Transcript PPT - UCLA Head and Neck Surgery

Marilene B. Wang, MD, FACS
Professor
UCLA Division of Head Neck Surgery
Chief of Otolaryngology
VA Greater Los Angeles Healthcare System
 From
Anterior Nasal Spine
◦ To Sphenoid Ostium 7 cm
◦ To Pituitary Fossa8.5 cm
 Middle
turbinate
 Lamina papyracea
 Ethmoid fovea
 Cribriform plate
 Sphenoid
 Facial
pain/pressure
 Nasal obstruction/blockage
 Nasal
discharge/purulence/discolo
red postnasal drip
 Hyposmia/anosmia
 Purulence
in nasal cavity on
examination
 Fever (acute rhinosinusitis
only)
 Headache
 Fever
 Halitosis
 Fatigue
 Dental
 Cough
 Ear
pain
pain/pressure/fullness
 Acute
 Subacute
 Chronic
 Recurrent,
acute
 Acute exacerbations of
chronic
 Duration
up to 4 weeks
 > 2 major factors
 1 major factor + 2 minor
factors
 Nasal purulence on exam
 Duration
4-12 weeks
 >2 major factors
 1 major factor + 2 minor
factors, or nasal purulence on
exam
 Complete resolution after
effective medical therapy
 Duration
> 12 weeks
 History same as for subacute
 Facial pain does not constitute
suggestive history in absence of
other nasal symptoms or signs
 >4
episodes/year + each
episode last >7-10 days.
 Absence of intervening signs
of chronic rhinosinusitis
 Sudden
worsening of chronic
rhinosinusitis
 Return to baseline after
treatment
 Allergies
 Immunodeficiency
 Genetic/congenital
 Endocrine
 Neuromechanism
 Anatomic
 Neoplastic
 Acquired
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%)
 S.
pneum (25-30%)
 H. influenzae (15-20%)
 M. catarrhalis (15-20%)
 S. pyogenes (2-5%)
 Anaerobes (2-5%)
 Sterile (20-35%)
 Mild
disease with no recent
antimicrobial use
 Augmentin, Amoxicillin
 Vantin
 Ceclor
 Omnicef
 Tequin,
Levaquin, Avelox
 Augmentin
 Combination (Amox or
clinda + Suprax)
 Bactrim
 Doxycycline
 Zithromax,
Biaxin,
Erythromycin
 Switch to quinolone if no
improvement in 72 hours
 Quinolone
 Augmentin
 Clindamcin
+ rifampin
 Consider IV abx
 Augmentin,
Amoxicillin
 Vantin
 Ceclor
 Omnicef
 Switch
if no improvement after
72 hours
 Bactrim
 Macrolide
 Augmentin
 Rocephin
 Bactrim,
macrolide
 Consider IV abx if no
improvement
 Afrin
for 3 days
 Normal saline sprays
 Decongestants
 Antihistamines
 ?Steroids
 Periorbital
cellulitis
 Preseptal cellulitis/abscess
 Orbital cellulitis
 Orbital abscess
 Cavernous 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
 Allergic
 Shiners
 Itchy,
salute
red conjunctiva
 Sneezing
 Post-nasal drip, rhinorrhea,
congestion
 Dust
 Mold,
 Plants
mildew
 Animal
dander
 Feathers/down
 Pollen
 Smog
 Trees,
grasses, weeds
 Dust, fertilizer, chemicals
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Asthma
Allergic fungal sinusitis
Cystic fibrosis
Mucociliary dysfunction
Connective tissue disorders
(Wegener’s granulomatosis,
sarcoid)
 Nasal
polyposis
 Samter’s triad (aspirin
sensitivity, nasal polyps,
asthma)
 Cocaine use
 Antibiotics
 Antihistamines
 Nasal
steroids
 Normal saline irrigations
 Allergy evaluation +/immunotherapy
 Sinus
CT scan
 Consider anatomic factors—
septal deviation, nasal
polyps, concha bullosa,
ostio-meatal blockage
 Nasal
polyposis
 Anatomic blockage—deviated
septum, enlarged turbinate,
concha bullosa
 Mucocele
 Orbital abscess
 Fungal
sinusitis—allergic vs.
invasive (mucor)
 Tumor of nasal cavity or
sinus
 Chronic,
recurrent sinusitis
 Failure to respond to
maximal medical therapy
 Obtain cultures
 Nasal
congestion
 Headache/sinus pain
 Fatigue
 Prolonged bleeding/crusting
 Breach
of lamina papyracea—
damage to extraocular muscles,
periorbital ecchymoses
 Damage to optic nerve—
blindness
 Breach of cribriform—CSF leak
 Meningitis
 May
be a lifelong disease
 Allergy control—
antiihistamines, nasal steroids,
immunotherapy
 Oral steroids—judiciously
 Antibiotics for acute
exacerbations
 Environmental
control—avoid
carpet, damp, mold, older
homes, smog
 Saline irrigations
 Alternative
therapies—
acupuncture, stress management,
herbal remedies
 Pain management
 Multi-disciplinary effort—work
with allergy, infectious disease,
neurology/pain management
services
4
types of allergic reactions (Gell
and Coombs)
 Type 1 – IgE
 Type 2 - IgG--antigen
 Type 3 – Immune complex
 Type 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
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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)
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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
 Avoid
medications which may
interfere
◦ Antihistamines
◦ Antidepressants
◦ Antacids
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Anaphylaxis
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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
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Pharmacotherapy
◦ Antihistamines, anti-leukotrienes, mast-cell
stabilizers, topical and systemic steroids
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Specific allergens
Vial test
◦ Intradermal test
◦ Smallest measurable dose
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Once or twice weekly injections
Dose escalated
Continue treatment 3-5 years
 Invasive
◦Acute fulminant
◦Chronic invasive
◦Granulomatous invasive
 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
 Not
all 5 criteria for diagnosis
 Gradual nasal airway
obstruction
 Thick nasal mucous/crusts
 May take years to manifest
 AFS-like syndrome
 Immunocompetent
 Normal
 Atopic
ESR, WBC
◦Asthma, hay fever, inhalant
allergy
• Nasal polyposis
 Hyperactive
allergic
inflammatory response
 Possible fungal toxin
 Inflammatory mediators
 Recurrent bacterial sinusitis
 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
 Allergic
response to fungus by
skin testing and in vitro
(radioallergosorbent)
methodology
 Variable culture results (64-100%)
from sinus contents
 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)
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MRI-T2 weighted
Hypointensity of signal in sinus (dehydrated
allergic fungal mucin)
 Enhancement of periphery of sinus (mucosal
edema)
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 Medical
 Surgical
 Break
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
 Complete
removal of allergic
fungal mucin and fungal debris
 Mucosal sparing
 Save middle turbinate
 Frontal sinus obliteration not
advised
 PREOPERATIVE
◦ Antibiotics
◦ Steroids
REGIMEN
 POSTOPERATIVE
REGIMEN
◦ Steroid taper
◦ Intranasal steroids
◦ Antibiotics
◦ Clinic endoscopy and
debridement
 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 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
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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 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
 Recurrence
of disease common
 Surgical treatment mandatory
 Multidisciplinary 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