acute and chronic rhinitis

Prepared by:Sobhan sabzi

Acute Rhinitis can be – •Viral •Bacterial •Irritative type

1) Common cold (Coryza) etiology : Several viruses (adeno virus,

picorna virus and its sub-groups sucha s rhinovirus, coxsackie, and ECHO)

Clinical features : Nasal stiffness, rhinorrhoea, sneezing, low grade fever, secondary bacterial invasion may occur.

Treatment : Bed rest, Plenty of fluids, Antihistaminics, Nasal decongestants, Analgesics, Antibiotics.

Complications : Sinusitis, pharyngitis, tonsillitis,

bronchitis, pneumonia and otitis media.

Influenzal rhinitis - Influenza viruses A, B or C.

c/f are similar to common cold

Rhinitis associated with exanthemas. Measles, rubella, chickenpox.

precede exanthemas by 2-3 days

Diphtheritic rhinitis : • Primary • Secondary to faucial diphtheria• May occur in acute or chronic form • Greyish membrane is seen covering the inferior

turbinate and the floor of nose; membrane is tenacious and its removal causes bleeding

Treatment : Isolation of the patient, systemic penicillin and diphtheria antitoxin.

Chronic non-specific inflammations of nose include :

1. Chronic simple rhinitis2. Hypertrophic rhinitis3. Atrophic rhinitis4. Rhinitis sicca5. Rhinitis caseosa.

etiology : Predisposing factors a. Persistence of nasal infection due to

sinusitis, tonsillitis, and adenoids.b. Chronic irritation from dust, smoke,

cigarette smoking, snuff.c. Nasal obstruction.d. Vasomotor rhinitise. Endocrinal or metabolic factors, e.g.

hypothyroidism. a. Pathology : Hyperemia and edema of

mucous membrane, Hypertrophy of seromucinous glands, increase in goblet cells.

Clinical features : a. Nasal obstruction b. Nasal discharge. It may be mucoid or

mucopurulent. Postnasal drip. c. Headached. Swollen turbinates – They pit on

pressure, shrink with application of vasoconstrictor drops (this differentiates the condition from hypertrophic rhinitis).

Treatment : a. Treat the predisposing factor.b. Nasal irrigations with alkaline solution.c. Nasal decongestants. d. Antibiotics help to clear nasal infection.

Characterized by thickening of mucosa, submucosa, seromucinous glands, periosteum and bone.

etiology : Recurrent nasal infections Chronic sinusitis Chronic irritation of nasal mucosa.

Symptoms : Nasal obstruction Nasal discharge :

thick and sticky. Headache Heaviness of head Transient anosmia.

Signs : Hypertrophy of

turbinates Turbinal mucosa is

thick, does not pit on pressure, little shrinkage with vasoconstrictor drugs due to underlying fibrosis.

Maximum changes in the inferior turbiante.

Mulberry appearance of inferior turbiante.

Treatment : Discover the cause and remove

it. Reduction in size of turbinates by

a. Liner cauterisationb. Submucosal diathermyc. Cryosurgery of turbinatesd. Partial or total turbinectomye. Submucous resection of turbinates

bone.f. Lasers

Chronic inflammation of nose characterized by atrophy of nasal mucosa and turbinate bones.

Primary atrophic rhinitis : etiology : Exact cause is not known,

Various theories regarding its causation are:

a. Hereditary factorsb. Endocrinal disturbances : Starts puberty,

involves females more than males, tends to cease after menopause.

c. Racial factors – White.d. Nutritional deficiency : Deficiency of

vitamin A, D or iron.e. Infective : Klebsiella ozaenae, (Perez

bacillus), diphtheroids, P.vulgaris, Esch. Coli, Staphylococci and Streptococci but they are all considered to be secondary invaders.

f. Autoimmune process : The body reacts by a destructive process to the antigens released from the nasal mucosa.

Pathology : Ciliated columnar epithelium is

replaced by stratified squamous type. Atrophy of seromucinous glands,

venous sinusoids and nerve elements.

Obliterative endarteritis. The bone of turbinates undergoes

resorption. Paranasal sinuses are small.

Type 1: charecterised by endarteritis and periarteritis of terminal arterioles

-result of chronic infection - benefits from vasodilator effect of

oestrogen therapy Type 2: vasodilatation of capillaries - which might be made worse by

oestrogen therapy

Clinical features : Commonly seen in females and starts around

puberty. Foul smell from the nose. Marked anosmia (merciful anosmia) Nasal obstruction Epistaxis when the crusts are removed. Nasal cavity full of greenish or greyish black

dry crusts. Nasal cavities appear roomy. Nasal mucosa appear pale. Septal perforation and dermatitis of nasal

vestibule. Nose shows saddle deformity.

Prognosis : Disease persists for years

Treatment : 1. Medical :

a. Nasal irrigation and removal of crusts.b. 25% glucose in glycerine. – Inhibits the

growth of proteolytic organisms which are responsible for foul smell.

c. Local antibiotics – KemicetineTM antiozaena solution contains chloromycetin, oestradiol and vitamin D2.

d. Oestradiol spray – increase vascularity of nasal mucosa and regeneration of seromucinous glands.

e. Placental extract injected submucosally.

f. Systemic use of streptomycin – reducing crusting and odour. Effective against Klebsiella organisms.

2. Surgical :a. Young’s operation – Both the nostrils are

closed completely just within the nasal vestibule by raising flaps. They are opened after 6 months or later. Modified young’s operation - Aims to

partially close the nostrils.b. Narrowing the nasal cavities. Among the

techniques followed, some are : Submucosal injection to teflon paste. Insertion of fat, cartilage, bone or teflon strips

under the mucoperiosteum of the floor and lateral wall of nose and the mucoperichondrium of the septum.

