3 Anatomy Maxillary sinus Frontal sinus: Largest, 10-20 cc. Med. = lat nasal wallSup = orbital floorFloor = alveolar process.Drainage via ostium in lower infundibulum.Frontal sinus:Absent unilat in 12%, bilat 5%.Drainage: into frontal recess posteromedially
4 Anatomy Ethmoid sinuses: 3-18 air cells Ant & post. Roof = fovea ethmoidalis, Lat = lamina papyracea, post = sphenoid, optic nerve.Ant mid meatus, post sup meatus.Medial wall: uncinate process, ethmoid bulla, in between hiatus semilunaris, infundibulum
7 29 years old male Nasal obstruction Runny nose Post-nasal drip Facial fullness
8 Rhinitis Rhinitis Classification Inflammatory Rhinitis Allergic rhinitisSeasonal allergic rhinitisPerennial allergic rhinitisPerennial nonallergic rhinitisEosinophilic nasal diseaseEosinophilic nonallergic rhinitis (ENR)Nonallergic rhinitis with eosinophilia syndrome (NARES)Associated with aspirin sensitivityAtrophic rhinitisPrimaryAcquiredInfectious rhinitisGranulomatous rhinitis (noninfectious)Irritant dust, chemical, or fume-induced rhinitisRhinitis induced by cold, dry airNoninflammatory RhinitisRhinitis medicamentosaTopicalSystemicHormonalIdiopathic vasomotor rhinitisStructurally Related RhinitisSeptal deviationNeoplasmsCerebrospinal fluid rhinorrheaMiscellaneous
9 Atrophic Rhinitisnasal mucosal atrophy with crusting and an extremely foul odorCuase : uknownBacterial: Klebsiella ozaenae, atoxic Corynebacterium diphtheriae, and the Perez-Hofer bacillusDeficiencies in vitamin A and ironRadical surgerySx & Sn: halitosis, nasal obstruction, epistaxis, and headache. Offensive nasal odor, crusting, and turbinate atrophy.\Tx: reversing nutritional deficiencies, saline irrigations, vitamin A, & systemic or topical antibiotics.Surgical(faliure of medical therapy): closure of the nostril and nasal vestibuloplasty to narrow the nostrils.
10 Vasomotor RhinitisOveractive parasympathetic stimulation of the nasal mucosa vasodilation, edema, and hypersecretion of mucusSx: nasal obstruction, profuse rhinorrhea, infrequent sneezing, stuffiness, and face pressure and headache.Trigger factors: changes in weather or humidity, the presence of irritating fumes, or air conditioning or stressTx:Medical: Systemic decongestants, Antihistamines, steroids, topical ipratropium bromide.Surgical: many procedures (inf turbinectomy, submucous resection, Cryotherapy ..etc)
12 Rhinitis Medicamentosa Nasal obstruction caused by overuse of topical decongestants or a systemic medications.Rebound vasodilatation after prolonged vasoconstriction with topical agentsTx:discontinuation of the offending medicationantihistamine-decongestant combinationstopical nasal corticosteroids +/- tapering oral prednisone dosage for 7 to 10 days.gentle submucosal Kenalog-40 injection!!
13 Allergic Rhinosinusitis Type I hypersensitivity reaction. Occur 2 to 5 minutes of antigen-antibody reaction.A second (late) phase: result of mediator release from cells (neutrophils, eosinophils) and occurs about 4 to 6 hours after the acute phase.
