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RHINITIS

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Title: RHINITIS


1
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2
RHINITIS
  • SAYED MOSTAFA HASHEMI MD
  • Isfahan university of medical sciences

3
Rhinitis
  • Rhinitis is defined as the occurrence of annoying
    nasal symptoms including discharge, itching,
    sneezing, congestion, and pressure.
  • The rhinitis syndromes are principally recognized
    by clinical patterns.

4
Rhinitis 1-allergic type 2-Non allergic
type
5
Allergy
  • Allergic reaction is an exaggerated or
    inappropriate immune reaction and causes damage
    to the host
  • Hypersensitivity
  • Type I anaphylactic reaction mediated by IgE
    antibodies, which trigger the mast cells and
    basophils to release pharmacologically active
    agents.

6
Epidemiologic Evidence
  • Extensive overlap among the diseases
  • Asthma occurs in up to 40 of patients with
    allergic rhinitis (general population rate 10)
  • Allergic rhinitis occurs in 80-90 of patients
    with asthma (general population rate 20)
  • Allergic rhinitis is present in 60-80 of
    patients with chronic rhinosinusitis
  • Among asthmatics, 40-60 have abnormal sinus
    radiographs magnitude of sinus abnormalities
    correlates with the severity of the patients
    asthma
  • Patients with allergic rhinitis are three times
    more likely than normal controls to develop
    asthma later in life

7
Pathophysiology of Allergic Rhinitis
Source Cummings Otolaryngology Head Neck
Surgery
8
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9
Pathophysiology contd.
  • So the main effects are
  • 1- vasodilation
  • 2-increased permeability of vessels
  • 3-gland stimulation

10
  • Symptoms with allergic rhinitis develop upon
    inhalation of allergens among individuals
    previously exposed to such allergens and against
    which they have made IgE antibodies

11
Allergic rhinitis
  • Allergic rhinitis, one of the rhinitis syndromes,
    )is associated with a symptom complex
    characterized by paroxysms of sneezing,
    rhinorrhea, nasal obstruction, and itching of the
    eyes, nose, and palate(It is also frequently
    associated with postnasal drip, cough,
    irritability, and fatigue

12
Diagnosis
  • History
  • Recurrent episodes of sneezing, rhinorrhea, nasal
    congestion, and lacrimation
  • Pruritis (nasal, ocular, oral, pharyngeal) is
    highly suggestive of allergy
  • Post-nasal drip, throat clearing
  • Eustachian tube dysfunctionear popping and
    clicking,
  • Systemic symptoms fatigue, irritability, sleep
    disturbance
  • Inquire about personal or family history asthma,
    eczema, atopic dermatitis, allergic rhinitis
  • Exposure to exacerbating substancestobacco
    smoke, smog

13
Diagnosis
  • Timing of symptoms and definitions
  • Traditionally classified as seasonal versus
    perennial
  • Seasonaldue to tree pollen, ragweed, grasses,
    outdoor molds
  • Perennial (symptoms for gt2 hours/day for gt9
    months/year)due to dust mites, pet dander,
    cockroaches, indoor molds

14
Common antigens (allergens) causing
  • seasonal allergic rhinitis are tree, grass, and
    weed pollens, and fungi.
  • perennial rhinitis frequently associated with
    Indoor allergens such as dust mites, cockroaches,
    animal proteins, and fungi

15
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16
Diagnosis
  • Physical Exam
  • Head adenoid facieselongated face, open mouth,
    retracted mandible, flattened malar eminences,
    pinched nostrils, raised upper lip
  • Ears middle ear effusion or retraction
  • Eyes allergic shiners (venous stasis from
    chronic nasal congestion)
  • Nose
  • External supratip crease (allergic salute)
  • Internal pale, boggy, edematous mucosa
    inferior turbinate hypertrophy polyps
  • Throat cobble stoning of the posterior
    pharyngeal wall

