ORIGINAL RESEARCH PAPER Volume - 10 | Issue - 02 | February - 2021 | PRINT ISSN No. 2277 - 8179 | DOI : 10.

36106/ijsr

INTERNATIONAL JOURNAL OF SCIENTIFIC RESEARCH

MUCORMYCOSIS OF MAXILLOFACIAL REGION IN A DIABETIC PATIENT: A
CASE REPORT, REVIEW OF LITERATURE AND AN INSIGHT INTO VARIUOS
MANAGEMENT MODALLITIES.
Dental Science
Srikanth MDS, Assistant Professor, Department of Oral and Maxilliofacial Surgery, St. Joseph
Kasaraneni* dental college, Duggirala, Eluru, 534003. *Corresponding Author
S. Ravi Raja MDS, Professor and HOD, Department of Oral and Maxilliofacial Surgery, St. Joseph
Kumar dental college, Duggirala, Eluru, 534003.
D. Vamsi Krishna MDS, Associate Professor, Department of Oral and Maxilliofacial Surgery, St. Joseph
Reddy dental college, Duggirala, Eluru, 534003.
Post graduate student, Department of Oral and Maxilliofacial Surgery, St. Joseph dental
Sowmya Mantha college, Duggirala, Eluru, 534003.
Soundarya Post graduate student, Department of Oral and Maxilliofacial Surgery, St. Joseph dental
Mopidevi college, Duggirala, Eluru, 534003.
Post graduate student, Department of Oral and Maxilliofacial Surgery, St. Joseph dental
K. Anant Nag college, Duggirala, Eluru, 534003.
ABSTRACT
Fungi of the order Mucorales causes an invasive and potentially lethal infection known as mucormycosis. It is a devastating disease in patients with
poorly controlled diabetes mellitus and immunocompromised conditions. The infection either begins in the nose and paranasal sinuses due to
inhalation of fungal spores or an ulcer or extraction of teeth aids as portal of entry. The infection can also spread to orbital and intracranial structures
either through direct invasion or the blood vessels. It is an aggressive infection that needs to be addressed promptly to prevent fatal consequences.
We report a case of maxillary necrosis in an uncontrolled diabetic patient due to mucormycois to emphasize importance early diagnosis and
treatment of this potentially fatal fungal infection. We briey review the literature of rhinocerebral mucormycosis in terms of its pathogenesis,
portal of entry and predisposing factors, incidence and forms, clinical features, diagnosis, differential diagnosis and various management options.
KEYWORDS
Mucormycosis, immunocompromised patient, diabetes mellitus, maxillary necrosis.
INTRODUCTION: tissues, further hematogenous spread to other vital organs can occur
Mucormycosis (also known as zygomycosis and phycomycosis) is the (lung, brain, and so on) and results in sepsis.5
name attributed to infections caused by nonseptate fungi that belong to
the class Zygomycetes (Phycomycetes).1 Paltauf 2 was credited with Type-2 diabetes is more frequently associated with mucormycosis.
the rst histologic description of generalized mucormycosis in a 52- Tugsel et al.7 also reported that Type I diabetes mellitus is most
year-old patient. Since this report appeared in 1885, opportunistic commonly associated with 40% of mucormycosis cases overall.
infections caused by fungi of the order Mucorales (genera Rhizopus, Diabetes mellitus is one among the most common endocrinal disorders
Mucor and Absidia) have been recognized, in association with which alter many physiological processes, presenting as diminished
diabetes, hematologic malignant disease, immunosuppressive therapy, resistance to infections, vascular and micro vascular changes, and
thermal burns and surgery. Mucormycosis rarely affects otherwise altered tissue response. Patients with diabetic ketoacidosis have a
healthy people.1 These fungi usually ubiquitory and found in fruits, signicantly high risk for mucormycosis.8 Early studies by Chinn et al 9
soil, and feces and also can be cultured from the nasal passages, oral and Artis et al 10 had proved that diabetic ketoacidosis impairs
cavity and throat of healthy disease-free individuals. The spores of chemotaxis and the phagocytic activity of neutrophils and increases
these organisms are usually dispersed into air from decaying material,3 available serum iron respectively. Since Iron is required for the growth
The fungi are usually avirulent; when the host resistance is of a variety of microorganisms, with its availability being especially
exceptionally low, they become pathogenic.4 important in the case of mucormycosis11 as has been proved by the
studies of Boelaert et al 12.
PORTAL OF ENTRY AND PREDISPOSING FACTORS:
Mucormycosis of the maxillofacial region can be of two different INCIDENCE AND FORMS:
origins. One is from disseminated infection where the portal of entry is The incidence of mucormycosis is not related to age or sex. There are
inhalational (through the nasal cavity) and the other is through direct six well-known clinical forms of mucormycosis, based on various
wound infection with dissemination to other vital organs as a common systemic-involvement-namely:
complication.5 The predisposing factors are uncontrolled diabetes, 1.Rhino-orbito-cerebral,
particularly in patients having ketoacidosis, malignancies such as 2.Pulmonary,
lymphomas and leukemias, renal failure, organ transplant, long-term 3.Gastrointestinal,
corticosteroid and immunosuppressive therapy, cirrhosis, burns, 4.Cutaneous,
