rhinitis & rhino-sinusitis - alexu.edu.eg

Zeyad MANDOUR- M.D; Ph.D.; A.F.S.A.Professor of O.R.L.Rhinology UnitORL department,Alexandria University

Rhinitis &Rhino-sinusitis

Rhinitis

Rhinosinusitis

Definition

As the lining of the nose and paranasalsinuses is continuous, inflammatoryprocesses tend to involve both areas.

Sinusitis

Defence- Mechanisms

1. Mucociliary system, √2. Epithelial integrity,3. Reflexes (cough, sneeze),4. Lysoszymes, opsonins &complement,5. Immnoglobulins (secetory IgA,

IgE)6. Macrophages & lymphocytes.

Mucociliary clearance:This depends upon

1.Amount of mucus.

2.Mucosal resorption

3.Patency of air current

4.Ciliary action.

Air current & Mucociliary clearance

safe

unsafe

unsafe

Rhinosinusitis

Allergic Infective viral& bacterial

Non allergicnon infective

Acute Chronic

Nonspecific

Chronicsimplerhinitis

SpecificCommon coldInfluenza

Atrophicrhinitis Syphilis

T.B.Scleroma

Granulomatous

SarcoidosisWegenerStewart

NARESVasomotor rhinitis

Rhinitismedicamentosa

Hypertrophicrhinitis

Infectivefungal

Allergic Rhinitis

• Allergic rhinitis is an Ig.E mediatedhypersensitivity of nasal mucous membranecharacterized by:

• Sneezing, itching, watery rhinorrhea and asensation of nasal obstruction.

• It may also involve the lining of paranasalsinuses.

• It occurs in atopic individuals who are exposed tocommon aero-allergens

• It is genetically inherited either:Autosomal recessive.Autosomal dominant.

DefinitionDefinition

Allergens:

Seasonal rhinitis Perennial allergic rhinitis Occupational allergens Food and drug induced rhinitis Role of pollution

Grass Pollen

Allergens:

Seasonal rhinitis Perennial allergic rhinitis Occupational allergens Food and drug induced

rhinitis Role of pollution

House dust mites

Allergens:

Seasonal rhinitis Perennial allergic

rhinitis Occupational

allergens Food and drug

induced rhinitis Role of pollution

Domestic animals

Allergens:



Allergens:

Seasonal rhinitis Perennial allergic rhinitis Occupational allergens Food and drug induced rhinitis Role of pollution

Allergens:



Intermittent Persistent

Mild Moderate toSevere

Classification

Intermittent

< 4 days/week Or< 4 days/week Or < 4 weeksconsecutive< 4 weeks

consecutive

Persistent

> 4 days/week & > 4 weeks

consecutive

Mild

Normal sleep

No impairment of daily activities

No troublesome Symptoms inuntreated patients

Moderate to Severe

Abnormal Sleep

Impairment of daily activity

Abnormal work

The Allergic reaction

Sensitization

Ig E Production

Arming of mast cells

Release of mediators

Clinical effects

IL-3, IL-5GM-CSF

Allergic rhinitis (mechanisms)

Allergen

Mast cell HistamineLeukotrienes

ProstaglandinsBradykinin, PAF

T lymphocytes(mast cells)

Immediate rhinitis symptomsSneezingItching

Watery dischargeNasal congestion

B lymphocytes

Ig E

IL-4

Eosinophilrecruitment

VCAM-1

Delayed ongoing rhinitisNasal blockageLoss of smell

Nasal hyper-reactivity

AR & Co-morbidities

Nasalpolyposis

AR & Co-morbidities

Clinical PicturePerennial

allergic rhinitisSeasonal

allergic rhinitis+

Mucoid + PND

+++

+++

++++

Watery

+

+

• Sneezing &Itching• Rhinorrhea

• Loss of tasteand smell• AssociatedsinusitisandEustachianDysfunction

Positive personal and family history of other atopic diseases

External signs

Allergic salute.

Mouth breathing.

Allergic shiners.

Pale bluish edematousnasal turbinates.

Polyps, septal deflection orprominent nasal turbinates.

