Acute and chronic rhinitis

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Acute and chronic rhinitis

  1. 1. Department of Otorhinolaryngology PIMS
  2. 2.  Acute Rhinitis can be – • Viral • Bacterial • Irritative type
  3. 3. 1) Common cold (Coryza) Aetiology : Several viruses (adeno virus, picorna virus and its sub-groups sucha s rhinovirus, coxsackie, and ECHO) Clinical features : Nasal stuffness, rhnorrhoea, sneezing, low grade fever, secondary bacterial invasion may occur. Treatment : Bed rest, Plenty of fluids, Anthihistaminics, Nasal decongestants, Analgesics, Antibiotics, when secondary infection supervenes.
  4. 4. Complications : Sinusitis, pharyngitis, tonsillitis, bronchitis, pneumonia and otitis media.Influenzal rhinitis - Influenza viruses A, B or C. c/f are similar to common coldRhinitis associated with exanthemas. Measles, rubella, chickenpox. precede exanthemas by 2-3 days
  5. 5.  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.
  6. 6.  Chronic non-specific inflammations of nose include : 1. Chronic simple rhinitis 2. Hypertrophic rhinitis 3. Atrophic rhinitis 4. Rhinitis sicca 5. Rhinitis caseosa.
  7. 7.  Aetiology : 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 rhinitis e. Endocrinal or metabolic factors, e.g. hypothyroidism.a. Pathology : Hyperaemia and oedema of mucous membrane, Hypertrophy of seromucinous glands, increase in goblet cells.
  8. 8.  Clinical features : a. Nasal obstruction b. Nasal discharge. It may be mucoid or mucopurulent. Postnasal drip. c. Headache d. Swollen turbinates – They pit on pressure, shrink with application of vasoconstrictor drops (this differentiates the condition from hypertrophic rhinitis). e. Post-nasal discharge. Mucoid or mucopurulent discharge.
  9. 9.  Treatment : a. Treat the predisposing factor. b. Nasal irrigations with alkaline solution. c. Nasal decongestants. d. Antibiotics help to clear nasal infection.
  10. 10.  Characterized by thickening of mucosa, submucosa, seromucinous glands, periosteum and bone.Aetiology : Recurrent nasal infections Chronic sinusitis Chronic irritation of nasal mucosa.
  11. 11. Symptoms : Signs : Nasal obstruction  Hypertrophy of Nasal discharge : thick turbinates and sticky.  Turbinal mucosa is Headache thick, does not pit on Heaviness of head pressure, little Transient anosmia. shrinkage with vasoconstrictor drugs due to underlying fibrosis.  Maximum changes in the inferior turbiante.  Mulberry appearance of inferior turbiante.
  12. 12. Treatment : Discover the cause and remove it. Reduction in size of turbinates by a. Liner cauterisation b. Submucosal diathermy c. Cryosurgeryof turbinates d. Partial or total turbinectomy e. Submucous resection of turbinates bone. f. Lasers
  13. 13. Compensatoryhypertrophic rhinitis • In cases of marked deviation of septum to one side. • Roomier side of the nose shows hypertrophy of inferior and middle turbinates. • To reduce the wide space to overcome the ill effects of drying and crusting.
  14. 14.  Chronic inflammation of nose characterized by atrophy of nasal mucosa and turbinate bones.Primary atrophic rhinitis : Aetiology : Exact cause is not known, Various theories regarding its causation are: a. Hereditary factors b. Endocrinal disturbances : Starts puberty, involves females more than males, tends to cease after menopause.
  15. 15. 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.
  16. 16. 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.
  17. 17.  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
  18. 18. 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.
  19. 19. Prognosis : Disease persists for yearsTreatment :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.
  20. 20. 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.g. Potassium iodide by mouth promotes and liquefies nasal secretion.
  21. 21. 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. a. 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.
  22. 22. 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.
  23. 23.  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.
  24. 24.  Unilateral and mostly affecting males. Nose is filled with offensive purulent discharge and cheesy material. Sinus mucosa becomes granulomatous. Bony walls of sinus may be destroyed.Treatment : Removal of debris and granulation tissue Free drainage of the affected sinus.
  25. 25. ALLERGICRHINITIS
  26. 26.  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
  27. 27. AETIOLOGY : Inhalant allergens – Pollen from the trees and grasses, mold spores, house dust, debris from insects or house mite are common offenders. Genetic predisposition
  28. 28. Sensitized Antigen Mast cell Release of mediatorsPerformed Newly synthesized• Histamine • Prostaglandins e.g. PGD2• ECF – A • Leukotrienes e.g. SRS-A• NCF – A • PAG• Heparin • Thromboxane A•Others • TNFa
  29. 29.  Clinically allergic response occurs in 2 phases : 1. Acute or early phase : Within 5-30 min, sneeing, rhinorrhoea nasal blockagte 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.
  30. 30.  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 oedema, postnasal drip, chronic cough. Signs of allergy may be seen in the nose, eyes, pharynx or larynx.
  31. 31. Nasal signs : • Transverse nasal crease • Allergic salute • Pale and oedematous nasal mucosa • Thin, watery or mucoid dischargeDiagnosis : • Detailed history and physical examination.
  32. 32. 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.
  33. 33. Complications :1. Recurrent sinusitis.2. Nasal polyp3. Serous otitis media4. Bronchial asthma.
  34. 34. Treatment :1. Avoidance of allergen.2. Treatment with drugs. a. Antihistaminics b. Corticosteorids Oral corticosteorids Use should be limited to acute episodes Several systemic side effects Topical steroids such as beclomethasone dipropionate, budesonide, flunisolide acetate, fluticasone are used as aerosols, very effective in the control of symptoms. Fewer systemic side effects.
  35. 35. c. Sodium chromoglycate Stabilizes 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.
  36. 36.  Non-allergic rhinitis but clinically simulating nasal allergy. Condition usually persists throughout the year.
  37. 37. 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.
  38. 38. 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.
  39. 39. 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.
  40. 40. 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).
  41. 41. 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.
  42. 42. 3. Rhinitis of pregnancy : Due to hormonal changes. Local measures such as limited use of nasal drops.4. Honeymoon rhinitis5. 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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