Outline Basics Types of fungal sinusitis Management What's new
Forms yeast or mold Yeast Unicellular Reproduce asexually by buddingPseudohyphae – when bud doesn’t detach from yeast Mold Multicellular Grow by branching – hyphae
How to differentiate ? 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
Fungal Ball Sequestration of fungal elements within a sinus without invasion or granulomatous changes Presents similar to rhinosinusitis, Cocosmia peanut-butter like appearance Frontal/ Maxillary sinus most common followed by sphenoid sinus Surgical Removal with restoration of drainage of the sinus
Saprophytic Fungal Infestation After sinonasal surgery Visible growth of fungus on mucus crusts without invasion Diagnosis: Endoscopic visualization of crusts with fungi Treatment: Weekly nasal endoscopy with removal of crusts until disease process resolves
Allergic Fungal Rhinosinusitis Most common form Hypersensitivity reaction to inhaled fungal organisms Typical allergic Mucin Diagnostic criteria (Brent & Khun ) : 1) Nasal Polyps 2)The presence of eosinophilic mucin 3) Characteristic CT 4) + ve Fungal culture and/or smear 5) Fungus-specific IgE is demonstrated 6) immunocompetent
AFRS
MRI
Microscopic examination Charcot - Leyden crystals
Managment Surgical removal of allergic mucin restoration of normal sinus drainage is goal Stepwise management : Topical Steroids Antileukotrienes inhibitors Antifungal Biologics Oral steroids Experemental Therapies
Acute Invasive Fungal Sinusitis Mortality 50 - 80% Typically Immunocompromised 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
Acute Invasive Fungal Sinusitis Spores inhaled = fungus grows in warm, humid sinonasal cavity Fungi invade neural and vascular structures with thrombosis of feeding vessels Mucor causes obliterative vascular invasion leading to ischemia. Necrosis and loss of sensation = acidic environment = further fungal growth Extrasinus extension occurs via bony destruction , perineural and perivascular invasion
CT scan Unilateral ethmoid involvement with bone destruction intraorbital spread and proptosis
MRI
Managment 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 once the acute stage has passed Reversal of cause of immunosuppression if possible Intracranial spread is most predictive of mortality
Chronic Invasive Fungal Sinusitis Slower disease process than acute Biggest difference: Most patients are immunocompetent Usually persistent and recurrent disease Noncontrast CT – Hyperattenuating soft tissue mass withing one or more of paranasal sinuses, bone involvement with or without sclerosis MRI – decreased signal on T1& T2
Management Similar to acute – surgical + medical Start with Amphotericin B until can rule out Mucormycosis Best length of treatment not well studied Most recommend 3-6 months of therapy Close F/U and debridement required Biopsy anything that is suspicious as asymptomatic recurrence is not uncommon
Granulomatous Invasive Fungal Sinusitis Same entity as chronic invasive fungal sinusitis Primarily found in Africa and Southeast Asia, only few case reports in US Immunocompetent Caused by Aspergillus flavus Characterized by noncaseating granulomas in the tissues