rhinology review part 2
DESCRIPTION
RHINOLOGY REVIEW part 2. Marilene B. Wang, MD, FACS Professor UCLA Division of Head Neck Surgery Chief of Otolaryngology VA Greater Los Angeles Healthcare System. Sphenoid Sinus Distances. From Anterior Nasal Spine To Sphenoid Ostium7 cm To Pituitary Fossa8.5 cm. - PowerPoint PPT PresentationTRANSCRIPT
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Marilene B. Wang, MD, FACSProfessor
UCLA Division of Head Neck SurgeryChief of Otolaryngology
VA Greater Los Angeles Healthcare System
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From Anterior Nasal Spine◦To Sphenoid Ostium 7 cm
◦To Pituitary Fossa 8.5 cm
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Middle turbinateLamina papyraceaEthmoid foveaCribriform plateSphenoid
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Facial pain/pressureNasal obstruction/blockage
Nasal discharge/purulence/discolored postnasal drip
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Hyposmia/anosmiaPurulence in nasal cavity on examination
Fever (acute rhinosinusitis only)
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HeadacheFeverHalitosisFatigue
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Dental painCoughEar pain/pressure/fullness
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AcuteSubacuteChronicRecurrent, acuteAcute exacerbations of chronic
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Duration up to 4 weeks> 2 major factors1 major factor + 2 minor factors
Nasal purulence on exam
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Duration 4-12 weeks>2 major factors1 major factor + 2 minor factors, or nasal purulence on exam
Complete resolution after effective medical therapy
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Duration > 12 weeksHistory same as for subacuteFacial pain does not constitute suggestive history in absence of other nasal symptoms or signs
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>4 episodes/year + each episode last >7-10 days.
Absence of intervening signs of chronic rhinosinusitis
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Sudden worsening of chronic rhinosinusitis
Return to baseline after treatment
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AllergiesImmunodeficiencyGenetic/congenital
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EndocrineNeuromechanism
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AnatomicNeoplasticAcquired mucociliary dysfunction
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• Microorganisms—viral, bacterial, fungal
• Noxious chemicals, pollutants, smoke
• Medications• Trauma• Surgery
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• 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%)
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S. pneum (25-30%)H. influenzae (15-20%)M. catarrhalis (15-20%)S. pyogenes (2-5%)Anaerobes (2-5%)Sterile (20-35%)
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Mild disease with no recent antimicrobial use
Augmentin, AmoxicillinVantinCeclorOmnicef
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Tequin, Levaquin, AveloxAugmentinCombination (Amox or clinda + Suprax)
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BactrimDoxycyclineZithromax, Biaxin, Erythromycin
Switch to quinolone if no improvement in 72 hours
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QuinoloneAugmentinClindamcin + rifampinConsider IV abx
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Augmentin, AmoxicillinVantinCeclorOmnicefSwitch if no improvement after 72 hours
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BactrimMacrolide
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AugmentinRocephinBactrim, macrolideConsider IV abx if no improvement
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Afrin for 3 daysNormal saline spraysDecongestantsAntihistamines?Steroids
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Periorbital cellulitisPreseptal cellulitis/abscess
Orbital cellulitisOrbital abscessCavernous sinus thrombosis
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• Widespread affliction—the 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
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Allergic saluteShinersItchy, red conjunctivaSneezingPost-nasal drip, rhinorrhea, congestion
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DustMold, mildewPlantsAnimal danderFeathers/down
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PollenSmogTrees, grasses, weedsDust, fertilizer, chemicals
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• Asthma• Allergic fungal sinusitis• Cystic fibrosis• Mucociliary dysfunction• Connective tissue disorders (Wegener’s granulomatosis, sarcoid)
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Nasal polyposisSamter’s triad (aspirin sensitivity, nasal polyps, asthma)
Cocaine use
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AntibioticsAntihistaminesNasal steroidsNormal saline irrigationsAllergy evaluation +/- immunotherapy
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Sinus CT scanConsider anatomic factors—septal deviation, nasal polyps, concha bullosa, ostio-meatal blockage
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Nasal polyposisAnatomic blockage—deviated septum, enlarged turbinate, concha bullosa
MucoceleOrbital abscess
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Fungal sinusitis—allergic vs. invasive (mucor)
Tumor of nasal cavity or sinus
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Chronic, recurrent sinusitis
Failure to respond to maximal medical therapy
Obtain cultures
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Nasal congestionHeadache/sinus painFatigueProlonged bleeding/crusting
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Breach of lamina papyracea—damage to extraocular muscles, periorbital ecchymoses
Damage to optic nerve—blindness
Breach of cribriform—CSF leakMeningitis
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May be a lifelong diseaseAllergy control—antiihistamines, nasal steroids, immunotherapy
Oral steroids—judiciouslyAntibiotics for acute exacerbations
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Environmental control—avoid carpet, damp, mold, older homes, smog
Saline irrigations
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Alternative therapies—acupuncture, stress management, herbal remedies
Pain managementMulti-disciplinary effort—work with allergy, infectious disease, neurology/pain management services
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4 types of allergic reactions (Gell and Coombs)
Type 1 – IgEType 2 - IgG--antigenType 3 – Immune complexType 4 – Delayed hypersensitivity
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• Mast cells bind IgE via their Fc(ε) 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
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• 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
