Slide 1

Marilene B. Wang, MD, FACS Professor UCLA Division of Head Neck Surgery Chief of Otolaryngology VA Greater Los Angeles Healthcare System Slide 2 Slide 3 Slide 4 From Anterior Nasal Spine To Sphenoid Ostium7 cm To Pituitary Fossa8.5 cm Slide 5 Middle turbinate Lamina papyracea Ethmoid fovea Cribriform plate Sphenoid Slide 6 Facial pain/pressure Nasal obstruction/blockage Nasal discharge/purulence/discolo red postnasal drip Slide 7 Hyposmia/anosmia Purulence in nasal cavity on examination Fever (acute rhinosinusitis only) Slide 8 Headache Fever Halitosis Fatigue Slide 9 Dental pain Cough Ear pain/pressure/fullness Slide 10 Acute Subacute Chronic Recurrent, acute Acute exacerbations of chronic Slide 11 Duration up to 4 weeks > 2 major factors 1 major factor + 2 minor factors Nasal purulence on exam Slide 12 Duration 4-12 weeks >2 major factors 1 major factor + 2 minor factors, or nasal purulence on exam Complete resolution after effective medical therapy Slide 13 Duration > 12 weeks History same as for subacute Facial pain does not constitute suggestive history in absence of other nasal symptoms or signs Slide 14 >4 episodes/year + each episode last >7-10 days. Absence of intervening signs of chronic rhinosinusitis Slide 15 Sudden worsening of chronic rhinosinusitis Return to baseline after treatment Slide 16 Allergies Immunodeficiency Genetic/congenital Slide 17 Endocrine Neuromechanism Slide 18 Anatomic Neoplastic Acquired mucociliary dysfunction Slide 19 Microorganismsviral, bacterial, fungal Noxious chemicals, pollutants, smoke Medications Trauma Surgery Slide 20 S. pneum (20-43%) H. influenzae (22-35%) Strep spp. (3-9%) Anaerobes (0-9%) M. catarrhalis (2-10%) S. aureus (0-8%) Other (4%) Slide 21 S. pneum (25-30%) H. influenzae (15-20%) M. catarrhalis (15-20%) S. pyogenes (2-5%) Anaerobes (2-5%) Sterile (20-35%) Slide 22 Mild disease with no recent antimicrobial use Augmentin, Amoxicillin Vantin Ceclor Omnicef Slide 23 Tequin, Levaquin, Avelox Augmentin Combination (Amox or clinda + Suprax) Slide 24 Bactrim Doxycycline Zithromax, Biaxin, Erythromycin Switch to quinolone if no improvement in 72 hours Slide 25 Quinolone Augmentin Clindamcin + rifampin Consider IV abx Slide 26 Augmentin, Amoxicillin Vantin Ceclor Omnicef Switch if no improvement after 72 hours Slide 27 Bactrim Macrolide Slide 28 Augmentin Rocephin Bactrim, macrolide Consider IV abx if no improvement Slide 29 Afrin for 3 days Normal saline sprays Decongestants Antihistamines ?Steroids Slide 30 Periorbital cellulitis Preseptal cellulitis/abscess Orbital cellulitis Orbital abscess Cavernous sinus thrombosis Slide 31 Widespread afflictionthe most common allergic disease Affects 10-30% of American adults >20 million people, adults and children Results in missed work and school days, poor quality of life Slide 32 Allergic salute Shiners Itchy, red conjunctiva Sneezing Post-nasal drip, rhinorrhea, congestion Slide 33 Dust Mold, mildew Plants Animal dander Feathers/down Slide 34 Pollen Smog Trees, grasses, weeds Dust, fertilizer, chemicals Slide 35 Asthma Allergic fungal sinusitis Cystic fibrosis Mucociliary dysfunction Connective tissue disorders (Wegeners granulomatosis, sarcoid) Slide 36 Nasal polyposis Samters triad (aspirin sensitivity, nasal polyps, asthma) Cocaine use Slide 37 Antibiotics Antihistamines Nasal steroids Normal saline irrigations Allergy evaluation +/- immunotherapy Slide 38 Sinus CT scan Consider anatomic factors septal deviation, nasal polyps, concha bullosa, ostio-meatal blockage Slide 39 Nasal polyposis Anatomic blockagedeviated septum, enlarged turbinate, concha bullosa Mucocele Orbital abscess Slide 40 Fungal sinusitisallergic vs. invasive (mucor) Tumor of nasal cavity or sinus Slide 41 Chronic, recurrent sinusitis Failure to respond to maximal medical therapy Obtain cultures Slide 42 Nasal congestion Headache/sinus pain Fatigue Prolonged bleeding/crusting Slide 43 Breach of lamina papyracea damage to extraocular muscles, periorbital ecchymoses Damage to optic nerve blindness Breach of cribriformCSF leak Meningitis Slide 44 May be a lifelong disease Allergy control antiihistamines, nasal steroids, immunotherapy Oral steroidsjudiciously Antibiotics for acute exacerbations Slide 45 Environmental controlavoid carpet, damp, mold, older homes, smog Saline irrigations Slide 46 Alternative therapies