17
Allergic shiners
18
Allergic salute
19
Diagnosis
  • History physical examination
  • Skin tests (in vivo)
  • Serologic tests (in vitro)

20
Diagnosis
  • Testing
  • Skin testing
  • Antigen introduced via skin puncture versus
    intradermal injection
  • Advantages rapid, inexpensive, more sensitive
  • Disadvantages affected by antihistamine therapy,
    cannot be used if patient has dermatographism,
    potential for systemic reaction
  • In vitro testingradioallergosorbent testing
    (RAST) and enzyme-linked immunosorbent testing
    (ELISA)
  • Identify antigen-specific IgE in the patients
    serum
  • Advantages No needles, can be used for patients
    with dermatographism, no potential for systemic
    reaction
  • Disadvantages longer turnaround time, more
    expensive, less sensitive

21
Serologic tests
  • RAST
  • Radioallergosorbent test
  • ELISA
  • enzyme-linked immunosorbent assay

22
treatment
  • Environmental control
  • Medical
  • antihistamins
  • corticosteroides
  • alpha adrenergics
  • mast cell stabilizers
  • antilukotians
  • immunotherapy

23
Avoidance of allergens and environmental controls
  • Patients who have seasonal allergies should avoid
    outdoor activities when allergens are in the air.
    The patient's house and workplace should be kept
    as clean as possible.

24
Avoidance of allergens and environmental controls
  • House dust mites increase in warm humid
    conditions, and the antigen is found in their
    feces. Control measures include removing
    reservoirs (eg, stuffed animals, carpets, heavy
    drapes), covering bedding with dust-miteproof
    covers, and washing potential reservoirs in hot
    water.

25
Avoidance of allergens and environmental controls
  • Frequent vacuuming with a high-efficiency
    particulate-arresting (HEPA) vacuum and use of
    acaricides (eg, benzyl benzoate) and products
    that denature dust mite antigen (eg, tannic acid)
    are encouraged.
  • In addition, lowering the relative humidity to
    less than 50 and lowering the temperature to
    less than 70F are helpful in controlling the
    dust mite population.

26
corticostroides
  • LOCAL
  • SYSTEMIC

27
Topical Nasal Steroids
28
Antihistamins
  • FAIRST GENERATION
  • CLEMASTINE
  • CLORPHNIRAMINE
  • DIPHENHYDRANINE
  • SECOUN GENERATION
  • LORATIDIN
  • ASALASTIN

29
Commonly Prescribed Antihistamines
30
Immunotherapy
  • Immunotherapy is indicated in patients whose
    symptoms are not well controlled with avoidance
    measures and pharmacotherapy. It also is
    appropriate for those with symptoms lasting more
    than 1 season and documented allergen-specific
    IgE antibodies.
  • Immunotherapy should be considered only in
    individuals who can comply with weekly injections
    for approximately 3 years.
  • Immunotherapy should be avoided in those
    receiving beta-blockers and those who have poorly
    controlled asthma, autoimmune disorders, or
    immunodeficiency disorders.
  • During pregnancy, injections should not be
    initiated, and doses should not be increased.
  • Although the exact mechanisms of immunotherapy
    are not known, they are associated with decreased
    allergen-specific IgE levels and increased
    allergen-specific immunoglobulin G (IgG) levels.
    These IgG molecules are thought to be blocking
    antibodies that are important in impeding the
    allergic reaction.
  • .

31
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32
Nonallergic Rhinitis
33
Define
  • Noninfectious rhinitis has been classified as
    either allergic or non-allergic.
  • Allergic rhinitis is defined as immunologic nasal
    response, primary mediated by immunoglobulin E
    (IgE).
  • Non-allergic rhinitis is defined as rhinitis
    symptoms in the absence of identifiable allergy,
    structure abnormality or sinus disease.

