Transcript Idiopathic Rhinitis

1
Amir A. Kargoshaie MD
Isfahan university of medical sciences
2


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.
3
Diseases arising primarily within the nasal cavity are discussed
here separately from those arising in the nasal sinuses, although
disease of the nose may originate in the sinuses and vice versa.
4
Allergic Rhinitis and its Impact on Asthma (ARIA)
guidelines classification of rhinitis
5
Acute Inflammations of the Nasal Cavity
Acute Rhinitis
Clinical Features. Since the common cold can be caused by different organisms,
the symptoms are not uniform. In the common form
--dry prodromal stage with generalized symptoms, including chills and a feeling of
cold alternating with a feeling of heat, headache, fatigue, loss of appetite, possibly
subfebrile temperature, but often a high temperature in children, as well as
itching, burning, a feeling of dryness in the nose and throat, and nasal irritation.
The nasal mucosa is usually pale and dry.
---The catarrhal stage usually begins a few hours later, with watery secretions,
nasal obstruction, temporary loss of smell, lacrimation, rhinolalia clausa, and
worsening of the constitutional symptoms. The nasal mucosa is deep red in color,
swollen, and secretes profusely.
-- After several days, the disease changes to a mucous phase. The generalized
symptoms begin to improve, the secretions thicken, the sense of smell improves,
and local symptoms gradually regress.
-- Resolution should be achieved within a week. The common cold, or viral
rhinosinusitis, is defined as duration of symptoms for less than 10 days.
6
Secondary bacterial infection may occur. The
secretions then turn greenish-yellow, and the
disease resolves more slowly.
Acute intermittent nonviral rhinosinusitis is
defined as an increase of symptoms after 10
days, with a duration of less than 12 weeks.
Initial catarrh occurs in influenza and
infection with other types of viruses such as
parainfluenza virus, adenovirus, reovirus,
coronavirus, enterovirus, myxovirus, and
respiratory syncytial virus.
The symptoms are as described above, but
are complicated by other manifestations
such as involvement of the entire respiratory
tract, the gastrointestinal tract (causing
diarrhea), the meninges, the pericardium, the
kidneys, and the muscles.
Purulent rhinosinusitis. The
mucosa is edematous and
hyperemic. A track of pus is
seen in the middle nasal
meatus.
7
-Pathogenesis. The infection is caused by a rhinovirus.
More than 100 types belonging to the picornavirus group have been
isolated. The disease may also be caused by numerous other viruses.
The incubation period of the rhinovirus is from 1 to 3 days. The disease
is spread by droplet infection and is exacerbated by cooling of the body.
The most common pathogens in purulent bacterial rhinosinusitis are
Streptococcus pneumoniae, Haemophilus influenzae, Moraxella
catarrhalis, Staphylococcus aureus, Streptococcus pyogenes, and
various anaerobes.
-Diagnosis. Initially, it is often not clear whether a runny nose is the initial
symptom or an accompanying symptom of a severe virus infection.
-Differential diagnosis. This can often be made only after a few days. It
includes the initial phase of an acute exanthema, allergic or vasomotor
rhinitis, congenital syphilis, and nasal diphtheria (usually in children).
8
•Treatment. There is no treatment for the basic cause. Symptomatic
treatment includes decongestant nose drops or oral decongestants.
Antibiotics should only be given for secondary bacterial infection, and
culture and sensitivity tests should be carried out beforehand. Steam
inhalations, treatment with infrared lamps, analgesics, and bed rest
should be prescribed if necessary.
•Prevention. While there is no scientific evidence that prevention is
possible, measures to improve general health may be helpful. These
include building up the patient’s overall resistance using sauna baths,
therapeutic regimens at health resorts, hydrotherapy, participation in
sports, administration of vitamin C, and scrupulous hygiene, especially in
contact with young children. Adenoidectomy may be necessary in
children . Immunization against rhinoviruses is not yet possible, but there
are vaccines against influenza.
9


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.
10

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 patient’s asthma
◦ Patients with allergic rhinitis are three times more
likely than normal controls to develop asthma later
in life
11
Source: Cumming’s Otolaryngology: Head & Neck Surgery
12
13
So the main effects are:
1- vasodilation
2-increased permeability of vessels
3-gland stimulation
14

