Lecture on Fungal Sinusitis

1. Dr Vasanthika Sanjeewanie Thuduvage
Consultant ENT and Head & Neck Surgeon
Senior Lecturer / Faculty of Medicine KDU

2.  400,000 known fungal species or which 400
are human pathogens and 50 of which cause
systemic or CNS infection
 Broadly categorized into invasive and
noninvasive

3.  Invasive
 Presence of fungal hyphae within the mucosa,
submucosa, bone, or blood vessels of the
paranasal sinuses
 Noninvasive
 Absence of fungal hyphae within the mucosa and
other structures of the paranasal sinuses

4.  Invasive
 Acute Invasive Fungal Sinusitis
 Chronic Invasive Fungal Sinusitis
 Chronic Granulomatous Invasive Fungal Sinusitis
 Noninvasive
 Allergic Fungal Sinusitis
 Fungus Ball (fungus mycetoma)

5.  Older individuals, female>male
 Immunocompetent
 May have a history of trauma or injury to
sinus
 Asymptomatic or minimal symptoms with
chronic pressure or nasal discharge
 Cacosmia (perception of foul odor when no
such odor exists)
 fumigatus and dematiaceous fungi most
commonly cause fungal ball

6.  Mass within the lumen of paranasal sinus and is
usually limited to one sinus
 peanut-butter like appearance
 Frontal/Maxillary sinus most common followed by
sphenoid sinus
 Noncontrast CT – hyperattenuating mass often with
punctate calcifications
 MRI – variableT1 and hypointenseT2 due to
absence of free water, calcifications and
paramagnetic metals also generate decreasedT2
signal – no central enhancement to differentiate
from neoplasm

7.  Noncontrast CT – hyperattenuating mass
often with calcifications
 MRI – variableT1 and hypointenseT2 due to
absence of free water, calcifications and
paramagnetic metals also generate
decreasedT2 signal – no central
enhancement to differentiate from neoplasm

9.  High density material with thickened walls of the
maxillary sinus due to chronic inflammation

11.  Surgical Removal with restoration of
drainage of the sinus
 Antifungal medications usually unnecessary
 Recurrence is rare

12.  Most common form of fungal sinusitis
 Common in warm, humid climates
 Hypersensitivity reaction to inhaled fungal
organisms resulting in chronic noninfectious
inflammatory reaction - IgE type I immediate
hypersensitivity and type III hypersensitivity are
involved
 Common organisms implicated – Bipolaris,
Curvularia, Alternaria, Aspergillus, and Fusarium
 “Allergic mucin” within affected sinus which is
inspissated mucous the consistency of peanut
butter with eosinophils on histology

13.  Younger individuals, third decade,
immunocompetent
 Often associated history of atopy with
allergic rhinitis or asthma
 Chronic headaches, nasal congestion, and
chronic sinusitis for years

14.  Usually bilateral with multiple sinuses involved if not
pansinus involement
 Often has a nasal component
 Noncontrast CT – high attenuation allergic mucin
within lumen of sinuses – can mimic a mucocele
with expansion of the sinus
 MRI – variableT1 appearance, lowT2 signal
(attributed to high concentration of iron,
magnesium, and manganese concentrated by
fungal organisms and also due to a high protein, low
free water content of allergic mucin

16.  Moderately highT1 signal, lowT2 signal with
expanded sinus can be seen in allergic fungal
sinusitis, mucocele, or sinonasal polyposis

17.  Surgical removal of allergic mucin with
restoration of normal sinus drainage is goal
 Longterm use of topical nasal steroids helps
suppress the immune response and minimize
recurrence
 ? Low dose oral steriods/ ? Immune therapy
 Topical or systemic antifungals are not
indicated

18.  Most lethal form of fungal sinusitis – mortality 50-
80%
 Rare in immunocompetent patients
 Two clinical populations
 Poorly controlled Diabetics – ususally caused by
fungi of order Zymocycetes (Rhizopus,
Rhizomucor, Absidia, and Mucor)
 Immunocompromised with severe neutropenia
(chemotheraphy patients, BMT, organ
transplants, AIDS) – Aspergillus accounts for 80%
of infection in this group