34
Introduction
  • Nasal function includes
  • Temperature regulation
  • Olfaction
  • Humidification
  • Filtration and Protection

35
Table   -- Causes of non-allergic rhinitis
  •   
  • Occupational 
  •  
  • Drug induced
  •   
  • Rhinitis medicamentosa
  • NARES
  • Hormonal
  • Idiopathic or vasomotor
  • Atrophic and other mimickers

36
Occupational
  • Arises from airborne agents at workplace.
  • Agents do not act through immune-mediated
    mechanism. They are direct irritants to the
    nasal mucosa and cause non-allergic
    hyper-responsive reactions.

37
Occupational Irritants
38
Occupational Irritants
  • Over 205 different chemicals entities identified,
    including cigarette smoke and chemicals and
    solvents like chlorine, metal salts, latex, glues
    and wood dusts.
  • Patients usually present with concurrent
    occupational asthma.
  • Diagnosis is based on history or results of nasal
    provocation with stimulus. About 70 of patient
    improve in symptoms when triggers are avoided.

39
Drug Induced Rhinitis
40
Drug Induced Rhinitis
  • Several common medications may induce rhinitis
    when administered topically or orally.
  • Drugs can be divided into pharmacologic or
    aspiring hypersensitivity.

41
MEDICATIONS CONTRIBUTING TO RHINITIS
  • Cocaine
  • Topical nasal decongestants
  • phosphodiesterase type-5 inhibitors
    (PDE-5)--Sildenafi
  • Alpha-adrenoceptor antagonists
  • Reserpine
  • Hydralazine
  • Angiotensin-converting enzyme inhibitors
  • Beta-blockers
  • Methyldopa
  • Guanethidine
  • Phentolamine
  • Oral contraceptives
  • Non steroidal anti-inflammatory medications
  • Aspirin
  • Psychotropic agents
  • Thioridazine
  • Chlordiazepoxide
  • Chlorpromazine
  • Amitriptyline
  • Perphenazine
  • Alprazolam

42
Drug Induced Rhinitis
  • Intolerance to aspirin and/or NSAIDS is
    unpredictable.
  • It is predominately produces rhinorrhea but may
    be a part of a ASA triad complex involving
    hyperplastic rhinosinusitis, nasal polyps and
    asthma.

43
Drug Induced Rhinitis
  • Pharmacologic rhinitis is infrequent and a
    predicable side effect.
  • Usually lead to nasal congestion, but watery
    secretions and PND can be accompanying symptoms.

44
Rhinitis Medicamentosa
  • Rhinitis medicamentosa (RM) is a drug induced
    non-allergic rhinitis associated with prolonged
    use of topical nasal decongestants. Also called
    rebound or chemical rhinitis
  • Incidence is btw 1-9, equal sex distribution and
    more common in young to middle age adults and
    pregnant women.

45
Rhinitis Medicamentosa
  • Nasal mucosa innervated predominately by
    sympathetic fibers. They release Norepinephrine,
    that stimulate alpha 1 and alpha 2 receptors that
    cause vasoconstriction.
  • Sympathomimetic amines (phenylephrine) and
    imidazoline derivatives (oxymetazoline) both
    produce vasoconstriction by endogenous release of
    norepinephrine.

46
Rhinitis Medicamentosa
  • Prolong use leads to reduced production of
    presynaptic norepinephrine and also leads to
    decrease sensitivity of alpha receptors causing
    need for larger dose for shorter acting time.
  • This leads to a cycle of excessive dose which
    worsens their original symptoms.

47
Rhinitis Medicamentosa
  • Risk of RM is accepted to be greatest after 10
    day use of medication.
  • Treatment is gradual stopping of decongestant
    with introduction of topical corticosteroid.
  • Pt should be warned of temporary worsening
    symptoms. Pt should be off nasal decongestants
    for 3 month before any other treatment, medical
    or surgical, can be used for original nasal
    disorder.