acupuncture, stress management, herbal remedies Pain management Multi-disciplinary effortwork with allergy, infectious disease, neurology/pain management services Slide 47 4 types of allergic reactions (Gell and Coombs) Type 1 IgE Type 2 - IgG--antigen Type 3 Immune complex Type 4 Delayed hypersensitivity Slide 48 Mast cells bind IgE via their Fc() receptors Mast cell degranulates and releases mediators--produce allergic reactions Hypersensitivity usually appears on repeated contact with the allergen. Examples of type I allergic reactions Anaphylaxis, atopic asthma, atopic eczema, drug allergy, hay fever Slide 49 Antibody (IgG or IgM) directed against antigen on an individual's own cells, or against foreign antibody (after blood transfusion) Cytotoxic action by killer cells, or to lysis mediated by the complement system. Autoimmune hemolytic anemia, Goodpasture's syndrome, hemolytic disese of the newborn, myasthenia gravis, pemphigus Slide 50 Immune complexes (antigen and usually IgG or IgM) deposited in the tissue Complement is activated and polymorphonuclear cells are attracted, causing local tissue damage and inflammation. Polyarteritis nodosa, post-streptococcal glomerulonephritis, systemic lupus erythematosus Slide 51 T cells, sensitized to antigen, release lymphokines following secondary contact with the antigen Cytokines induce an inflammatory response, activate and attract macrophages, release inflammatory mediators. Antibodies produced against fixed cellular or tissue antigens are usually autoantibodies Crohn's disease, leprosy, tuberculosis, sarcoidosis, schistosomiasis Slide 52 Parents with allergy greater likelihood of producing allergic children Food allergies Environment air pollution Smoking Slide 53 Historyenvironmental exposure, smoking, seasonal occurrence, pets, foods Examination Allergic shiners Allergic salute Supratip crease Dennies lines (skin fold under eyes) Adenoid facies Slide 54 Skin testing Prick/puncture (scratch or patch) Intradermal Dilutional intradermal (skin end-point titration-SET) In vitro testing RAST (radioactive marker) ELISA (enzymatic marker) Slide 55 Prickfew drops of purified allergen pricked onto skin surface (dust, dander, pollen) Patchlarge patch with different allergens (latex, medications, metal, fragrances, preservatives) Histamine or glycerin used as positive controls Slide 56 Intradermal injection of allergens at increasing concentrations to measure allergic response Start with a very dilute solution If 2mm of growth noted, then second injection at a higher concentration is given to confirm the response End point is concentration of antigen that causes an increase in the size of the wheal followed by confirmatory whealing Stop at 13 mm Slide 57 Avoid medications which may interfere Antihistamines Antidepressants Antacids Slide 58 Anaphylaxis Low-grade fever Lightheadedness or dizziness Wheezing or Shortness of breath Extensive skin rash Swelling of face, lips or mouth Difficulty swallowing or speaking Slide 59 RAST -radioallergosorbent testdetect specific IgE antibodies to allergens Improved sensitivity without loss of specificity Excellent reproducibility across the full measuring range of the calibration curve Not always necessary to remove patient from an anthihistamine medication regimen If skin conditions (such as eczema) are so widespread that allergy skin testing can not be done Slide 60 ELISA enzyme linked immunosorbent assay Used more for food allergies Not as sensitive as skin tests Slide 61 Environmental control Stop smoking, clean house, avoid mold, indoor plants, pets, HEPA filter Pharmacotherapy Antihistamines, anti-leukotrienes, mast-cell stabilizers, topical and systemic steroids Slide 62 Specific allergens Vial test Intradermal test Smallest measurable dose Once or twice weekly injections Dose escalated Continue treatment 3-5 years Slide 63 Invasive Acute fulminant Chronic invasive Granulomatous invasive Slide 64 Noninvasive Saprophytic fungal infestation Fungal ball, mycetoma Allergic fungal rhinosinusitis Slide 65 Corollary to allergic bronchopulmonary aspergillosis (ABPA) AFRS cycle Immune and eosinophilic response to protein components of fungi Sinonasal inflammation, viscid allergic fungal mucin, obstruction, stasis Slide 66 Bony remodeling Inflammatory mediators Major basic protein Eosinophilic peroxidase Tumor necrosis factor