Fungal Sinusitis Flashcards
Regarding fungal sinusitis, how is it typically classified?
FUNGAL SINUSITIS = INVASIVE VS. NON-INVASIVE
INVASIVE:
1. Acute/Fulminant Invasive
2. Chronic/Indolent Invasive
3. Granulomatous Invasive
NON-INVASIVE:
1. Saprophytic (now called Localized Fungal Colonization)
2. Mycetoma (aka. fungal ball)
3. Allergic fungal rhinosinusitis (aka Fungus related Eosinophilic)
Regarding acute invasive fungal sinusitis, discuss:
1. What are features on presentation? 7
2. What are the risk factors? 1
6. How is it diagnosed?
7. What is the treatment? Name 5
7. What is the mortality rate?
Mortality rate = 50-80%
PRESENTATION:
1. PODS features
2. Headaches
3. Fever
4. V2 paresthesias
5. Palatal or nasal necrosis
6. Proptosis or vision changes
7. Other cranial nerve deficits
RISKS:
1. Immunocompromised patients
DIAGNOSIS:
1. Physical Examination
- Endoscopic evaluation
- CT Sinuses
- biopsy in high risk patients (ideally ensuring coagulopathy and ensure platelets > 60 prior to doing biopsy)
TREATMENT:
1. Correct underlying immunodeficiency!!
2. Serial surgical debridement until circumferential healthy bleeding tissue
3. Systemic antifungals
- Amphotericin B IV 1mg/kg/day - lipid based is more expensive, less nephrotoxic and can maintain higher doses
- Voriconazole or Itraconazole if not mucor
- Posaconazole is used often for secondary prophylaxis (e.g. after an episode of AIFR)
- Nasal rinses (ampho B nasal rinses)
4. Correct hypoglycemia
5. ICU consultation
6. ID consultation
7. Hyperbaric oxygen (controversial)
Kevan Page 33
Acute invasive - common organsism? Name 5
CAUSATIVE ORGANISMS:
1. Aspergillus (more common in immune compromised with neutropenia)
2. Zygomycetes species (infection with this species is called mucormycosis; more common seen in DKA patients)
a/ Mucor
b/ Rhizomucor
c/ Absidia
d/ Rhizopus
e/ Apophysomyces
3. Bipolaris
4. Candida
Describe the histopathology of acute invasive fungal sinusitis.
Name 3 differences between mucormycosis and aspergillus.
Name 3 stains
PATHOLOGY FINDINGS:
Fungal stains:
A/ Gomori Methenamine silver (GMS) = Grocott
B/ Periodic Acid-Schiff (PAS)
C/ KOH stain
- Mucormycosis
- Broad and ribbon like (10-15µm)
- No septae
- Irregular, 90 degree branching
Think fast growing so no time to form septae; spreads quickly so 90deg branching pattern and broad - Aspergillus
- Narrow hyphae
- Regular septations
- Acute angle branching (e.g. 45degrees)
Think slower growing so septated, less rapid spread so acute branching and narrow
Discuss Chronic Invasive Fungal Sinusitis:
1. What is the most common organism cultured?
3. What is the most common risk factor?
4. What is the common histopathological finding?
Most common organism = Aspergillus Fumigatus most common (but other fungi from acute can also cause it)
Most common risk factor:
1. Diabetes (more commonly associated)
Histopathological finding: Associated with dense collections of fungal hyphae
- What is the most common clinical presentation of chronic invasive FS?
Most common presentation:
- Orbital apex syndrome is more commonly seen with CIFS (dysfunction of the optic nerve and CNs - vision loss, ptosis, complete internal and external ophthalmoplegia due to process in the optic canal and superior orbital fissure)
Regarding Granulomatous Invasive Fungal Sinusitis, discuss:
1. Where are common geographic locations this is seen? 4
2. What is the most common organism? 1
3. What is the common histopathology findings? 2
4. What is the main difference between this and Chronic Invasive Fungal Sinusitis clinically?
Historically known as primary paranasal aspergillosis granuloma in Sudan
Locations seen:
- North Africa
- India
- Pakistan
- Saudi Arabia
- Sudan area
Organism: Aspergillus Flavus
Pathology:
1. Non-caseating granulomas
2. Multinucleated giant cells
*Similar findings with GIFR and Chronic IFR. Major differentiating feature are the presence of enlarging granulomatous masses in the paranasal sinuses and face
What is Localized Fungal Colonization of Nasal/Paranasal mucosa? How is it treated?
Historically called: Saprophytic fungal sinusitis
Defined by visible growth of fungus on mucous crusts within the sinonasal cavity
- Fungus grows on CRUST, doesn’t involve the mucosa
Treatment:
1. Saline irritation and serial debridement
2. Systemic antifungals and imaging not needed
Vancouver 442
Regarding Mycetoma (fungal ball), discuss:
1. What are the common clinical features?
2. What is the most common organism?
3. What are imaging findings? 5
4. Histology findings? 3
5. What is the common treatment?
Mycetoma/fungal ball - not a true tumor
Features:
- Inspissated (thickened) fungal debris, without invasion
Most common organism:
1. Aspergillus Fumigatus (as with CIFS)
2. Dematioceous fungi
Imaging findings:
1. Usually a single sinus affected (Maxillary most common > Sphenoid > others)
2. CT: Double density sign - The fungal ball is hyperattenuated (bright, due to dense matted fungal hypae ± punctate calcifications) while the surrounding inflammed mucosa is hypoattenuated.