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• 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
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• 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
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Parents with allergy greater likelihood of producing allergic children
Food allergies Environment— air pollution Smoking
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History—environmental exposure, smoking, seasonal occurrence, pets, foods
Examination ◦ Allergic shiners◦ Allergic salute◦ Supratip crease◦ Dennie’s lines (skin fold under eyes)◦ Adenoid facies
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Skin testing◦ Prick/puncture (scratch or patch)◦ Intradermal◦ Dilutional intradermal (skin end-point
titration-SET) In vitro testing
◦ RAST (radioactive marker)◦ ELISA (enzymatic marker)
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Prick—few drops of purified allergen pricked onto skin surface (dust, dander, pollen)
Patch—large patch with different allergens (latex, medications, metal, fragrances, preservatives)
Histamine or glycerin used as positive controls
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• 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
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Avoid medications which may interfere◦Antihistamines◦Antidepressants◦Antacids
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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
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RAST -radioallergosorbent test—detect 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
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ELISA – enzyme linked immunosorbent assay
Used more for food allergies Not as sensitive as skin tests
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Environmental control◦ Stop smoking, clean house, avoid mold,
indoor plants, pets, HEPA filter Pharmacotherapy
◦ Antihistamines, anti-leukotrienes, mast-cell stabilizers, topical and systemic steroids
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Specific allergens Vial test
◦ Intradermal test◦ Smallest measurable dose
Once or twice weekly injections Dose escalated Continue treatment 3-5 years
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Invasive◦Acute fulminant ◦Chronic invasive◦Granulomatous invasive
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Noninvasive◦Saprophytic fungal infestation
◦Fungal ball, “mycetoma”◦Allergic fungal rhinosinusitis
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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
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Bony remodeling Inflammatory mediators
◦Major basic protein◦Eosinophilic peroxidase◦Tumor necrosis factor◦Interleukins◦Interferons
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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
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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
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Not all 5 criteria for diagnosis
Gradual nasal airway obstruction
Thick nasal mucous/crustsMay take years to manifest
AFS-like syndrome
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ImmunocompetentNormal ESR, WBCAtopic◦Asthma, hay fever, inhalant allergy
•Nasal polyposis
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Hyperactive allergic inflammatory response
Possible fungal toxinInflammatory mediatorsRecurrent bacterial sinusitis
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Role of IgENot consistently elevated in serum
Local IgE-mediated immune response in nasal mucosa
IgE as cause of inflammation or merely a marker
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Allergic response to fungus by skin testing and in vitro (radioallergosorbent) methodology
Variable culture results (64-100%) from sinus contents
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Allergic fungal mucin◦Sheets of eosinophils◦Charcot-Leyden crystals◦Extramucosal fungal elements
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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
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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)
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MedicalSurgicalBreak the Allergic Fungal Rhinosinusitis Cycle
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Functional endoscopic sinus surgery Complete ventilation of the sinuses Wide maxillary antrostomies Complete ethmoidectomies Sphenoid sinusotomies Frontal sinusotomies
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Complete removal of allergic fungal mucin and fungal debris
Mucosal sparingSave middle turbinateFrontal sinus obliteration not advised
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PREOPERATIVE REGIMEN◦Antibiotics◦Steroids
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POSTOPERATIVE REGIMEN◦Steroid taper◦Intranasal steroids◦Antibiotics◦Clinic endoscopy and debridement
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Long-term systemic steroids◦Effective ◦Multiple potential complications
◦Screen for DM, cataracts, glaucoma, + PPD, active hepatitis
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Systemic antifungal agents Amphotericin B, itraconazole,
voriconazole Mixed results Expensive Hepatotoxic Need regular evaluation of liver
function tests
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83 patients managed with ESS, itraconazole, low dose oral steroids, topical steroids
36,000 doses of itraconazole—no adverse effects
Reoperation required in only 20%
Rains et al. AJR 2003;17:1-8
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• Intranasal Amphotericin irrigation—chronic rhinosinusitis patients
Ponikau et al. J Allergy Clin Immunol 2002:110:862-866
Reduced mucosal inflammation on CT scanImprovement in symptoms and endoscopic staging in 75%
Ricchetti et al. J Laryngol Otol 2002;116:261-
263Disappearance of polyps in 62% of
mild and 42% of moderate chronic rhinosinusitis
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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
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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
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Caveats Ferguson (1993) reported patients
who received immunotherapy prior to surgery had worsening of symptoms-ongoing antigenic loadlocal reactions, immune complex deposits
Patients who received immunotherapy after surgery improved
Caution with concomitant ABPA, unable to surgically remove fungi in lower respiratory tract
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Recurrence of disease commonSurgical treatment mandatoryMultidisciplinary management
◦Steroids, antifungals—systemic vs. topical
◦Immunotherapy
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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