Intranasal signs

Complications

Otitis mediaSinusitis

Allergic rhinitis and bronchial asthmafrequently coexist.

• Aspiration of secretions.• Dryness of LRT.• Increase vagal stimulation.• Bacterial toxins.• Inflammatory cytokines.

Therefore, treatment of rhinitis with improvement in nasal airwaymay also improve symptoms of bronchial asthma.

Investigations

Skin allergy test

An allergen extract is placedinto skin by either scratching

or pricking with a sharpdevice or by intradermal

injection using a syringe &needle.

Investigations

Blood test:

• Total IgE.

• Specific IgE (RAST test)

About 50% of patients with allergic rhinitis have normal levels oftotal IgE and 20% of non-affected individuals can have elevated

total IgE levels.

Investigations

Eosinophils:

Blood sample

Nasal smear

Only supports the diagnosis of allergicneither sensitive orrhinitis but it is

specific.

Non-allergic eosinophilic rhinitis.

Parasitic infection.

Management of Allergic Rhinitis

•Allergen Avoidance

•Pharmacotherapy

•Immunotherapy

Drug and Symptom MatrixDrugs and Symptoms Sneezing Itching Rhinorrhea CongestionAntihistamines ***** **** ***Anticholinergics(Ipratropium bromide) *****Corticosteroids ***** ***** *** ***Decongestants *****Mast Cell Stabilisers ***** *** *Antileukotrines *** ** ****

Adjunctive management1.Antibiotics

2.Mucolytic

3.Anti- leukotrienes

4.Irrigations- Saline douches

5.GERD control

6.FESS

7.Myringotomy +/- Grommettube insertion

Infective Rhinosinusitis

Infective Rhino-sinusitis-Non-specific or specificClassification• Acute Rhino-sinusitis• Chronic Rhino-sinusitis• Sub acute Rhino-sinusitis• Recurrent ARS• Acute Rhino-sinusitis superimposed on

CRS

Rhinosinusitis



Acute Chronic

Nonspecific




T.B.Scleroma

Granulomatous





Infectivefungal

Infective viral RhinosinusitisAcuteCommon coldInfluenza

Common Cold

Rhinovirus Coronavirus

The commenst viral infection in human

Mode of Transmission

Predisposing factors

Cold weather. High humidity. Immune deficiency. Nutritional & Vitamin deficiency. Fatigue & stress. Nasal obstruction. Foci of chronic infection. General disease.

Viral Invasion

Release of mediators from infected cellse.g. IL-8, kinins, prostaglandins

Vasodilatation.Increase permeability.

Increase glandular secretion.Stimulation of parasympathetic

nerve endings.

Viral Invasion

Release of mediators from infected cellse.g. IL-8, kinins, prostaglandins

Clinical Picture

Clinical picture:• Fever, headache,malaise.• Dryness of nose.• Sore throat.• Sneezing.• Nasal obstruction.• Watery rhinorrhea.• MucopurulentRhinorrhea.• Resolution within5-10 days.

Complications:• Sinusitis.• Pharyngitis.• Adenoiditis.• Tonsillitis.• Otitis media.• Laryngotrachitis.• Bronchitis.• Pneumonia.• Nephritis.• Rheumatic fever.

Treatment: Bed rest. Vitamins. Fluids. Analgesic. Antipyretics. Antihistaminics. Anticholenergic. Decongestant. Antibiotics.

Influenza

One of the most common infectious diseases in human.

It is caused by influenza virusthat is classified as type A, B & C.

InfluenzaIt may occur in epidemics.

Spanish flu epidemic 1918 killed 20 millions all over the world.

InfluenzaTwo types of influenza virus.

Human influenzaAvian influenza

InfluenzaTwo types of influenza virus.

Human influenzaA person infected with a particular flu virusstrain develops antibody against that virus.

As newer virus strains appear throughantigenic shift and drift , the antibodiesagainst the older strains no longer recognizethe "newer" virus, and infection with a newstrain can occur.