48
NARES
49
NARES
  • NARES, non-allergic rhinitis with eosinophilia
    syndrome, is characterized on the basis of 20-25
    or greater eosinophils in nasal smears of pt with
    rhinitis.
  • There is lack of allergy by skin test, or IgE
    antibodies.
  • Prevalence ranges from 13-33 of non-allergic
    rhinitis.

50
Numerous eosinophils on nasal mucosa
51
NARES
  • Etiology is unknown, however, NARES is believed
    to be associated with ASA triad.
  • This is due to the fact that NARES patients
    frequently develop nasal polyps and asthma later
    in life.
  • Also, abnormal prostaglandin metabolism has been
    implicated as cause of NARES
  • However, eosinophil counts are elevated in 20 of
    nasal smears of general population and not
    everyone with eosinophilias has symptoms of
    rhinitis.

52
Hormonal Rhinitis
53
Hormonal Rhinitis
  • Defined as rhinitis during periods of known
    hormonal imbalance
  • Estrogens are know to affect the autonomic
    nervous system by increasing central
    parasympathetic activity, acetyl choline
    transferase and acetycholine content. Also,
    increased inhibition of sympathetic neurons of
    alpha-2 receptors noted in pregnancy.
  • Estrogen also believed to increase hyaluronic
    acid in nasal mucosa.

54
Hormonal Rhinitis
  • Therefore, the most common causes are pregnancy,
    menstruation, puberty and exogenous estrogen.
    Hormonal rhinitis in pregnancy usually manifest
    in the second month and continues throughout the
    pregnancy.
  • Cumulative incidence of pregnancy rhinitis was
    22, 69 in women who were smokers.

55
Hormonal Rhinitis
  • Hypothyroidism may also be a known cause of
    hormonal rhinitis. In pt with hypothyroidism,
    edema increases in the turbinates as a result of
    TSH release. However, evidence is inconclusive
    at this time.
  • Nasal congestion and rhinorrhea are the most
    common symptoms of hormonal rhinitis.

56
Idiopathic rhinitis
  • Also known as vasomotor rhinitis is characterized
    by nasal blockage and rhinorrhea, but sneezing
    and pruritus is lower than allergic rhinitis.
  • Etiology is unknown, however attempts have been
    made to differentiate idiopathic rhinitis on
    basis hyperactivity to histamine, methacholine,
    cold dry air or capsaicin.
  • None of the test have been able to differentiate
    it from other forms of rhinitis

57
Idiopathic Rhinitis
  • Idiopathic rhinitis (IR) is usually diagnosis of
    exclusion.
  • Therefore, it is solely diagnosed on patient
    complaints.

58
Idiopathic Rhinitis
  • Exclusion criteria for IR
  • Positive allergy test
  • Smoking
  • Nasal polyps
  • Pregnancy
  • Medications affecting nasal function
  • Beneficial effects of nasal corticosteroid spray
    (NARES)

59
Idiopathic Rhinitis
  • Studies have suggested autonomic dysregulation,
    neuropeptide or nitric oxide hyperactivity.
  • However, non of these studies have been conclusive

60
Atrophic rhinitis et al
  • A number of conditions can produce the same signs
    and symptoms of rhinitis.
  • Structural conditions mimic rhinitis include
    deviated septum, nasal tumors, enlarged adenoids,
    hypertrophic turbinates, and atrophic rhinitis.
  • Immunologic conditions include Wegeners
    granulomatosis, sarcoidosis, and polychondritis.

61
Occupational Irritants
62
Diagnosis
63
  • A comprehensive head and neck examination
    includes nasal endoscopy.
  • Boggy and edematous mucosa with clear mucoid
    secretions suggest noninfectious rhinitis.
  • Inflammation and purulent discharge from middle
    meatus suggest active infection.
  • Areas of blanched mucosa with prominent vessels
    suggest chemical exposure
  • Atrophy of mucosa is seen in aging, prior surgery
    or drug abuse
  • Look for septal deviations, choanal stenosis,
    polyps.

