2. RHINITIS
AN INFLAMMATION OF THE LINING MEMBRANE OF THE NOSE.
• ACUTE RHINITIS:
A. ACUTE NON-SPECIFIC RHINITIS E.G. ACUTE CORYZA (COMMON COLD) AND
INFLUENZA RHINITIS.
B. ACUTE SPECIFIC RHINITIS E.G. NASAL DIPHTHERIA.
• CHRONIC RHINITIS:
a. CHRONIC NON-SPECIFIC RHINITIS
b. CHRONIC SPECIFIC RHINITIS E.G. SCLEROMA AND SYPHILIS.
3. COMMON COLD (CORYZA):
ADENOVIRUS, RHINOVIRUS, RESPIRATORY SYNCYTIAL VIRUS AND PARA INFLUENZAE VIRUS
A SECONDARY BACTERIAL INFECTION USUALLY SUPERVENES.
• PREDISPOSING FACTORS:
*GENERAL FACTORS:
• BAD VENTILATION.
• FATIGUE.
• MALNUTRITION AND VITAMIN DEFICIENCY.
• LOW GENERAL RESISTANCE E.G. RENAL, HEPATIC, DIABETIC AND IMMUNODEFICIENT PATIENTS.
*LOCAL FACTORS:
• NASAL OBSTRUCTION.
• FOCI OF CHRONIC INFECTION IN THE SINUSES AND NASOPHARYNX.
4. • CLINICAL PICTURE:
FOUR STAGES INCLUDE :
• PRODROMAL STAGE: NASAL DRYNESS, IRRITATION AND
SNEEZING.
• HYPERAEMIC STAGE: NASAL OBSTRUCTION, WATERY DISCHARGE
AND GENERAL SYMPTOMS OF MILD TOXAEMIA AND FEVER. THE
MUCOUS MEMBRANE APPEARS RED AND SWOLLEN.
• STAGE OF SECONDARY INFECTION: THE DISCHARGE THICKENS,
DIMINISHES AND BECOMES MUCOPURULENT. NASAL
OBSTRUCTION AND TOXAEMIA ARE AT THEIR MAXIMUM.
• RESOLUTION STAGE: THE SYMPTOMS AND SIGNS GRADUALLY
DIMINISH AND RECOVERY TAKES PLACE AFTER 5-10 DAYS.
5. • COMPLICATIONS:
• SINUSITIS.
• OTITIS MEDIA.
• TONSILLITIS AND PHARYNGITIS.
• LARYNGITIS, TRACHEITIS, BRONCHITIS, PNEUMONIA AND ASTHMA
EXACERBATION.
6. TREATMENT:
• SELF-LIMITING.
• ANALGESIC ANTIPYRETIC SUCH AS ASPIRIN OR PARACETAMOL.
• STEAM INHALATION AND TOPICAL NASAL DECONGESTANTS MAY PROVIDE SOME
RELIEF FROM NASAL OBSTRUCTION.
• ANTIBIOTICS MAY BE REQUIRED FOR CONTROL OF SECONDARY INFECTION.
7. NASAL DIPHTHERIA
RARE.
CORYNEBACTERIUM DIPHTHERIAE.
IT IS USUALLY SECONDARY TO FACIAL DIPHTHERIA, BUT VERY RARE
MAY BE PRIMARY.
• CLINICAL :
• OBSTRUCTION
• FETID DISCHARGE WHICH IS WATERY AT FIRST AND LATER BECOMES
BLOOD STAINED AND MUCOPURULENT.
• THE INFERIOR TURBINATE, THE FLOOR OF THE NOSE AND
SOMETIMES THE SEPTUM ARE COVERED WITH A GREYISH ADHERENT
MEMBRANE.
• REMOVING THIS MEMBRANE LEAVES A RAW BLEEDING SURFACE.
NASAL SWABS ARE ESSENTIAL FOR DIAGNOSIS.
8. • TREATMENT:
• SYSTEMIC ANTIBIOTICS, USUALLY PARENTERAL PENICILLIN AND NASAL TOILET.
• SYSTEMIC ANTITOXINS ARE ALSO INDICATED.
N.B :PATIENTS SHOULD BE ISOLATED UNTIL NEGATIVE 3 SUCCESSIVE NASAL SWABS
9. CHRONIC HYPERTROPHIC RHINITIS
AETIOLOGY:
• RECURRENT ACUTE RHINITIS OR SINUSITIS.
• ALLERGIC RHINITIS.
• VASOMOTOR RHINITIS.
PATHOLOGY: HYPERTROPHY OF THE NASAL MUCOSA AND SUBMUCOSA.