protein energy malnutrition and AIDS. 6 5.Disseminated,
6.Miscellaneous.
PATHOGENESIS:
Mucormycosis infection is caused by an asexual spore formation. Rhino-orbito-cerebral mucormycosis is the most common among the
These tiny spores become airborne and eventually settle on the oral and six forms and is noted commonly in uncontrolled diabetic patients.
nasal mucosa of humans. In most of the immune-competent hosts, Pulmonary form is usually seen in patients with leukemia and
these spores will be narrowed by a phagocytic response. In case this receiving chemotherapy, may develop due to inhalation or by vascular
response fails, germination will continue and hyphae will be mode. Gastrointestinal mucormycosis is rare, and if occurs believed to
developed. In immunocompromised hosts as polymorphonuclear occur in extremely malnourished children. Cutaneous forms are
leukocytes are less effective in removing hyphae, the infection usually noted in patients with disruption of the normal protective skin,
becomes established, and further progresses as hyphae begin to invade especially in cases of burns. Dissemination form is seen more
the arteries, wherein they propagate within the vessel walls cause frequently in patients with pulmonary mucormycosis while it is less
thrombosis, ischemia, and infarction with dry gangrene of the affected common in gastrointestinal or cutaneous form. The most common site
72 International Journal of Scientific Research
Volume - 10 | Issue - 02 | February - 2021
for dissemination mucormycosis is brain, but is also noted in other
parts of the body.13
CLINICAL FEATURES:
Clinically, rhinocerebral mucormycosis can present with atypical
signs and symptoms similar to bacterial rhinosinusitis, such as:
headache, fever, unilateral facial swelling 14 or to orbital cellulitis, with
the presence of palpebral oedema, ptosis, chemosis, and
ophtalmoplegia. Cranial nerves V and VII can also be affected.
Affected tissue may appear normal initially, after progressing to
erythema, violaceous aspect and nally developing a black necrotic
eschar due to the occlusion vessels and tissue necrosis. This black
eschar, in the palatal or intranasal region, is highly suggestive of
mucormycosis, but it is not always present 15. Progression of infection
to central nervous system is heralded by development of confusion and
disorientation 16, with bloody nasal discharge also reported as a
potentially early sign of disease extension to the brain. Central nervous
system damage may also result from cavernous sinus thrombosis and
internal carotid artery encasement leading to cerebral infractions and
hematogenous dissemination of the disease to other organ sites17.
DIAGNOSIS:
Diagnosis of mucormycosis requires thorough clinical history and
evaluation of underlying medical illness. Moreover, presence nasal or
palatal necrosis raises strong suspicion of this condition. Computed
tomography (CT) is considered to be one of the initial imaging
methods of choice for the detection of mucormycosis, but in the early
stages of the disease ndings may be non-specic (Dhiwakar et al.,
2003) 18 and even invasive mucormycosis may be present with a
normal sinus CT. Evidence of bony erosion and extra sinus spread are
strongly suggestive of the diagnosis. Magnetic resonance imaging
(MRI), is a better and more sensitive system for detecting invasive soft
tissue being the imaging method of choice to identify its extra sinus
spread (Rapidis, 2009) 19.
Denitive diagnosis can only to achieve through of histological study
identifying the characteristic hyphae, after performing a biopsy of
involved area.20 Histologically, it is characterized by extensive tissue
necrosis and the presence of numerous and irregular broad, nonseptate,
hyphae that branch in right angle (Ferguson, 2000) 21. Other methods
for helping diagnosis have been described. These include ne needle
aspiration and nasal scraping, calcouor uorescence and quantitative
polymerase chain reaction system. In the present case, the same
histopathology was revealed. The histopathological differential
diagnosis includes aspergillosis where the hyphae of Aspergillus
species are septate, smaller in width and branch at more acute angles.
DIFFERENTIAL DIAGNOSIS:
Differential diagnosis of this entity should include squamous cell
carcinoma, chronic granulomatous infection like tuberculosis, tertiary
syphilis, midline lethal granuloma, Wegener's granulomatosis and
other deep fungal infection. 22,7
MANAGEMENT:
Mucormycosis was considered to be fatal until the 1960s, when
amphotericin B was introduced as a treatment. Amphotericin B is a
fungistatic rather than fungicidal agent, which contributes to the
lengthiness of treatment23. Treatment of mucormycosis consists of
surgical debridement; systemic antifungal therapy and treatment of
any underlying condition are most effective methods. Control and
prevention of opportunistic fungal infection in patients suffering from
debilitating diseases such as diabetic ketoacidosis,
immunodepression, blood dyscrasia, solid organ transplant, patients
on long term steroids and bone marrow transplant is very important.
Once mucormycosis infection diagnosed in debilitated patients, it