Common Uncommon

PneumoniaOtitis media Tracheobronchitis

Acute sinusitis

Reye's syndromePericarditis

MyositisMyoglobinuria Encephalitis

Transverse myelitisGuillain-Barré syndrome

Rhabdomyolysis

Complications

• Healthy children six to 23months of age.• Adults 65 years and older.• Persons six months to 64 yearswith cardiopulmonary, respiratory,renal, metabolic, orimmunodeficient conditions.• Pregnant women

Features Influenza Common cold

Onset Abrupt More gradualFever Common up to 40.0°C Uncommon only 0.5°C

Myalgia Severe, common UncommonArthralgia Severe, common UncommonAnorexia Common UncommonHeadache Severe, common Severe, common

Cough (dry) Common, severe Mild to moderateMalaise Severe Mild

Fatigue, weakness More common Very mild, short lastingChest discomfort Common, severe Mild to moderate

Stuffy nose Occasional CommonSneezing Occasional Common

Sore throat Occasional Common

1. Children aged 6–23 months.2. Adults aged ≥50 years.3. Persons aged 2–64 years with underlying

chronic medical conditions.4. Women who will be pregnant during the

influenza season.5. Residents of nursing homes and long-term

care facilities.6. Children aged 2–18 years on chronic

aspirin therapy.7. Health-care workers involved in direct

patient care; and8. Out-of-home caregivers and household

contacts of children aged <6 months.

Vaccination

Rhinosinusitis



Acute Chronic

Nonspecific




T.B.Scleroma

Granulomatous





Infectivefungal

Infective bacterial Rhinosinusitis

Chronic non-specific• Simple chronic rhinitis• Chronic hypertrophic rhinitis• Chronic atrophic rhinitis

1. Simple chronic rhinitis• Repeated attacks of acute rhinitis• Maintenance of acute

inflammatory condition by one ormore of the following factors:

1. Neighboring infection (sinusitis,tonsillitis or adenoiditis)

2. Chronic nasal obstruction(deviated septum or vasomotorrhinitis)

3. Ciliary stasis (ciliarydyskinesia))

Simple chronicrhinitis4. Chronic irritation (smoke,

tobacco, dust orvasoconstrictor abuse )

5. Metabolic imbalance (dietimbalance, excessivecarbohydrate, gout orvitamins deficiency)

6. Endocrine factors (diabetes,thyroid)

Simple chronic rhinitis- clinicalfeatures• Nasal obstruction (chronic

hyperaemia, nasopulmonary reflex)• Post nasal discharge• Headache• Transient anosmia

Simple chronic rhinitis-Examination

• Red mucosa (active infection)• Purple mucosa (venous stasis)• Other areas (pal and edematous)• Mucous strands

Simple chronic rhinitis-Management• Correcting predisposing factors• Nasal wash• Topical +/_ systemic steroids• ABCS +/_

2. Chronic hypertrophicrhinitis

• Advanced stage of non specificchronic with permanent wholemucosa hypertrophy

• Thick, nodular mucosa especiallyat the posterior end of the inferiorturbinate (mulberry like)

• Sometimes polyps may form• +/_ Rhinitis medicamentosa

Chronic hypertrophicrhinitis

• Same os simple chronic rhinitis• +/_ surgical trimming• +/_ out fracture

Chronic nasal disease characterized by progressive atrophy ofnasal mucosa and the underlying bone of the turbinates withformation of scanty viscid secretions that rapidly dries toform crusts that emit a characteristic foul odor (ozaena).There is associated abnormal patency of nasal passages.

3. Atrophic rhinitis

The exact cause is unknown1) Chronic bacterial infection; Klebsiela, Pertussis,

Diphtheria.

2) Nutritional Deficiency; Vit-A deficiency, Fedeficiency.

3) Endocrinal Factor; estrogenic deficiency.

4) Autoimmune.

Etiology (primary)

Incidence

• Endemic in subtropical & temperate climates.

• In Egypt, it affects 1% of the population.

• More in those living in unhygienic conditions.

• It occurs more commonly in females at the time of

puberty and this supports the hormonal theory of

the role of estrogen in the etiology of atrophic

rhinitis.