Interleukins Interferons Slide 67 Evidence of Type I hypersensitivity (IgE mediated) Nasal polyposis Characteristic CT findings Eosinophilic mucous Positive fungal smear Kuhn and Javer: Otolaryngol Clin North Am 2000,33:2;419-432 Slide 68 Asthma Unilateral predominance Radiographic bone erosion Fungal culture Charcot-Leyden crystals Serum eosinophilia Kuhn and Javer: Otolaryngol Clin North Am 2000,33:2;419-432 Slide 69 Not all 5 criteria for diagnosis Gradual nasal airway obstruction Thick nasal mucous/crusts May take years to manifest AFS-like syndrome Slide 70 Immunocompetent Normal ESR, WBC Atopic Asthma, hay fever, inhalant allergy Nasal polyposis Slide 71 Hyperactive allergic inflammatory response Possible fungal toxin Inflammatory mediators Recurrent bacterial sinusitis Slide 72 Role of IgE Not consistently elevated in serum Local IgE-mediated immune response in nasal mucosa IgE as cause of inflammation or merely a marker Slide 73 Allergic response to fungus by skin testing and in vitro (radioallergosorbent) methodology Variable culture results (64-100%) from sinus contents Slide 74 Allergic fungal mucin Sheets of eosinophils Charcot-Leyden crystals Extramucosal fungal elements Slide 75 Slide 76 CT Unilateral or asymmetric Sinuses Expanded--Bony attenuation or erosion Displacement of adjacent structures Signal heterogeneity Manning S et al. Laryngoscope 1997;107:170-176 Slide 77 Slide 78 Slide 79 MRI-T1 weighted Variable signal intensity in involved sinuses Signal void at periphery (mucosal edema) MRI-T2 weighted Hypointensity of signal in sinus (dehydrated allergic fungal mucin) Enhancement of periphery of sinus (mucosal edema) Slide 80 Slide 81 Slide 82 Slide 83 Medical Surgical Break the Allergic Fungal Rhinosinusitis Cycle Slide 84 Functional endoscopic sinus surgery Complete ventilation of the sinuses Wide maxillary antrostomies Complete ethmoidectomies Sphenoid sinusotomies Frontal sinusotomies Slide 85 Complete removal of allergic fungal mucin and fungal debris Mucosal sparing Save middle turbinate Frontal sinus obliteration not advised Slide 86 PREOPERATIVE REGIMEN Antibiotics Steroids Slide 87 POSTOPERATIVE REGIMEN Steroid taper Intranasal steroids Antibiotics Clinic endoscopy and debridement Slide 88 Long-term systemic steroids Effective Multiple potential complications Screen for DM, cataracts, glaucoma, + PPD, active hepatitis Slide 89 Systemic antifungal agents Amphotericin B, itraconazole, voriconazole Mixed results Expensive Hepatotoxic Need regular evaluation of liver function tests Slide 90 83 patients managed with ESS, itraconazole, low dose oral steroids, topical steroids 36,000 doses of itraconazoleno adverse effects Reoperation required in only 20% Rains et al. AJR 2003;17:1-8 Slide 91 Intranasal Amphotericin irrigationchronic rhinosinusitis patients Ponikau et al. J Allergy Clin Immunol 2002:110:862-866 Reduced mucosal inflammation on CT scan Improvement in symptoms and endoscopic staging in 75% Ricchetti et al. J Laryngol Otol 2002;116:261-263 Disappearance of polyps in 62% of mild and 42% of moderate chronic rhinosinusitis Slide 92 Beneficial Mabry, Marple et al. (1997 and 1998) Prospective study, immunotherapy after surgery, patients improved, did not require systemic steroids, recurrences decreased Retrospective study, 11 patients matched with controls, immunotherapy patients had improved quality of life and objective endoscopic measures of mucosal edema Slide 93 Both fungal and nonfungal antigens, administered in separate vials Weekly immunotherapy, dosage advancement as tolerated Include wide variety of mold antigens Continue for 3-5 years Regular endoscopy and cleaning Slide 94 Caveats Ferguson (1993) reported patients who received immunotherapy prior to surgery had worsening of symptoms-ongoing antigenic load local reactions, immune complex deposits Patients who received immunotherapy after surgery improved Caution with concomitant ABPA, unable to surgically remove fungi in lower respiratory tract Slide 95 Recurrence of disease common Surgical treatment mandatory Multidisciplinary management Steroids, antifungalssystemic vs. topical Immunotherapy Slide 96 Better control with prolonged postoperative medical therapy Probably immunological disease, not infectious Therapy evolving as understanding of disease process improves Prolonged, close follow-up needed