must be treated proptly, without any delay, by different modalities,
medically and surgically.24
The agent of choice is AmB. Two formulations of amphotericin B are
available namely amphotericin B deoxycholate (ABD), Liposomal
amphoterecin B (LAMB). This polyene agent binds to sterols and
forms transmembrane channels; consequently, forming pores that
disrupt the fungal cell wall synthesis. Conventional AmB (1–1.5
mg/kg/d IV) can be used, but the dose should be temporarily reduced
when serum urea nitrogen level exceeds 40 mg/100 mL or serum
creatinine level exceeds 3.0 mg/100 ml. conventional AmB is
associated with more toxic effects like nephrotoxicity 25. So, lipid
preparations of AmB (liposomal AmB) are used which appear to be
PRINT ISSN No. 2277 - 8179 | DOI : 10.36106/ijsr
less toxic and provide the same therapeutic effect. Liposomal AmB
increases circulation time and alters the biodistribution of the AmB, so
they are able to localize and reach in greater concentrations in infected
and inamed tissues. Further, a 50 % lethal dose of liposomal AmB is
approx. 10–15 times higher than that of conventional Amphoterecin.26
Posaconazole, a triazole, is considered as a second-line drug for
management of Mucormycosis. It has been effectively used in
sequential therapy at a dosage of 400 mg twice daily after the
administration of liposomal amphotericin, as achieving steady-state
plasma concentrations of the drug take approximately one week. This
drug is shown to be safe despite use varying from months to years by
several studies.27
Isavuconazole is a novel azole that shows in vitro activity against
mucorales comparable to that of posaconazole. A water-soluble
prodrug, isavuconazonium sulfate, which is suitable for intravenous
and oral administration, is under clinical development and is rapidly
cleaved into the isavuconazole active moiety with an oral
bioavailability in humans that approaches 100 %. 28
Surgery is the mainstay in management for any form of mucormycosis.
Early and aggressive surgical debridement of all infected and
devitalized tissue is considered to be the best approach without which
mucormycosis almost always is fatal. Surgical treatment for
mucormycosis is based on the overall general condition of the patient
and response to the medical therapy. Wide surgical debridement of the
infected tissue is essential and may include partial or total
maxillectomy, mandibulectomy and orbital exenteration. Surgery
should be initiated without delay once the diagnosis is conrmed, and
repeat surgical debridement may be required for local control of the
condition. Although it has been reported that surgery alone is not
curative, an aggressive surgical approach appears to improve survival.
Orbital exenteration must be assessed on a case-by-case basis as,
29
although it may life-saving, it is not necessary in all patients with
evidence of orbital disease. The decision is dependent of the
aggressiveness of presentation, the type of underlying disease process
and response to initial therapy. Surgical treatment can be
complemented with systemic antifungal agents (polyenes, azoles, etc.)
that permit control of infection in regions where vital tissue cannot be
completely resected.
Total duration of therapy for mucormycosis should be individualized
for each patient, being continued until resolution of infection and
radiographic imaging shows absence or stabilization of the disease
with resolution of underlying immunosuppression.
Hyperbaric oxygen therapy aids neovascularization, promoting
healing in poorly perfused acidotic and hypoxic but viable areas of
tissue. It should consist of exposure to 100 % oxygen for 90 min at
pressures from 2.0 to 2.5 atm with 1 or 2 exposures daily, for a total of
40 treatments. Hyperbaric oxygen therapy may prove to be effective in
patients who appear to be deteriorating despite optimal medical and
surgical therapies. 30 Other therapies may include nebulized/local
irrigation with AmB, topical hydrogen peroxide, leukocyte
transfusions, treatment with interferon-gamma, polyvalent
immunoglobulin, and the combination of AmB with ucytosine,
rifampin, or uconazole.
Due to the role of iron metabolism in the pathogenesis of
mucormycosis, it is possible that iron chelators serve as adjuants in
combination with antifungal therapies.31
Prompt removal of the involved soft tissue and bones is necessary for
achieving disease-free status locally. Conrmation of disease-free
status by combining tissue diagnosis and clinical examination is an
essential prerequisite before reconstruction.
Mucormycosis is the most fatal fungal infection in humans, with
mortality rates of 15–34. Death may occur within several days to a few
weeks, even when appropriate treatment has been instituted.19
Mucormycosis once regarded as fatal, now with early medical and
surgical management survival rates, is thought to exceed 82 %.32
CASE REPORT:
A 50-year-old female patient reported to the Maxillofacial Surgery
Department, St. Joseph dental college, Duggirala, Eluru in March
2019 with exposed bone in the upper jaw and pain for one-month
duration.
International Journal of Scientific Research 73
Volume - 10 | Issue - 02 | February - 2021 PRINT ISSN No. 2277 - 8179 | DOI : 10.36106/ijsr