Symptoms with allergic rhinitis develop upon
inhalation of allergens among individuals
previously exposed to such allergens and
against which they have made IgE antibodies
15

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
16

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 dysfunction—ear popping and clicking,
◦ Systemic symptoms: fatigue, irritability, sleep
disturbance
◦ Inquire about personal or family history asthma, eczema,
atopic dermatitis, allergic rhinitis
◦ Exposure to exacerbating substances—tobacco smoke,
smog
17

Timing of symptoms and definitions
◦ Traditionally classified as seasonal versus perennial
 Seasonal—due to tree pollen, ragweed, grasses,
outdoor molds
 Perennial (symptoms for >=2 hours/day for >=9
months/year)—due to dust mites, pet dander,
cockroaches, indoor molds
18


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
19
20
21

Physical Exam
◦ Head: adenoid facies—elongated 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
22
23
Allergic salute
24
History
Skin
& physical examination
tests (in vivo)
Serologic
tests (in vitro)
25

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 testing— radioallergosorbent testing (RAST) and
enzyme-linked immunosorbent testing (ELISA)
 Identify antigen-specific IgE in the patient’s serum
 Advantages: No needles, can be used for patients with
dermatographism, no potential for systemic reaction
 Disadvantages: longer turnaround time, more expensive,
less sensitive
26
 RAST
Radioallergosorbent test
 ELISA
enzyme-linked immunosorbent assay
27


Environmental control
Medical
antihistamins
corticosteroids
alpha adrenergics
mast cell stabilizers
antileukotrians
 immunotherapy
28
 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.
29
◦ House dust mites increase in warm
humid conditions, and the antigen is
found in their feces. Control
measures include removing
reservoirs (e.g., stuffed animals,
carpets, heavy drapes), covering
bedding with dust-mite–proof
covers, and washing potential
reservoirs in hot water.
30
 Frequent vacuuming with a highefficiency particulate-arresting (HEPA)
vacuum and use of acaricides (e.g.,
benzyl benzoate) and products that
denature dust mite antigen (e.g., tannic
acid) are encouraged.
 In addition, lowering the relative humidity to
less than 50% and lowering the temperature
to less than 21° C(70°F) are helpful in
controlling the dust mite population.
31
Treatment. Symptomatic:
The World Health Organization (WHO)has published guidelines on Allergic
Rhinitis and its Impact on Asthma (ARIA) , which make the following
recommendations:
● Mild to moderate symptoms (e. g., first manifestation of allergic
rhinoconjunctivitis): a third-generation oral antihistamine (e. g., levocetirizine,
desloratadine)or a topical antihistamine (e. g., an azelastine nasal spray), if
necessary with concomitant use of antihistamine eye-drops.
● Marked nasal symptoms: a combination of an oral antihistamine and a topical
steroid (e. g., mometasone, fluticasone, triamcinolone).
● Severe nasal obstruction: brief application of a nasal decongestant containing
an α-sympathomimetic drug.
Hyposensitization: short-term titration and co-seasonal hyposensitization
treatment.
Causative therapy: specific immune therapy is the only treatment modality to
address the underlying cause. It can prevent the development of allergic asthma.
32


LOCAL
SYSTEMIC
33
34

FAIRST GENERATION
◦ CLEMASTINE
◦ CLORPHNIRAMINE
◦ DIPHENHYDRANINE

SECOND GENERATION
◦ LORATIDIN
◦ AZELASTIN
THIRD GENERATION
◦ Desloratadine
◦ levocetirizine
35
36