• CLINICAL :
1. BILATERAL NASAL OBSTRUCTION.
2. BILATERAL MUCOID NASAL AND POSTNASAL DISCHARGE.
10. • SIGNS:
1. CONGESTED HYPERTROPHIED NASAL MUCOSA.
2. CONGESTED HYPERTROPHIED INFERIOR
TURBINATE.
IT DOES NOT SHRINK WITH DECONGESTIVE DROPS
INDICATING IRREVERSIBLE CHANGES.
• TREATMENT:
• TREATMENT OF THE CAUSE.
• TOPICAL STEROIDS.
• REDUCTION OF THE INFERIOR TURBINATE BY:
A. SURGICAL PARTIAL INFERIOR TURBINECTOMY.
B. SUBMUCOUS DIATHERMY.
C. LASER TURBINATE REDUCTION.
11. ATROPHIC RHINITIS (OZAENA):
• ATROPHIC RHINITIS IS A CHRONIC NON-SPECIFIC RHINITIS CHARACTERIZED BY
PROGRESSIVE ATROPHY OF THE NASAL MUCOSA AND UNDERLYING BONY
TURBINATES.
• IT USUALLY COMMENCES AT PUBERTY.
12. Primary atrophic rhinitis : Secondary atrophic rhinitis
common in females
unknown
Infection: cocobacillus ozaenae, klebsiella
ozaenae and other gram negative organisms
have been isolated from cultures.
· Endocrine imbalance: oestrogen deficiency
has been suspected.
· Malnutrition: iron and vitamin A deficiency
have been claimed.
· Autoimmune disease.
· Autonomic imbalance.
· Hereditary factors.
· Long standing purulent rhinitis or sinusitis
during childhood.
· Excessive surgical destruction of the nasal
mucous membranes
e.g. radical turbinectomy and repeated
cautery.
13. CHRONIC SPECIFIC RHINITIS E.G. SCLEROMA
AND SYPHILIS
SEVERELY DEVIATED NASAL SEPTUM (IN THE WIDER SIDE).
POST-IRRADIATION.
• PATHOLOGY:
• ATROPHY OF THE MUCOSA, SUBMUCOSA AND BONY TURBINATES.
• ATROPHY OF THE SERO-MUCINOUS GLANDS.
• ENDARTERITIS OF THE ARTERIOLES.
• CLINICAL PICTURE:
CRUSTY NASAL DISCHARGE, FOUL ODOUR. (USUALLY NOT SMELLED BY THE PATIENT, AS HE HAS ANOSMIA DUE TO ATROPHY OF THE OLFACTORY
MUCOSA).
SENSE OF NASAL OBSTRUCTION; IN SPITE OF ROOMY NOSE DUE TO DULLNESS OF SENSATION OF AIR ON THE ATROPHIC MUCOSA,
EPISTAXIS ON REMOVING THE CRUSTS
SORE THROAT, DUE TO ASSOCIATED ATROPHIC PHARYNGITIS.
• CLINICAL EXAMINATION
CONFIRMS THE PRESENCE OF FETOR AND GREEN OR BLACK CRUSTS IN ROOMY NASAL CAVITIES. NASAL MUCOSA IS THIN, PALE, DRY (ATROPHIC) WITH
ATROPHIC INFERIOR TURBINATES.
14. • TREATMENT:
• CONSERVATIVE:
REGULAR NASAL DOUCHING WITH AN ALKALINE SOLUTION SHOULD BE
CONSIDERED TWICE DAILY.
25% GLUCOSE IN GLYCERINE PACK
TOPICAL OESTROGEN, ORAL POTASSIUM IODIDE AND HUMAN
PLACENTAL EXTRACTS.
ANTIBIOTICS AFTER CULTURE AND SENSITIVITY TESTS CAN BE USED AS
WELL.
• SURGICAL:
NARROWING THE NASAL CAVITIES
TEMPORARY CLOSING THE NOSTRILS FOR 6-12 MONTHS.
15. • Crust formation seen in patients who work in hot
dry surroundings
• Confined to anterior1/ 3rd Nose
• Treatment
• Correction of occupational surroundings,
• Local application of ointment, Nasal
douche.
Rhinitis sicca
16. • Mostly affects males
• Nose filled with offensive,cheesy
material
• Secondary to chronic sinus infection
• Treatment-Removal of debris,
drainage of sinus.
73
Rhinitis
Caseous
17. RHINOSCLEROMA (NASAL GRANULOMA) :
• AN ENDEMIC CHRONIC SPECIFIC INFECTION OF THE NOSE IN EGYPT. MORE COMMON IN
YOUNG ADULT FEMALES.
KLEBSIELLA RHINOSCLEROMATIS: GRAM -VE FRISCH DIPLOBACILLUS.