Etiology

Chronic bacterial infection: Coccobacillus. Bacillus pertussis or

mucosus. Klebsiella ozaenae. Diphtheroid bacilli.

Etiology

Nutritional Deficiency:

▫ Vitamin A deficiency.▫ Iron deficiency.

Etiology

Autoimmune Disease:Due to loss of tolerance

• Viral infection.• Malnutrition.• Immunodeficiency.

Etiology

Endocrinal factorMainly estrogen deficiency; the proof is:

Occurrence in girls around puberty. Aggravation of symptoms during menstruation. Improvement of some cases by estrogen therapy.

Etiology (secondary)

1. Excessive surgicaldestruction of nasal mucosa.

2. Chronic exposure to irritant,cocaine or toxic agents

3. Healed stage ofgranulomatous disease.T.B., Scleroma.

4. Radiotherapy.

Endarteritis & Periarteritis

Atrophy of mucosal & submcosal structures

Decrease nasal secretions Abnormal nasal patency

Dryness of secretions & crust formation

Histopathology

• Sub epithelial cellular infiltration (Accumulation of chronic inflammatory cells e.g.lymphocytes and plasma cells).• Ciliary destruction. )•Atrophy of the boney turbinates ( Decrease insize of mucosal & submucosal structures) and(Decrease in number and size of compoundalveolar glands).• Metaplasia from ciliated columnar to squamousepithelium.•Endarteritis obliteransIn Type I : Endarteritis obliteransIn Type II: Dilated capillaries.

Clinical Picture

Symptoms Signs

•Nasal obstruction.•Headache.•Epistaxis.•Bad odor from thenose.•Pharyngitis sicca.•Chocking.

• Fetor oris.• Green, yellow or blackcrusts.• Ulcerated bleedingmucosa.• Atrophy of inferior &middle turbinates.

Characteristic CT findings

Mucosal thickening of the paranasalsinuses.

Loss of definition of the ostiomeatalcomplex secondary to resorption of

the ethmoid bulla ad uncinateprocess.

Hypoplasia of the maxillary sinuses.

Enlargement of the nasal cavitieswith erosion and bowing of the

lateral nasal wall.

Bony resorption and mucosal atrophyof the inferior and middle turbinates.

Conservative measuresNasal cleaning; Regular nasal cleaning , lubricant

oil drops, glucose and glycerin.2) Vit E and iron supplement3) Hormonal therapy.4) Corticosteroids.5) Vasodilators.6) Antibiotics

Treatment

Surgical techniques---1Cavity narrowing techniques:Nasal closure1) Complete closure; Skin flaps.2) Partial closure; 3 mm hole.3) Post choana closure.Aim: decrease dryness, crustation.

Nasal Implants1) Auto grafts; cartilage.2) Autogenous osteoperiosteal flaps.3) Submucosa Teflon4) Synthetic implants as silicon

Surgical techniques---2

PharyngoplastyCaudally based pharyngeal flaps.

Cavity moistening techniques

1) Salivary irrigation procedures.2) Dennervation procedures.

Surgical techniques---3

Rhinosinusitis



Acute Chronic

Nonspecific




T.B.Scleroma

Granulomatous





Infectivefungal

Infective bacterial RhinosinusitisChronic specific• Syphilis• T.B• Rhinoscleroma

1. Syphilis• May be encountered in

primary, secondary, tertiary orcongenital forms (snufflespurulent rhinitis)

• Mucous membrane ulcerationand discharge occur incongenital and secondarysyphilis

Syphilis• Gummas of the tertiary stage give rise to

septal perforations (bone and cartilage)

• Destroy the surrounding nasal skeleton

with a shrunken bridge deformity

• DX : clinical features and Treponema

Pallidium identification in smears from

primary and secondary lesions

• Also by serological tests in tertiary stage

2. Tuberculosis• Rare complication of pulmonary TB• Ranging from ulcerative,

hypertrophic (tuberculoma) andfibrotic types

• Fibrotic often affects surroundingfacial skin (lupus)

• Cartilaginous septum Tuberculomamay lead to ulceration andperforation (no bone involvement)

