RHINITIS

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RHINITIS

• SAYED MOSTAFA HASHEMI MD
• Isfahan university of medical sciences

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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.

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Rhinitis1-allergic type 2-Non allergic
type
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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.

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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

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Pathophysiology of Allergic Rhinitis
Source Cummings Otolaryngology Head Neck
Surgery
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Pathophysiology contd.

• So the main effects are
• 1- vasodilation
• 2-increased permeability of vessels
• 3-gland stimulation

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

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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

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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

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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

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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

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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

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Allergic shiners
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Allergic salute
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Diagnosis

• History physical examination
• Skin tests (in vivo)
• Serologic tests (in vitro)

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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

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Serologic tests

• RAST
• Radioallergosorbent test
• ELISA
• enzyme-linked immunosorbent assay

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treatment

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

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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.

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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.

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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.

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corticostroides

• LOCAL
• SYSTEMIC

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Topical Nasal Steroids
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Antihistamins

• FAIRST GENERATION
• CLEMASTINE
• CLORPHNIRAMINE
• DIPHENHYDRANINE
• SECOUN GENERATION
• LORATIDIN
• ASALASTIN

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Commonly Prescribed Antihistamines
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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.
• .

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Nonallergic Rhinitis
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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.

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Introduction

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

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Table   -- Causes of non-allergic rhinitis

•   
• Occupational 
•  
• Drug induced
•   
• Rhinitis medicamentosa
• NARES
• Hormonal
• Idiopathic or vasomotor
• Atrophic and other mimickers

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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.

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Occupational Irritants
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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.

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Drug Induced Rhinitis
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Drug Induced Rhinitis

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

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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

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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.

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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.

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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.

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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.

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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.

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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.

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NARES
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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.

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Numerous eosinophils on nasal mucosa
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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.

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Hormonal Rhinitis
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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.

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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.

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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.

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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

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Idiopathic Rhinitis

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

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Idiopathic Rhinitis

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

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Idiopathic Rhinitis

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

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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.

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Occupational Irritants
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Diagnosis
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• 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.

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Treatment
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Treatment of NAR

• Medical
• specific treatment
• nonspecific treatment
• surgical

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• 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.

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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.

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• 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.

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Topical Nasal Steroids
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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

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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.

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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.

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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.

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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

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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.

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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.

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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.

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Treatment

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

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