• CLINICAL PICTURE:
1. CATARRHAL STAGE: RESEMBLE ACUTE RHINITIS.
2. ATROPHIC STAGE: CLINICALLY SIMILAR TO ATROPHIC RHINITIS.
3. HYPERTROPHIC (GRANULATION) STAGE: BILATERAL HARD, NON-ULCERATING SUBMUCOUS
GRANULOMATOUS NODULES APPEAR AT THE MUCO-CUTANEOUS JUNCTION, THEN SPREAD AND
COALESCE TO FILL THE NASAL CAVITIES AND BROADEN THE NOSE. NODULES MAY SPREAD TO
THE SUBCUTANEOUS TISSUES OF THE NASAL TIP, UPPER LIP AND DORSUM OF THE NOSE.
4. FIBROTIC (CICATRIZING) STAGE: DENSE FIBROSIS LEADING TO NASAL STENOSIS AND EXTERNAL
NASAL DEFORMITY.
18. Pathology:
Submucosal chronic inflammatory cellular infiltration
characterized by: Mikulicz cells: (large foamy cells
containing the Frisch bacilli within its vacuoles)
Russel bodies: (red-stained degenerated plasma
cells), Plasma cells, lymphocytes and fibroblasts.
19. • INVESTIGATIONS:
1. BIOPSY AND PATHOLOGICAL EXAMINATION.
2. CULTURE AND ANTIBIOTIC SENSITIVITY TEST.
SEQUELAE: THE PHARYNX (PHARYNGOSCLEROMA), LARYNX (LARYNGOSCLEROMA),
RARELY MIDDLE EAR (TYMPANOSCLEROMA) OR LACRIMAL SAC
(DACRYOSCLEROMA).
20. • TREATMENT:
MEDICAL:
LONG COURSE OF ANTIBIOTICS FOR A MINIMUM 4-6 WEEKS AS THE FRISCH
BACILLI ARE INTRACELLULAR AND THE ANTIBIOTICS DO NOT REACH IT
EASILY.
• STREPTOMYCIN: 1GM I.M. DAILY, FOR 40 DAYS (OTOTOXIC AND
NEPHROTOXIC DRUG).
• RIFAMPICIN: 300 MG ORALLY TWICE DAILY, FOR 40 DAYS (HEPATOTOXIC).
• ACCORDING TO THE CULTURE AND SENSITIVITY TEST.
SURGICAL:
RE-ESTABLISHMENT OF THE NASAL OR LARYNGEAL AIR WAY BY REMOVAL OF
THE GRANULOMATOUS MASSES OR FIBROUS TISSUE BY SURGERY OR CO2
LASER.
TRACHEOSTOMY IN CASE OF SEVERE LARYNGOSCLEROMA WITH UPPER
RESPIRATORY OBSTRUCTION.
21. NASAL LUPUS VULGARIS
ATTENUATED FORM OF T.B. BACILLI.
• CLINICAL PICTURE:
NASAL OBSTRUCTION
NASAL DISCHARGE WITH APPLE-JELLY NODULES AT THE MUCO-CUTANEOUS
JUNCTION OF THE VESTIBULE AND NASAL SEPTUM.
THEY APPEAR ON BLANCHING THEM BY PRESSING IT WITH GLASS SLIDE OR
DECONGESTIVE DROPS.
LATER ON IT GIVES, NODULAR ULCERATION WITH PERFORATION OF THE
CARTILAGINOUS SEPTUM AND ATROPHIC RHINITIS.
• INVESTIGATIONS:
1. BACTERIOLOGICAL SMEAR FOR T.B. BACILLI.
2. BIOPSY REVEALS T.B GRANULOMA.
• TREATMENT:
• ANTI-TUBERCULOUS DRUGS AND CALCIFEROL (VITAMIN D2).
22. ALLERGIC RHINITIS
IG-E MEDIATED (TYPE I ) HYPERSENSITIVITY REACTION OF THE MUCOUS MEMBRANE OF THE NOSE TO SPECIFIC ALLERGENS.
• AETIOLOGY:
GENETIC PREDISPOSITION : RELATIVES OF THE PATIENT MAY HAVE ANY ATOPIC MANIFESTATION (NASAL ALLERGY,
BRONCHIAL ASTHMA OR ALLERGIC DERMATITIS).
• TYPES:
• SEASONAL ALLERGIC RHINITIS: OCCURS IN SEASONS E.G. HAY FEVER.
• PERENNIAL ALLERGIC RHINITIS: PERSISTENT ALL OVER THE YEAR.
• ALLERGENS IN THE FORM OF:
1.INHALANTS (COMMON) :
• SEASONAL: POLLENS OF TREES AND GRASSES.
• PERENNIAL: HOUSE DUST MITES, FUNGUS SPORES ANIMAL DANDER, FEATHER AND OCCUPATIONAL INHALANTS E.G. FLOUR,
WOOD AND LATEX
2. INGESTANTS (RARE): EGG, STRAWBERRY, BANANAS, FISH, AND MILK.
3. DRUGS: ASPIRIN, PENICILLIN AND PLASMA.
23.