14 Allergic Rhinosinusitis Sx: tching, sneezing, rhinorrhea, and postnasal drainage (throat-clearing and cough). Seasonal or perennial, & linkage with known exposure to allergens.Signs:open-mouthed “adenoid facies.”, (“allergic salute”), “allergic shiners”and puffiness around the eyes.high arched palate, prominent pharyngeal lymphoidDxNasal smears (Hansel’s stain) eosinophils (> 25% of the cells). total IgESkin test
15 Allergic Rhinosinusitis Management:Level I: Prevention and Control of Symptoms.Environmental ControlFirst-line Pharmacotherapy:Antihistamines compete with histamine for H1-receptor sites on the target organs during the allergic responseDecongestants are sympathomimetic substances that cause vasoconstriction within turbinate stroma, producing shrinkage of congested tissue (Pseudoephedrine & Phenylpropanolamine)Cromolyn nasal spray: stabilizes and protects mast cells from degranulationLevel II: Recognition and Management of Complicating Factors Treat other types of rhinitis: vasomotor, medicamentosa…
16 Allergic Rhinosinusitis Level III: Corticosteroids for Control of Severe or Chronic SymptomsLevel IV: Immunotherapysymptoms are not controlled with pharmacotherapy, allergens that cannot be avoided, symptoms span two or more allergy seasons, willing to cooperate in a program of immunotherapyparenteral administration of antigens formation of allergen-specific IgG-blocking antibodies compete with IgE antibodies for target sites on mast cells or basophils.
17 Paranasal Sinusitis3 factors essential to normal physiology of the paranasal sinuses: patency of the ostia, function of the cilia, & quality of the nasal glandular secretions.Most significant pathophysiology that produces sinusitis: mucosal edema in and around the sinus ostium:Hypooxygenation of the involved sinus.Ciliary function is disturbed stagnation of the secretion.Local host resistance factors are diminished darainage & perfect milieu for the growth of bacterial pathogensInflammation (e.g. allergic rhinitis, URTI..) increased secretions and edema in the sinonasal mucosa.
19 Paranasal Sinusitis Classification Acute: infectious lasting from 1 day up to 4 weeks. Management is medical, and rarely surgical treatment.Subacute: infection lasts from 4 weeks to 3 months. inflammatory process is still reversible Medical management.Chronic: sinusitis persists longer than 3 months. Results from acute sinusitis that has been either inadequately treated or completely untreated. The process is irreversible surgical treatment is indicated.
20 Paranasal Sinusitis Acute sinusitis: Bacterial: Adults: Streptococcus pneumoniae, Staphylococcus aureus, Streptococcus pyogenes groups ABC, and Haemophilus influenzae (gram-negative).Children: S. pneumoniae, Branhamella catarrhalis (formerly known as Neisseria catarrhalis), Haemophilus influenzae, Streptococcus pyogenes groups A and C, and Streptococcus pyogenes a-hemolytic type
21 ManagementAntibiotics clinical improv. In 2-3 days, Ab should continue for daysPenicillin GAmoxicillinCefaclorTrimethoprim sulfateErythromycin sulfateAugmentinAnalgesicsMucolyticsSaline irrigationsTopical decongestion edema around the ostia oxygenation and facilitate drainage (reverse the hypoxia)Shrinkage and suction with Argyrol: packing the nose removal of pus & oxygenationSurgical management: presence of mucopurulent material in immunosuppressed pt , pt with acute max. sinusitis, no Improvement or worsening of symptoms.
