Presentation on theme: "Diseases of the Nose & Sinuses Khalid H. Al-Sebeih, MD, FRCSC, ABO Assistant Professor, Department of Surgery Faculty of Medicine, Kuwait University. Department."— Presentation transcript:
Diseases of the Nose & Sinuses Khalid H. Al-Sebeih, MD, FRCSC, ABO Assistant Professor, Department of Surgery Faculty of Medicine, Kuwait University. Department of Otolaryngology, Sabah Hospital
Anatomy 1. Maxillary sinus Largest, 10-20 cc. Med. = lat nasal wall Sup = orbital floor Floor = alveolar process. Drainage via ostium in lower infundibulum. 2. Frontal sinus: Absent unilat in 12%, bilat 5%. Drainage: into frontal recess posteromedially
Anatomy 3. 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
Atrophic Rhinitis nasal mucosal atrophy with crusting and an extremely foul odor Cuase : uknown Bacterial: Klebsiella ozaenae, atoxic Corynebacterium diphtheriae, and the Perez-Hofer bacillus Deficiencies in vitamin A and iron Radical surgery Sx & 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.
Vasomotor Rhinitis Overactive parasympathetic stimulation of the nasal mucosa vasodilation, edema, and hypersecretion of mucus Sx: 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 stress Tx: Medical: Systemic decongestants, Antihistamines, steroids, topical ipratropium bromide. Surgical: many procedures (inf turbinectomy, submucous resection, Cryotherapy..etc)
Nasal obstruction caused by overuse of topical decongestants or a systemic medications. Rebound vasodilatation after prolonged vasoconstriction with topical agents Tx: discontinuation of the offending medication antihistamine-decongestant combinations topical nasal corticosteroids +/- tapering oral prednisone dosage for 7 to 10 days. gentle submucosal Kenalog-40 injection!! Rhinitis Medicamentosa
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.
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 shinersand puffiness around the eyes. high arched palate, prominent pharyngeal lymphoid Dx Nasal smears (Hansels stain) eosinophils (> 25% of the cells). total IgE Skin test Allergic Rhinosinusitis
Management: Level I: Prevention and Control of Symptoms. Environmental Control First-line Pharmacotherapy: a) Antihistamines compete with histamine for H1-receptor sites on the target organs during the allergic response b) Decongestants are sympathomimetic substances that cause vasoconstriction within turbinate stroma, producing shrinkage of congested tissue (Pseudoephedrine & Phenylpropanolamine) c) Cromolyn nasal spray stabilizes and protects mast cells from degranulation Level II: Recognition and Management of Complicating Factors Treat other types of rhinitis: vasomotor, medicamentosa… Allergic Rhinosinusitis
Level III: Corticosteroids for Control of Severe or Chronic Symptoms Level IV: Immunotherapy symptoms are not controlled with pharmacotherapy, allergens that cannot be avoided, symptoms span two or more allergy seasons, willing to cooperate in a program of immunotherapy parenteral administration of antigens formation of allergen-specific IgG-blocking antibodies compete with IgE antibodies for target sites on mast cells or basophils. Allergic Rhinosinusitis
Paranasal Sinusitis 3 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 pathogens Inflammation (e.g. allergic rhinitis, URTI..) increased secretions and edema in the sinonasal mucosa.
Obstruction of the sinus ostium Retained secretions
Classification 1. Acute: infectious lasting from 1 day up to 4 weeks. Management is medical, and rarely surgical treatment. 2. Subacute: infection lasts from 4 weeks to 3 months. inflammatory process is still reversible Medical management. 3. 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. 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 Paranasal Sinusitis
Management 1.Antibiotics clinical improv. In 2-3 days, Ab should continue for 10-14 days Penicillin G Amoxicillin Cefaclor Trimethoprim sulfate Erythromycin sulfate Augmentin 2.Analgesics 3.Mucolytics 4.Saline irrigations 5.Topical decongestion edema around the ostia oxygenation and facilitate drainage (reverse the hypoxia) 6.Shrinkage and suction with Argyrol: packing the nose removal of pus & oxygenation 7.Surgical management: presence of mucopurulent material in immunosuppressed pt, pt with acute max. sinusitis, no Improvement or worsening of symptoms.