24. • CLINICAL PICTURE: SYMPTOMS:
• REPEATED AND PAROXYSMAL ATTACKS OF SNEEZING.
• ITCHING IN THE NOSE AND PALATE.
• BILATERAL WATERY NASAL DISCHARGE (RHINORRHEA).
• BILATERAL AND INTERMITTENT NASAL OBSTRUCTION
• ASSOCIATED CONJUNCTIVAL ALLERGY AND BRONCHIAL
ASTHMA.
• SIGNS:
• HYPERTROPHY OF THE TURBINATES
• OEDEMATOUS PALE OR VIOLET COLOURED MUCOSA OF
THE NOSE.
• WATERY OR MUCOID NASAL SECRETION.
• SEQUELAE: · CHRONIC HYPERTROPHIC RHINITIS. ·
ALLERGIC NASAL POLYP
26. • INVESTIGATIONS
1. SKIN SENSITIVITY TESTS: WITH SEVERAL ALLERGENS TO DETECT THE CAUSATIVE
ALLERGEN.
2. NASAL PROVOCATION TESTS: A SPRAY OF THE SUSPECTED ALLERGEN APPLIED INTO
THE NOSE PRODUCES SNEEZING AND RHINORRHEA.
3. BLOOD TESTS: RADIO-IMMUNO-SORBENT TEST: INCREASED TOTAL PLASMA IG E
LEVEL. RADIO-ALLERGO-SORBENT TEST: INCREASED PLASMA IG E LEVEL TO SPECIFIC
ALLERGEN.
• TREATMENT:
• AVOIDENCE: AVOID EXPOSURE OR INTAKE OF THE ALLERGEN IF POSSIBLE.
• ORAL ANTIHISTAMINES: NON-SEDATING ANTIHISTAMINES ARE TOLERABLE.
• LOCAL ANTIHISTAMINES: LEVOCABASTINE NASAL SPRAY.
• LOCAL AND ORAL CHROMOGLYCATES: WHICH ARE MAST CELL STABILIZERS.
• LOCAL AND SYSTEMIC CORTICOSTEROIDS .
• IMMUNOTHERAPY: IF MEDICAL TREATMENT FAILS.
27. VASOMOTOR RHINITIS:
• ABNORMAL REACTION OF THE NASAL MUCOSA TO NON-
ALLERGIC FACTOR DUE TO OVER ACTIVITY OF THE NASAL
PARASYMPATHETIC SUPPLY (CHOLINERGIC HYPERACTIVITY)
CAUSING VASODILATATION AND WATERY NASAL
SECRETION.
1. UNKNOWN.
2. ENVIRONMENTAL TRIGGERS: DUST, TOBACCO, AND
CHANGES IN HUMIDITY.
3. ENDOCRINAL FACTORS: PREGNANCY, MENOPAUSE, MENSES,
AND HYPOTHYROIDISM.
4. DRUGS: ANTIHYPERTENSIVE DRUGS, CONTRACEPTIVE PILLS,
AND ABUSE OF DECONGESTIVE NASAL DROPS (RHINITIS
MEDICAMENTOSA DUE TO REBOUND CONGESTION).
5. EMOTIONAL UPSET.
28. • CLINICAL PICTURE:
SIMILAR TO ALLERGIC RHINITIS WITH NEGATIVE ALLERGIC
TESTS.
• INVESTIGATIONS: NEGATIVE OF ALL TESTS FOR ALLERGY
• TREATMENT:
• MEDICAL: IPRATROPIUM (ANTICHOLINERGIC) NASAL SPRAY.
• SURGICAL: VIDIAN NERVE (NERVE OF PTERYGOID CANAL)
NEURECTOMY IF NO RESPONSE TO MEDICAL TREATMENT.
Notas del editor
Sensitization · The inhaled allergens stimulate specific IgE production by plasma cells. These immunoglobulins fix to the cell membrane of the mast cells. Such cells become sensitized to the allergen.
2. Hypersensitivity · The allergens bind to the fixed IgE on the sensitized mast cells causing degranulation of the mast cells leading to release of chemical mediators: e.g. histamine, leukotrienes, prostaglandins and chemotactic factors manifested by:1) Stimulation of nerve endings causes sneezing and nasal itching. 2)Stimulation of seromucinous glands causes rhinorrhea.3) Vasodilatation congestion increased capillary permeability causes oedema leads to nasal obstruction. § Cellular infiltration of eosinophils and basophils attracted by chemotactic factors. Basophils release vasoactive mediators which cause nasal obstruction and rhinorrhea. The nasal mucosa is continuous with the sinus mucosa, so sinuses are usually involved with thickening of the lining mucosa and fluid effusion.
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