22 Complications Mucocele chronic, cystic lesion of the paranasal sinuses. Expand slowly and concentrically bony erosion & extrasinus expansion.Most common in the frontal sinus.Sx: frontal headache and proptosis, displacement of the globe in a downward and outward direction and diplopia but no nasal obstruction and rhinorrheaTx: surgery
24 Complications classification (Chandler): Inflammatory edema — lid edema; no limitation of extraocular movement with normal acuityOrbital cellulitis — diffuse edema of orbital contents; no discrete abscess formationSubperiosteal abscess —purulent collection beneath periosteum of lamina papyracea; displacement of globe downward and laterallyOrbital abscess—purulent collection within orbit; proptosis and chemosis with ophthalmoplegia and decreased visionCavernous sinus thrombosis—bilateral eye findings; prostration; meningismus
34 Complications Intra-cranial complications direct extension through a defect in the posterior wall of the frontal sinusRetrograde thrombophlebitis of the valveless ophthalmic vesselsThe subdural space abscesscerebral abscess, seizures, and neurologic deficits.Meningitis (rare).Septic thrombosis of major dural sinusesTx:High-dose antibiotic therapymanagement of increased intracranial pressure, and prevention of seizures.Surgical drainage
35 Fungal Rhinosinusitis Classification:Acute invasive fungal sinusitisLife threatiningMucor mycosis, immunocompromised hostTx: radical resection, correct underlying medical problem, systemic antifungal.Chronic invasive fungal sinusitisSimilar to ch. Sinusitis, caused by aspergillusEndemic in hot dry climates e.g. SudanMycetoma (fungus ball): concentric hyphae of aspegillusTx: simple excision.Allergic fungal sinusitisMost common, Demitaceous groubNasal polyps, +ve skin test, Charcot-Layden crystalsTx: surgery & steroidsSaprophytic infection: fungal contamination
38 Epistaxis Local Systemic 10% of cases unknown Trauma (facial fractures, Vasculardigital trauma) Blood dyscrasiaInflammatory reactions DrugsAnatomical or structural Systemic toxic (heavy metals)deformities InfectiousForeign bodies CardiovascularToxic chemicalSurgeryIntranasal tumors (benign, malignant)10% of cases unknown
39 EpistaxisOsler-Rendu-Weber’s disease (hereditary hemorrhagic telangiectasiaautosomal dominant diseaseLack of contractile elements in the vessel walls arteriovenous fistulae are formed.Precipitating factors include mucosal fragility and trauma.Blood dyscrasiasIdentified early in lifeMost common Factor VIII (80% of cases).Von Willebrand’s: prolonged bleeding time, deficiency in antihemophilic Factor VIII, and impaired platelet adhesiveness.Drugs (acetylsalicylic acid, anticoagulants), Systemic toxic agents (phosphorous, mercury), infectious diseases (scarlet fever, smallpox).
63 Surgical management Spontaneous CSF Leak Unlikely stops with conservative therapy2 patients responded to medical managementOur experience consistent with Mayo Clinic experienceSurgical interventionCombined team:Otolaryngology & neurosurgery
64 Surgical management Intracranial Advantage: Disadvantage: ability to achieve a fluid-tight dural closurerepair multiple areas of leakage.Treat associated problems e.g. tumorsDisadvantage: morbidity, mortalityprolonged hospitalization periodLoss of olfaction
65 Surgical management Extracranial (Extranasal & Intranasal) Advantage: minimal morbidity and mortality while still achieving excellent visualization of the dural defectDisadvantage:precise, preoperative localization of the leakage site
69 Olfactory DisordersOlfactory bulb lies on top of the cribriform plate at the base of the brainOlfactory epithelium: upper septum & lat nasal cavityEpithelium:olfactory receptor (bipolar neuron)microvillar cell (another type of olfactory receptor cell)supporting, or sustentacular, cellsbasal cells (stem cells to replace the dying olfactory receptors)
70 Olfactory Disorders Causes Obstructive Nasal and Sinus Disease Olfactory Loss Following Upper Respiratory Infectiondamage to olfactory neurons at the level of the epithelium, the bulb, or the central olfactory tracts1/3 of patients will regain olfactory ability in 3 to 6 monthsHead Trauma5% to 10% of adults who have sustained both major and minor head traumashearing of the delicate fila olfactoria nerves as they pass through the cribriform plate8% to 39% of the patients recovery of olfactory function usually within 3 months
71 Olfactory Disorders Toxins Aging Congenital Formalduhyde, benzene, smokingPermenantAgingolfactory loss in old people can occur from dementia-related diseasestwo dementia-related diseases: Alzheimer’s disease and Parkinson’s diseaseCongenitalhypogonadotrophic hypogonadism (Kallmann’s syndrome
72 Midline Nasal Masses Congenital masses of neuroectodermal origin Lesion Dural connection Transillumination Furstenberg’s test Meningitis HistologyGlioma None No Negative No Solid mass of glial tissuewith a fibrous stalkEncephalocele Always Yes Positive Yes Ependymal-lined spacethat communicates withthe ventriclesDermoid Rare Rarely Negative Rare Fluctuating cyst withsinus tract leading to skin