3. CT: Soft tissue opacification of the sinus ± calcification
4. CT: No bony erosion, but bones of the sinus might be thick
5. MRI: the mucosa is hyperenhacing while the fungal ball is not (absence of free water, T1/T2 both hypointense)
6. MRI: Calcifications and paramagnetic metals (iron, magnesium, manganese) –> areas of signal void on T2
Histology:
1. “Ripple” effect of fungal hyphae separate from adjacent mucosa, fungal hyphae without invasion inflammatory response
2. Fungus stains with GS and PAS
Treatment:
1. Complete surgical debridement/removal of the fungal ball
2. Thorough irrigation
Regarding allergic fungal rhinosinusitis, discuss:
1. What is the type of hypersensitivity reaction?
2. What are the possible causative organisms? 8
Type of hypersensitivity reaction:
- Type 1 and Type 3 hypersensitivity reaction to fungal antigens
Organisms (“ABCDEFGH”)
A: Alternaria
B: Bipolaris
C: Curvularia, Cladosporium
D: Drechslera
E: Exserohilum, Exophilia
F: Fusarium
G: AsperGillus
H: Helminthosporium
In order of frequency:
1. Bipolaris (most common)
2. Curvularia
3. Aspergillus
4. Alternaria
Nadia Rhinology Resident lecture
Staging of AFRS
KUPFERBERG STAGING SYSTEM
1. Stage 0: No evidence of disease (no edema/mucin)
2. Stage 1: Mucosal edema
3. Stage 2: Polypoid edema
4. Stage 3: Polyps
- Vancouver modification adds suffixes
- A: Without allergic mucin
- B: With allergic mucin
AFRS:
Pathologic findings - 3
Radiologic findings - 4
PATHOLOGIC FINDINGS
1. Charcot-Leyden Crystals: Formed frombreakdown of granules of eosinophils (allergic inflammation) – therefore seen in lots of eosinophilic/allergy entities
2. Eosinophilic mucin
3. May have sparse fungal hyphae on KOH/PAS/Grocott
RADIOLOGIC FINDINGS: “ABDDES”
1. Asymmetric sinus (AFS unilateral up to 50%)
2. Bone erosion
3. Heterogenous opacification (double density)
4. Displacement of neighbouring structures
5. Expansion of the sinus
6. Serpiginous (Scattered) areas of high attenuation “star-filled sky” pattern
What is the diagnostic criteria for allergic fungal rhinosinusitis
DIAGNOSTIC CRITERIA: BENT & KUHN CRITERIA
- 5 major criteria (need to meet all 5)
- 6 minor criteria (support diagnosis only)
Major Criteria (PEN1S)
P: Pathology (Fungal stains/smears)
E: Eosinophilic Mucin with non-invasive fungal hyphae
N: Nasal polyposis
1: Type 1 Hypersensitivity reaction to fungus (testing or history positive for fungal atopy)
S: Scan findings
- Serpiginous (Scattered) areas of high attenuation “star-filled sky” pattern, bony/sinus wall erosion, unilateral/asymmetric propensity
Minor Criteria (ABCDEF)
A: Asthma
B: Bony Erosion
C: Charcot-Leyden Crystals
D: Directionality (unilateral disease)
E: Eosinophilia (serum)
F: Fungal cultures
Treatment of AFRS. List 5 things
Treatment:
1. Identical to CRSwNP - systemic and nasal steroids (e.g. pulmicort rinses)
2. FESS is the cornerstone of AFRS treatment, but has high recurrence rate without adjunctive therapy
3. Insufficient data for antifungal therapy, however some sources (Vancouver notes) - need to monitor liver function:
- Amphotericin B irrigations
- Itraconazole 200mg TID (40% improved, 20% worse)
4. Biofilm management (topical agents that can be added to nasal saline irrigation to reduce biofilms):
- Baby shampoo 1% irrigation
- Manuka honey irrigation (not proven)
- Mupirocin (bactroban)
- Xylotil, Xyloglucan, Sodium Hyaluronate
5. Biologics:
- Omalizumab (Xolair) monoclonal Anti-IgE
- Mepolizumab (Nucala) monoclonal anti-IL5
Follow up:
1. Serum total IgE (level correlates with mucosal disease burden)
2. Regular debridement/medication
What does eosinophilic mucin look like on histopathology in fungal sinusitis? 4
- Presence of eosinophils
- Charcot-leyden crystals (by-product of eosinophil degranulation)
- Fungal elements and hyphae
- Necrotic inflammatory cellular debris
Plus CEMEN
Charcot Leyden Crystals
Eosinophil cationic protein
Major basic protein
Eosinophil peroxidase
Neurotoxin