• Biopsy is diagnostic and treatmentsimilar to lung condition

3. Scleroma• Chronic specific infection of the respiratory tract

esp. the nose (rhinoscleroma)• Klebsiella rhinoscleromatis• Mode of infection (unknown)• Not uncommon in Egypt• Teenagers especially in females (poor classes)• Granulomatous tissue infiltrates the submucosa

of the nose with accumulation of chronicinflammatory cells (plasma cells, lymphocytesand fibroblasts)

Scleroma• Spread to involve (nose, nasopharynx,

oropharynx) with soft palate fibrosis,subglottic stenosis and rarely trachealand bronchial, maxillary sinus andmiddle ear or ET or lacrimal sacinvolvement

Hebra nose

Scleroma- pathology• The infiltration is charecterized by

the presence of:• Miculicz cells (large foam cells

containing the causative bacilliwithin its vacuoles)

• Russel bodies (degeneratedplasma cells with an eosinophilstaining cytoplasm)

Scleroma- pathology

• Electron microscopy showsanother

type of cells called Mott cellswhich are

(plasma cells containinginclusion bodies)

They are intermediate stage b/wplasma cells and Russel bodies

Scleroma- clinical features• Catarrhal• Hypertrophic: overgrowth of

dense fibrous tissue• Atrophic : process of

reabsorption and breakdownof tissues

• Cicatricial: scar left by theformation of new connectivetissue over a healing sore orwound.

Scleroma- pathological features

• Hypertrophic: overgrowth ofdense fibrous tissue

• Atrophic : process ofreabsorption and breakdownof tissues

• Cicatricial: scar left by theformation of new connectivetissue over a healing sore orwound.

Scleroma- management• The organism can nevertheless be extremely difficult to

be eradicated by antimicrobials.• Once the diagnosis has been confirmed by biopsy,

treatment must be intense and prolonged.• Bactericidal antibiotics in large doses are given in large

doses for a minimum of four to six weeks and arecontinued until two consecutive cultures from biopsymaterial are proven negative.

• Initial surgical debridement prior to chemotherapy is reportedto be useful in granulomatous stage.

• The traditional antibiotics used are streptomycin andtetracycline, but the lenghthly nature o the treatment can leadto problems with adverse effects and compliance.

• Recent reports have emphasized the good results achieved withoral therapy with rifampicin, sulphamethoxazole- trimethoprimcombination, and ciprofloxacin.

• Local application of 2 percent acriflavin for a period of eightweeks has been noted to be both efficacious and non-toxic.

• Locally applied rifampicin has been used with success.

Scleroma- management

• Radiation to total dose of 3000 - 3500 Gy over three weeksdestroys scleroma but, the currently available antimicrobials, isunlikely to be required.

• In late cases where disease has been eradicated, further plasticreconstructive surgery may be required.

• This may be carried out by nasal endoscopy and laser, ifappropriate.

Scleroma- management

Rhinosinusitis



Acute Chronic

Nonspecific




T.B.Scleroma

Granulomatous





Infectivefungal

Granulomatous Rhinosinusitis• Sacoidosis• Wegener’s granuloma• Midline leathal granuloma (Stewart’s

granuloma)

1. Sarcoidosis• Idiopathic systemic

granulomatous disease• Frequent head and neck

manifestations• In the nose, the mucosa

becomes swollen and granular• Crusting and stenosis• +/_ neck adenopathy, hilar

adenopathy, eye and boneproblems

Sarcoidosis• Biopsy from nasal septum or

turbinates is often diagnostic

• Topical steroid sprays are

useful to control symptoms

2. Wegener’s granuloma• Autoimmune collagen

disorgers with multisysteminvolvement

• The respiratory tract, kidneysand skin are the most ofteninvolved

• Charecterized by a necrotizingvasculitis

• Ulceration of the septum withcrusting and saddle nose arecommon nasal presentations