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 rhinorrhea Tx: surgery
Complications classification (Chandler): 1. Inflammatory edema lid edema; no limitation of extraocular movement with normal acuity 2. Orbital cellulitis diffuse edema of orbital contents; no discrete abscess formation 3. Subperiosteal abscess purulent collection beneath periosteum of lamina papyracea; displacement of globe downward and laterally 4. Orbital abscesspurulent collection within orbit; proptosis and chemosis with ophthalmoplegia and decreased vision 5. Cavernous sinus thrombosisbilateral eye findings; prostration; meningismus
Complications Intra-cranial complications direct extension through a defect in the posterior wall of the frontal sinus Retrograde thrombophlebitis of the valveless ophthalmic vessels The subdural space abscess cerebral abscess, seizures, and neurologic deficits. Meningitis (rare). Septic thrombosis of major dural sinuses Tx: High-dose antibiotic therapy management of increased intracranial pressure, and prevention of seizures. Surgical drainage
Fungal Rhinosinusitis Classification: 1. Acute invasive fungal sinusitis Life threatining Mucor mycosis, immunocompromised host Tx: radical resection, correct underlying medical problem, systemic antifungal. 2. Chronic invasive fungal sinusitis Similar to ch. Sinusitis, caused by aspergillus Endemic in hot dry climates e.g. Sudan 3. Mycetoma (fungus ball): concentric hyphae of aspegillus Tx: simple excision. 4. Allergic fungal sinusitis Most common, Demitaceous groub Nasal polyps, +ve skin test, Charcot-Layden crystals Tx: surgery & steroids 5. Saprophytic infection: fungal contamination
Epistaxis LocalSystemic Trauma (facial fractures,Vascular digital trauma)Blood dyscrasia Inflammatory reactionsDrugs Anatomical or structuralSystemic toxic (heavy metals) deformitiesInfectious Foreign bodiesCardiovascular Toxic chemical Surgery Intranasal tumors (benign, malignant) 10% of cases unknown
Epistaxis Osler-Rendu-Webers disease (hereditary hemorrhagic telangiectasia autosomal dominant disease Lack of contractile elements in the vessel walls arteriovenous fistulae are formed. Precipitating factors include mucosal fragility and trauma. Blood dyscrasias Identified early in life Most common Factor VIII (80% of cases). Von Willebrands: 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).
History Examination Confirm CSF Conservative Tx
Medical Management Effective for traumatic leak Strict bed rest, no straining Head elevation 30 0 10 – 14 days Prophylactic antibiotic (controversial) L.P Carbonic-anhydrase inhibitors (acetazolamide) ??
History Examination Confirm CSF Conservative TX Failure Localization
Surgical management Spontaneous CSF Leak Unlikely stops with conservative therapy 2 patients responded to medical management Our experience consistent with Mayo Clinic experience Surgical intervention Combined team: Otolaryngology & neurosurgery
Intracranial Advantage: ability to achieve a fluid-tight dural closure repair multiple areas of leakage. Treat associated problems e.g. tumors Disadvantage: morbidity, mortality prolonged hospitalization period Loss of olfaction Surgical management
Extracranial (Extranasal & Intranasal) Advantage: minimal morbidity and mortality while still achieving excellent visualization of the dural defect Disadvantage: precise, preoperative localization of the leakage site Surgical management
Graft selection: a. Connective tissue grafts: Fascia lata, temporalis fascia, nasal septal cartilage b. Mucosal grafts: Contralateral inf. turbinate c. Other grafts: Lyophilized dura, synthetic dura, glass-ionomer bone cement Surgical management
Olfactory Disorders Olfactory bulb lies on top of the cribriform plate at the base of the brain Olfactory epithelium: upper septum & lat nasal cavity Epithelium: 1. olfactory receptor (bipolar neuron) 2. microvillar cell (another type of olfactory receptor cell) 3. supporting, or sustentacular, cells 4. basal cells (stem cells to replace the dying olfactory receptors)
Causes 1. Obstructive Nasal and Sinus Disease 2. Olfactory Loss Following Upper Respiratory Infection damage to olfactory neurons at the level of the epithelium, the bulb, or the central olfactory tracts 1/3 of patients will regain olfactory ability in 3 to 6 months 3. Head Trauma 5% to 10% of adults who have sustained both major and minor head trauma shearing of the delicate fila olfactoria nerves as they pass through the cribriform plate 8% to 39% of the patients recovery of olfactory function usually within 3 months Olfactory Disorders
4. Toxins Formalduhyde, benzene, smoking Permenant 5. Aging olfactory loss in old people can occur from dementia- related diseases two dementia-related diseases: Alzheimers disease and Parkinsons disease 6. Congenital hypogonadotrophic hypogonadism (Kallmanns syndrome Olfactory Disorders
Midline Nasal Masses Congenital masses of neuroectodermal origin LesionDural connectionTransilluminationFurstenbergs testMeningitisHistology GliomaNoneNoNegativeNoSolid mass of glial tissue with a fibrous stalk EncephaloceleAlwaysYesPositiveYesEpendymal-lined space that communicates with the ventricles DermoidRareRarelyNegativeRareFluctuating cyst with sinus tract leading to skin