The patient's medical history showed that she is diabetic and was under
regular treatment with oral anti diabetics. The patient gave a history of
pain in the left front tooth region 1month prior to that she visited our
department. She used clove oil for pain, then after 1week she visited a
local dentist, as her blood sugar levels were not under control the
extraction of tooth was postponed till blood sugar level were under
control. Within these days' patient observed whitish discoloration of
palate and again went to local dentist and got extraction of 22 without
bothering high blood sugar values. As the extracted socket site and
palatal area didn't heal properly, her blood glucose levels were
rechecked and found to be very high. Patient was started insulin
therapy by a local physician and was referred to our institute for further
management.

On extra oral examination there was diffuse swelling over the left
cheek region (FIGURE 1). An intra oral examination revealed
exposed necrotic greyish white coloured tissue over the anterior palate
region, and missing 22 teeth (FIGURE 2). On removing then necrotic
tissue, there was exposed bone in the anterior palate region and pus in
the left vestibule. The tissue was sent for HPE. On palpation there was Fig. 4: 3DCT Images.
mobility of exposed bony segment on the left side. Biochemical investigation revealed elevated blood sugar levels (FBS:
211mg/dl), and a provisional diagnosis of chronic osteomyelitis of
maxilla was made. Patient was started with IV clindamycin, metrozyl
regimen and debridement and irrigation with saline was done. Her
blood sugar values were thoroughly maintained and insulin therapy
was initiated.

Histopathologic evaluation of submitted tissue revealed features

suggestive of mucomycosis. Since there were concomitant opacities in
frontal, ethmoidal and sphenoidal sinuses the patient was referred to a
neurosurgeon for review regarding the cerebral involvement.

The neurosurgeon advised to continue with the surgery as there were

Fig. 1: Diffuse Swelling Over The Left Cheek Region.
no cerebral signs and symptoms. A subtotal maxillectomy was planned
under general anaesthesia. Based on the CT scan image, margins of
resection were planned. Extraction of 14 was done and osteotomy cut
was made thus cuts socket labially and palatally. The palatal osteotomy
cut was made to cross the midline in an angulated manner to join
pterygoid plates on the left side. The labial cut from 14 was extended in
a horizontal manner above the root apices of 13,12 and 11. Now it is
extended along the lateral nasal rim on the left side to reach 2mm below
infraorbital foramen and then angulated down to join the pterygo
tuberosity region on the left side (FIGURE 5). Now the osteotomised
maxilla was removed in one piece (FIGURE 6) followed by through
curettage and debridement. The resultant defect was meticulously
cleaned and surgical obturator was secured in position (FIGURE 7).
The specimen was sent for histopathological evaluation.

Fig. 2: Necrotic Greyish White Coloured Tissue

A CT of maxillofacial region was advised and which revealed as non-

homogenous thickening in the left maxillary sinus, erosion of bone
involving pterygoid plates on left side, left maxillary sinus wall, hard
palate and greater wing of sphenoid and adjacent temporal bone left
side. Opacities in frontal, ethmoidal and sphenoidal sinuses with
orbital cellulites in the inferior aspect of the left orbit (FIGURE 3,4).