Wegener’s granuloma• Biopsy id diagnostic• ESR is raised• Microscopic haematuria and

proteinuria• Can be controlled for many

years with steroids andcyclophosphamide

3. Midline lethal granuloma(Stewart’s granuloma)

• A rare locally destructive lesion• Radiotherapy and

chemotherapy may halt theprocess

• Most cases progress rapidly todeath

Rhinosinusitis



Acute Chronic

Nonspecific




T.B.Scleroma

Granulomatous





Infectivefungal

Non-allergic, non-infectiverhinosinusitis1. NARES2. Vasomotor rhinitis3. Rhinitis medicamentosa4. Chronic atrophic rhinitis5. Chronic hypertrophic rhinitis

Non-allergic, non-infective-ClassificationI. (NARES) (Jacobs, 1987) is characterized by the

presence of nasal eosinophilia in subjects whoare often middle-aged and who have perennialsymptoms of sneezing paroxysms, nasalitching, rhinorrhoea and occasionally loss ofsense of smell.

• However, they lack evidence of allergic diseaseas determined by skin tests and IgE levels.

Non-allergic, non-infective-ClassificationII. Vasomotor rhinitis

III. Rhinitis medicamentosa

IV. Chronic atrophic rhinitis √√

V. Chronic hypertrophic rhinitis √√

Rhinosinusitis



Acute Chronic

Nonspecific




T.B.Scleroma

Granulomatous





Infectivefungal

Infective fungal rhinosinusitis1. Invasive2. Non-invasive

Fungal Sinusitis• Invasive

▫ Presence of fungal hyphae within the mucosa,submucosa, bone, or blood vessels of theparanasal sinuses

• Non-invasive▫ Absence of fungal hyphae within the mucosa and

other structures of the paranasal sinuses

Fungal Sinusitis - Classification• Invasive

1. Acute Invasive Fungal Sinusitis2. Chronic Invasive Fungal Sinusitis3. Chronic Granulomatous Invasive Fungal Sinusitis

• Non-invasive1. Allergic Fungal Sinusitis2. Fungus Ball (fungus mycetoma)

1. Acute Invasive Fungal Sinusitis• Most lethal form of fungal sinusitis – mortality

50-80%• Rare in immunocompetent patients• Two clinical populations

▫ Poorly controlled Diabetics – ususally caused byfungi of order Zymocycetes (Rhizopus, Rhizomucor,Absidia, and Mucor)

▫ Immunocompromised with severeneutropenia (chemotheraphy patients, BMT, organtransplants, AIDS) – Aspergillus accounts for 80% ofinfection in this group

2. Chronic Invasive FungalSinusitis

• Usually immunocompetent• History of chronic rhinosinusitis• Usually persistent and recurrent disease• Maxillofacial soft tissue swelling, orbital

invasion with proptosis, cranial neuropathies,decreased vision, can invade cribiform platecausing headaches, seizures, decreased mentalstatus

3. Chronic GranulomatousInvasive Fungal Sinusitis

• Primary paranasal granuloma and indolentfungal sinusitis

• Primarily found in Africa (Sudan) and SoutheastAsia, only few case reports in US

• Immunocompetent• Caused by Aspergillus flavus• Characterized by non-caseating

granulomas in the tissues

4. Allergic Fungal Sinusitis

• Most common form of fungal sinusitis• Common in warm, humid climates of

Southern US• Hypersensitivity reaction to inhaled

fungal organisms resulting in chronicnoninfectious inflammatory reaction - IgEtype I immediate hypersensitivity and type IIIhypersensitivity are involved

• Common organisms implicated – Bipolaris,Curvularia, Alternaria, Aspergillus, andFusarium

Allergic Fungal Sinusitis – Clinical-cont.• “Allergic mucin” within affected sinus

which is inspissated mucous theconsistency of peanut butter witheosinophils on histology

• Younger individuals, third decade,immunocompetent

• Often associated history of atopy withallergic rhinitis or asthma

• Chronic headaches, nasal congestion, andchronic sinusitis for years

5. Fungus Ball

• Older individuals, female>male• Immunocompetent• Asymptomatic or minimal symptoms with

chronic pressure or nasal discharge• Cacosmia (perception of foul odor when no

such odor exists)

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rhinitis & rhino-sinusitis - alexu.edu.eg

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