19.  Necrotic nasal septum ulcer (eschar), sinusitis, rapid
orbital and intracranial spread resulting in death
 Angioinvasion and hematogenous dissemination
common
 Present with fever, facial pain, nasal congestion,
epistaxis progressing to proptosis, visual
disturbance, headache, mental status changes,
seizures as spread occurs
 73% of patients with intracranial spread die

20.  Noncontrast CT
 Severe unilateral nasal cavity soft tissue
thickening is most consistent (but nonspecific)
early CT finding
 Hypoattenuating mucosal thickening within
lumen of paranasal sinus with rapid aggressive
bone destruction of sinus walls occurs as disease
progresses
 Unilateral involvement of ethmoids, sphenoids
 Intracranial extension can result in cavernous
sinus thrombosis, carotid artery invasion,
occlusion, or pseudoaneurysm

21.  Unilateral ethmoid involvement with bone
destruction, intraorbital spread and proptosis

22. Aspergillus involving the sphenoid sinus with invasion of the left
cavernous sinus, thrombosis, extension to the left sylvian fissure and
infratemporal fossa with cerebral infarctions.

23.  MRI – better for evaluating intracranial and
intraorbital extension
 Evaluate for inflammatory change in orbital fat
and extraocular muscles
 Obliteration of periantral fat is a subtle sign of
extension
 Leptomeningeal enhancement progressing to
cerebritis and abscess

24. Aspergillus in left maxillary sinus with extension anterior and
posterior to the retroantral space. There is diffuse involvement of
the muscles of mastication.

25.  Aggressive surgical debridement and
systemic antifungal therapy
 High doses of Amphotericin B (1-1.5
mg/kg/d) are recommended. Oral
Itraconazole (400 mg/d) can replace
Amphotericin B once the acute stage has
passed
 Reversal of cause of immunosuppression if
possible
 Intracranial spread is most predictive of
mortality

26.  Inhaled fungal organisms deposited in nasal
passageways and paranasal sinuses
 Progression over months to years with fungal
organisms invading mucosa, submucosa,
blood vessels, and bony walls
 Organisms – Mucor, Rhizopus, Aspergillus,
Bipolaris, and Candida

27.  Usually immunocompetent
 History of chronic rhinosinusitis
 Usually persistent and recurrent disease
 Maxillofacial soft tissue swelling, orbital
invasion with proptosis, cranial neuropathies,
decreased vision, can invade cribiform plate
causing headaches, seizures, decreased
mental status

28.  Noncontrast CT – Hyperattenuating soft tissue mass
withing one or more of paranasal sinuses, bone
involvement often gives mottled appearance with
or without sclerosis
 May mimic malignancy with masslike appearance and
extension beyond sinus confines
 MRI – decreased signal onT1, markedly decreased
signal onT2 weighted images

30.  Surgical exenteneratin of affected tissues and
systemic antifungal
 Amphotericin B (2 g/d) is recommended; this
can be replaced by Ketoconazole or
Itraconazole
 Needs aggressive treatment

31.  Primarily found in Africa (Sudan) and
Southeast Asia, only few case reports in US
 Immunocompetent
 Caused by Aspergillus flavus
 Characterized by noncaseating granulomas in
the tissues

32.  Chronic indolent course similar to chronic
invasive fungal sinusitis
 Considered by some as same entity as
chronic invasive fungal sinusitis
 Imaging characertistics are similar to those
of chronic invasive fungal sinusitis
 Often resembles a mass/neoplasms
 Treatment is surgical debridement and
systemic antifungals

33.  Amphotericin B
Acute renal failure, anemia, agranulocytosis,
acute liver failure, cardiopulmonary
hypertension, and hemorrhagic
gastroenteritis.
 Itraconazole and fluconazole
Drug-induced cardiac dysrhythmias, hepatic
dysfunction, urticaria, and anaphylaxis.

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