Fig.5: Osteotomy Cuts

Fig.3: CT Images Fig.6: Defect After Debridement

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Volume - 10 | Issue - 02 | February - 2021
Fig.7: Surgical Obturator Secured
Histopathological evaluation of the surgically excised specimen
revealed Para keratinised stratied squamous epithelium and ciliated
pseudo stratied epithelium in some areas. The underlying
brovascular connective tissue shows endothelium lined capillaries
with thick walls and dilated arterioles. inammatory inltrate with
lymphocytes, plasma cells, large macrophages, with hyphae within
and multinucleated giant cells are present. PAS stain positive aseptate
fungal hyphae are evident within the connective tissue (FIGURE 8,9).
These features are suggestive of mucormycosis.
Fig.8: H&E Staining
Fig.9: PAS stain
The patient was administered single daily dose of liposomal
amphoterecin –B 1mg /kg body weight was an infusion in 100ml of NS
over 1-2hr period for 3 weeks, the blood urea, creatine levels and liver
function tests were monitored for nephrotoxicity .The patient was sent
home on 22nd day with oral antibiotics and tab. ketoconazole 200mg
and advised to come for regular follow up 2 weeks sign of healthy
granulation tissue were seen and wound was healed uneventfully in
around 3 months , the patient was now under regular follow-up for the
past 2 years with no evidence of recurrence (FIGURE 10). Patient was
now suggested with denitive obturator prosthesis.
Fig.10: 2nd year post-op
PRINT ISSN No. 2277 - 8179 | DOI : 10.36106/ijsr
DISCUSSION:
The rising trend of mucormycosis associated with diabetes is
commonly seen in uncontrolled DM and has a fatality rate ranging
from 32% to 57%. In this present case, the patient had uncontrolled
diabetes mellitus, which is a very well-known predisposing factor and
also showed non healing extraction site, which might have played a
vital role, as the entrance point for infection.
In our present case the patient did not have any advanced stages signs
and symptoms, where patient presented with unilateral facial swelling,
ptosis, erythema, necrotic eschar on palate this is considered as
rhinocerebral form of mucormycosis.
CBCT shows bony erosion, involvement of sinus, and nasal cavity,
mucosal thickening as in our case. These features may be seen in other
diseases, but if CBCT shows bony erosion and sinus involvement in an
immunocompromised patient, invasive fungal sinusitis should be one
of the differential diagnosis. However, invasive fungal infections with
intracranial and orbital extensions are incompletely evaluated in
CBCT. Besides, soft tissue inltration with fat stranding is unlikely to
be recognized in CBCT in such cases, magnetic resonance imaging
(MRI) or Multidetector computed tomography (MDCT) are better
imaging modalities.8
Considering the imaging constraints, the gold standard of validating
diagnosis is tissue based pathologic examination on permanent
sections. Stains of xed tissues with hematoxylin and eosin or
specialized fungal stains, such as Grocott methenamine-silver or
periodic acid-Schiff stains, show broad-based, ribbon like, nonseptate
hyphae with wide-angle branching (approximately 90◦). 34 In the
present case, the same histopathology was revealed. The
histopathological differential diagnosis includes aspergillosis where
the hyphae of Aspergillus species are septate, smaller in width and
branch at more acute angles.
Treatment of this entity is multifactorial. The risk stratication for the
severity of the disease condition and early clinical and laboratory
diagnosis. Effective antifungal therapy (monotherapy or combination
therapy), aggressive surgical debridement of necrotic debris, a reversal
of immunosuppression, and management of the underlying medical
cause are the treatment modalities followed in mucormycosis 35. We
followed the same protocol in our case we rst started with managing
of underlying condition, a combined medical and surgical
management and reconstruction of the defect after long follow-up to
conrm its disease-free state.
CONCLUSION:
Because mucormycosis is associated with extensive local tissue
destruction and rapid progression, the condition warrants prompt
surgical debridement. Frequently, serial debridements may be
required. The urgency of diagnosis is underscored by the contribution
of immunosuppression; restoration of immune competency is an
additional cornerstone of therapy. Prognosis usually depends on
several factors such as infection site, rapidity of diagnosis, type and
severity of immunosupression and the like. The mortality rates were
nearly 85% in earlier days; however, after the introduction of
combined therapy, more than 80% of the patients can be expected to
survive.
CONFLICTS OF INTEREST:
The authors declare they have no potential conict of interests
regarding this article.
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