Section and medial displacement of lateral wall of nose.

SECONDARY ATROPHIC RHINITIS : Specific infections like syphilis,

lupus, leprosy and rhinoscleroma. Longstanding purulent sinusitis,

radiotherapy or nose or excessive surgical removal of turbinates.

UNILATERAL ATROPHIC RHINITIS :

Extreme deviation of nasal septum. Atrophic rhinitis on the wider side.

Crust-forming disease Seen in patients who work in hot, dry

and dusty surroundings. Confined to the anterior third of nose. The ciliated columnar epithelium

undergoes squamous metaplasia. Atrophy of seromucinous glands (Crusts,

epistaxis, septal perforation).Treatment : Bland ointment or an antibiotic and

steroid. Nasal douche.

ALLERGIC RHINITIS

IgE – mediated immunologic response to nasal mucosa to air-borne allergens.

Two clinical types 1. Seasonal. Symptoms appear in or

around a particular season. 2. Perennial. Symptoms are present

throughout the year

AETIOLOGY : Inhalant allergens – Pollen from the

trees and grasses, mold spores, house dust, debris from insects or house mite are common offenders.

Genetic predisposition

SensitizedMast cell Antigen

Release of mediators

Performed • Histamine• ECF – A• NCF – A• Heparin •Others

Newly synthesized• Prostaglandins e.g. PGD2 • Leukotrienes e.g. SRS-A• PAG• Thromboxane A• TNFa

Clinically allergic response occurs in 2 phases :

1. Acute or early phase : Within 5-30 min, sneezing, rhinorrhea nasal blockage and/or bronchospasm. Due to release of vasoactive amines like histamine.

2. Late or delayed phase : 2-8 hours after exposure to allergen without additional exposure. Due to infiltration of inflammatory cells eosinophils, neutrophils, basophil, monocytes and CD4+ T cells at the site of antigen deposition.

No age or sex predilection Symptoms of seasonal nasal allergy. Paroxysmal sneezing, 10-20 sneezes at

a time, nasal obstruction, watery nasal discharge and itching in the nose.

Symptoms of perennial allergy. Frequent colds, persistently stuffy nose,

loss of sense of smell due to mucosal edema, postnasal drip, chronic cough.

Signs of allergy may be seen in the nose, eyes, pharynx or larynx.

Nasal signs : • Transverse nasal crease• Allergic salute• Pale and edematous nasal mucosa• Thin, watery or mucoid discharge

Diagnosis : • Detailed history and physical

examination.

Investigations : 1. Total and differential count. Peripheral

eosinophilia.2. Nasal smear shows large number of

eosinophils.3. Skin tests. Prick, scratch and

intradermal tests.4. Radioallergosorbent test (RAST).

Measures specific IgE antibody concentration in the patient’s serum.

5. Nasal provocation test.

Complications : 1. Recurrent sinusitis.2. Nasal polyp3. Serous otitis media4. Bronchial asthma.

Treatment : 1. Avoidance of allergen.2. Treatment with drugs.

a. Antihistaminicsb. Corticosteorids

Oral corticosteoridsUse should be limited to acute episodesSeveral systemic side effectsTopical steroids such as beclomethasone dipropionate, budesonide, flunisolide acetate, fluticasone are used as aerosols, very effective in the control of symptoms.Fewer systemic side effects.

c. Sodium chromoglycateStabilizes the mast cells and prevents them from degraulation.2% solution for nasal drops or spray or as an aerosol powder.

3. Immunotherapy Allergen is given in gradually increasing doses till the maintenance dose is reached.Immunotherapy suppresses the formation of IgE.

Non-allergic rhinitis but clinically simulating nasal allergy.

Condition usually persists throughout the year.

Pathogenesis : Parasympathetic stimulation causes

vasodilation and engorgement. Over activity of parasympathetic system also causes excessive secretion from the nasal glands.

Autonomic nervous system is under the control of hypothalamus therefore emotions play a great role in vasomotor rhinitis.

Nasal mucosa is also hyper-reactive and responds to several non-specific stimuli e.g. change in temperature, humidity.

Symptoms : Paroxysmal sneezing. In the morning. Excessive rhinorrhoea. Profuse and

watery. Nasal obstruction Postnasal drip. Signs : Nasal mucosa over the turbinates is

generally congested and hypertrophic.Complications : Nasal polypi, hypertrophic rhinitis and

sinusitis.

TREATMENT :Medical :1. Avoidance of physical factors

which provoke symptoms.2. Antihistaminics and oral nasal

decongestants.3. Topical steroids.4. Systemic steroids – for a short

time in very severe cases.5. Psychological factors should be

removed.

Surgical : 1. Nasal obstruction can be relieved

by measures which reduce the size of nasal turbinates.

2. Excessive rhinorrhoea, relived by sectioning the parasympathetic secretomotor fibres to nose (vidian neurectomy).

Other forms of non-allergic rhinitis : 1. Drug-induced rhinitis : Several

antihypertensive drugs. Some anticholinesterase drugs e.g. neostigmine. Contraceptive pills because of oestrogens.

2. Rhinitis medicamentosa : Topical decongestant nasal drops cause rebound phenomenon. Their excessive use causes rhinitis. Treated by withdrawal of nasal drops, short course of systemic steroid.

3. Rhinitis of pregnancy : Due to hormonal changes. Local measures such as limited use of nasal drops.

4. Honeymoon rhinitis 5. Emotional rhinitis : due to several

emotional stimuli.6. Rhinitis due to hypothyroidism :

Predominance of parasympathetic activity.

7. Non air-flow rhinitis : Seen in patients of laryngoectomy and tracheostomy.

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