Diseases of the Nose & Sinuses

Khalid H. Al-Sebeih, Khalid H. Al-Sebeih, MD, FRCSC, MD, FRCSC, ABOABO

Assistant Professor, Department of Surgery Assistant Professor, Department of Surgery

Faculty of Medicine, Kuwait University.Faculty of Medicine, Kuwait University.

Department of Otolaryngology, Sabah HospitalDepartment of Otolaryngology, Sabah Hospital

Anatomy Nasal cavity:

Roof: nasal bones, frontal bone, CFP of ethmoid, fovea ethmoidalis, sphenoid.

Septum: PPE, vomer, quadranqular cartilage, memb. septum, columella.

Floor: maxillary & palatine bone.

Lat wall: maxilla, inf. turbinate, ethmoid bone, lacrimal bone, palatine bone.

Anatomy1. 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

Anatomy3. 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

Anatomy

Anatomy 4. Sphenoid sinus:

Variable pneumatization

Above: pituitary gland & optic nerve

Lat: carotid, cavernous sinus, orbital apex structures.

Drainage: sphenethmoidal recess

29 years old male Nasal obstruction Runny nose Post-nasal drip Facial fullness

RhinitisRhinitis Classification Inflammatory RhinitisAllergic rhinitis Seasonal allergic rhinitis Perennial allergic rhinitisPerennial nonallergic rhinitis Eosinophilic nasal disease Eosinophilic nonallergic rhinitis (ENR) Nonallergic rhinitis with eosinophilia

syndrome (NARES) Associated with aspirin sensitivity Atrophic rhinitis Primary Acquired Infectious rhinitis Granulomatous rhinitis (noninfectious) Irritant dust, chemical, or fume-induced rhinitis Rhinitis induced by cold, dry air

Noninflammatory Rhinitis

Rhinitis medicamentosa

Topical

Systemic

Hormonal

Idiopathic vasomotor rhinitis

Structurally Related Rhinitis

Septal deviation

Neoplasms

Cerebrospinal fluid rhinorrhea

Miscellaneous

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)

Infectious Rhinitis Rhinoscleroma TB, Syphilis, leprosy. Rhinosporidiosis, histoplasmosis,

aspirgellosis.

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 shiners”and puffiness around the eyes. high arched palate, prominent pharyngeal lymphoid

Dx Nasal smears (Hansel’s 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

OO22

Vasodilatation Vasodilatation Ciliary dysfunctionCiliary dysfunction Mucous gland dysfunctionMucous gland dysfunction

TransudationTransudation stagnationstagnation Viscid fluidViscid fluid

Retained secretionsRetained secretions

Classification1. 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. Analgesics3. Mucolytics4. Saline irrigations5. 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 & oxygenation7. 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 abscess—purulent collection within orbit; proptosis and chemosis with ophthalmoplegia and decreased vision

5. Cavernous sinus thrombosis—bilateral 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

Local SystemicTrauma (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

Epistaxis Osler-Rendu-Weber’s 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 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).

Management1. ABC, IV fluid, cross matching.2. Silver Nitrate Cauterization 3. Electrical Cauterization 4. Cryotherapy 5. Nasal Packing

Anterior Nasal Packing Posterior Nasal Packing

6. Greater Palatine Foramen Block 7. Embolization

8. Surgery Septoplasty/Submucous Resection Internal Maxillary Artery Ligation Transantral Sphenopalatine Artery Ligation Anterior and Posterior Ethmoidal Artery Ligation External Carotid Artery Ligation Laser Photocauterization (HHT) Septodermoplasty (HHT) Cutaneous/Myocutaneous Flaps - Microvascular Free

Flaps (HHT)

Epistaxis

Epistaxis

Epistaxis

CSF Leak traumatic 95% (Accidental trauma

80%, iatrogenic 15%) nontraumatic 5% (tumors,

hydrocephalus, congenital anomalies or osteomyelitis

Violation of arachnoid, dura, bone, and mucosa

Cerebrospinal Fluid Leak

Ommaya Classification

CSF Leak

Non-Traumatic 5% Traumatic 95%

High PressureNormal Pressure

congenital, osteomyelitis

Tumors 50%Hydrocephalus

communicationg or obstructive

Accidental 80% Surgical 15%

History

History

Trauma Surgery Sinonasal

disease: sinusitis, Rhinitis, allergy

Symptoms

Symptoms No. of patients

Rhinorrhea 8

Headache 5

Sinus congestion

3

Anosmia 1

Meningitis 1

History

Examination

Cerebrospinal Fluid Leak

Physical examination: Valsalva

maneuver Endonasal scope:

00,300

Collecting CSF

History

Examination

Confirm CSF

Lab. Tests:

Glucose (> 30mg/100ml)

-2 transferrin

Confirm CSF Leak

History

Examination

Confirm CSF Conservative Tx

Medical Management Effective for traumatic leak

Strict bed rest, no straining

Head elevation 300

10 – 14 days

Prophylactic antibiotic (controversial)

L.P

Carbonic-anhydrase inhibitors

(acetazolamide) ??

History

Examination

Confirm CSF Conservative TX

FailureLocalization

Radiology:1. Radionuclide Cisternography: 2. High Resolution CT Scan 3. MRI (+/- FLAIR)

Cerebrospinal Fluid Leak

4. Water-Soluble Contrast CT

Cisternography

5. MRI after intrathecal injection of diluted

Gadolinium (Gd) ( Gd MRI

Cisternography)

History

Examination

Confirm CSF Conservative TX

FailureLocalization

Surgical repair

Surgical management Spontaneous CSF Leak

Unlikely stops with conservative therapy

2 patients responded to medical management

Our experience consistent with Mayo Clinic experienceSurgical 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

Orbit

Dura

Graft

Cerebrum

Orbit

Dura

Graft

Cartilage

Cerebrum

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)

Causes1. 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: Alzheimer’s

disease and Parkinson’s disease

6. Congenital hypogonadotrophic hypogonadism (Kallmann’s

syndrome

Olfactory Disorders

Midline Nasal Masses

 

Congenital masses of neuroectodermal origin

Lesion Dural connection Transillumination Furstenberg’s test Meningitis Histology

Glioma None No Negative No Solid mass of glial tissue

with a fibrous stalk

Encephalocele Always Yes Positive YesEpendymal-lined space

that communicates with

the ventricles

Dermoid Rare Rarely Negative Rare Fluctuating cyst with

sinus tract leading to skin

Midline Nasal Masses