64
Treatment
65
Treatment of NAR
  • Medical
  • specific treatment
  • nonspecific treatment
  • surgical

66
  • Patient education is key for initial treatment.
  • Pt are frequently not aware of triggers that
    incites their congestion
  • Avoidance of inciting factors, change in
    environment, using mask and protective equipment
  • Associated medications can be discontinued or
    changed
  • If exposure and medications cannot be changed,
    then medical therapy is next line of treatment.

67
Treatment
  • Immunologic therapy has no benefit to
    non-allergic rhinitis and therefore it is
    important to distinguish the disease before
    considering starting immunotherapy.
  • Nasal saline lavage has minor decongestant
    benefits and improves mucociliary function in
    both allergic and non-allergic rhinitis.

68
  • Topical nasal steroids are widely used for
    treatment of NAR.
  • They work on the nasal mucosa by decreasing
    neutrophils and eosinophil chemotaxis, reduced
    mast cell release and thus decrease edema and
    inflammation.

69
Topical Nasal Steroids
70
Treatment
  • Fluticasone propionate, budesonide and
    beclomthasone are the only topical steroids
    approved for NAR.
  • Efficacy is inconsistent. They must be tried for
    a minimum of 6 wks.
  • With the exception of NARES, topical steroids
    sprays do not provide the same reliefs as they do
    to allergic rhinitis

71
Treatment
  • Antihistamines have been shown to have
    inconsistent results.
  • Histamine release is the pathophysiology
    indicated for AR.
  • For this reason, they are considered a poor
    choice for NAR.

72
Treatment
  • Of the antihistamines, Azelastine intra-nasally
    has been efficacious for all forms of NAR,
    including Idiopathic Rhinitis.
  • It is an H1 receptor antagonist, that also
    inhibits synthesis of leukotrienes, kinins,
    cytokines and free radicals.
  • However, the exact mechanism of action for relief
    of symptoms is unknown.

73
Treatment
  • The anticholinergic drug Ipratropium bromide,
    which is mainly used for treatment of asthma, has
    been shown to be effective in reducing the
    severity and duration of rhinorrhea in NAR.
  • The strength of 0.03 is the dose for NAR,
    initially two sprays TID. Once symptoms abate,
    the dose should be lowered slowly until one spray
    BID.

74
Treatment
  • Mast cell stabilizers such as cromolyn, are
    effective only for allergic rhinitis and have no
    benefit with non-allergic disease.
  • No studies to date have been identified looking
    at the efficacy of leukotriene modifiers in
    treatment of non-allergic rhinitis

75
Treatment
  • Capsaicin has been shown to be of benefit to
    Idiopathic Rhinitis.
  • Nasal Capsaicin, the pungent agent of hot red
    peppers, results in rhinorrhea, nasal blockage
    and sneezing through c-fibers (pain receptors).
  • Repeated application of capsaicin, however, lead
    to desensitization and degeneration of C-fibers.

76
Treatment
  • Dosage is five high dose treatments of intranasal
    capsaisin over 1 day at 1 hr intervals after
    local anesthesia or five treatments spread out
    over 2 wks.
  • Up to 75 of patients will show long lasting
    (from 4 month to over 1 yr.) relief of symptoms.
  • Even after symptom free period is over, a repeat
    dose of capsaisin will most likely repeat itself.
  • A lower dose capsaicin formulations nasal sprays
    can be found OTC at pharmacies and used in higher
    frequencies.

77
Treatment
  • Surgery is reserved for failed medical therapy
    only.
  • Nasal polyps, inferior turbinate hypertrophy and
    septal spurs may obstruct nasal cavity and block
    the action of topical medications.

78
Treatment
  • Submucosal resection, vidian neurectomy or the
    combination of the two have been shown to be
    efficacious in treatment of symptoms.

79
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