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.
 .
37
Principle of specific immune therapy: Standardized allergen extracts of
dominant single allergens (major allergens), native or polymerized
(chemically modified) extracts—i. e., so-called allergoids—are used. They
are bound to a carrier such as aluminum hydroxide, tyrosine, or calcium
phosphate.
Application may be subcutaneous (subcutaneous immune therapy, SCIT)
or sublingual (sublingual immune therapy, SLIT).
Immunologic effects: T lymphocytes are influenced by the activation of
regulatory CD4+ T cells (IL-10, transforming growth factor β(, inducing
immediate hyposensitivity (lowered cytokine production) and replacement
of T helper subset 2 (TH2) dominance (IL-4, IL-5, IL-13) with a TH1
response.
This in turn affects the production of immunoglobulins by B lymphocytes
and inhibits effector cells (e. g., mast cells, basophilic leukocytes, and
eosinophilic granulocytes).
Effectiveness: Pollen allergy: symptoms decreased in 30 %; grass and
birch allergies in 45 %; dust allergies in 30 %.
38
39
40
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.
41
Nasal function
includes
Temperature
regulation
Olfaction
Humidification
Filtration and
Protection
42










Occupational
Drug induced
Rhinitis medicamentosa
NARES
Hormonal
Idiopathic or vasomotor
Atrophic and other mimickers
43
Arises from airborne agents at workplace.
Agents do not act through immunemediated mechanism. They are direct
irritants to the nasal mucosa and cause
non-allergic hyper-responsive reactions.
44
Chronic Inflammations of the Nasal Cavity
Rhinitis Sicca Anterior
•Clinical Features. These include a feeling of dryness,
irritation, formation of crusts in the nose, and also occasional
mild nasal bleeding .
•Pathogenesis. Several factors are responsible, such as
injury to the exposed parts of the anterior nasal mucosa,
dust, nose-picking, extremes of temperature, etc.
•Diagnosis. The nasal mucosa on the anterior part of the
nasal septum immediately posterior to the mucocutaneous
junction is dry. The mucosal surface is raw, roughened, and
granular. Crusts form, followed by ulceration and at times a
subsequent septal perforation.
•Treatment. Mild nasal oils that adhere well to the mucosa are
applied. Saline spray is also useful.
45
Chronic Rhinitis (Nonspecific Inflammation of the Nasal Mucosa)
Chronic rhinitis is one of the most common healthcare problems, with a
severe impact on lower airway disease and overall health. It is
characterized by hypertrophy of the nasal mucosa, especially around the
nasal turbinates, as well as by either hyperemia and edema, or true tissue
hypertrophy.
•Clinical Features. The main symptom is nasal obstruction, which
fluctuates markedly in the early stages and also alternates from side to
side. Later, it becomes continual and severe, and usually affects both
sides. The secretions are viscous, stringy, colorless, and only rarely
purulent. Postnasal catarrh is particularly prominent, with sniffles and
compulsive throat clearing. Other symptoms include rhinolalia clausa,
epiphora, secondary dacryocystitis, and secondary pharyngitis.
• In severe cases, fatigue, insomnia, an unsteady or woozy feeling in the
head, and, occasionally, headache and a feeling of pressure in the head
may occur. There is a general loss of psychological and physical wellbeing.
46
•Pathogenesis. The nasal mucosa is the human immunologic
“front line.” It is constantly forced to react to countless allergens
and antigens. The most important prerequisite for this function is
an intact mucociliary apparatus, which supports a wide range of
reactions—e. g., absorption, secretion, transportation, cellular or
humoral defenses . So-called inflammatory cells (macrophages,
granulocytes, leukocytes, and mast cells) are always found on
histopathological examination.
Chronic inflammation occurs when the normal capacity to react is
overstrained, and it has many etiologies. On the one hand,
recurrent inflammatory exacerbations (viral or bacterial) may cause
progressive damage to the mucociliary apparatus; on the other
hand, variations in anatomic shape (e. g., septal deviation, vomer
spur, maxillary crest, polyps, papillomas, adenoids) may elicit
chronic rhinopathy.
47
Chronic inflammation may be due to tobacco smoke and dust, chemicals,
environmental toxins, persistent extremes of temperature, abnormal
humidity, pregnancy, menstruation, menopause, endocrine disorders (e.
g., of the thyroid and adrenal glands, diabetes mellitus),diseases of the
heart and circulation, side effects of drugs, or infective allergy.
•Diagnosis. The disease is long-standing, and the history often reveals
one or more of the toxins named above. Examination shows a dark red
and partially bluish-violet swelling, affecting the inferior turbinate
especially. The nasal lumen is narrowed or obstructed. The thickened
mucosa responds to decongestant nose drops in simple chronic rhinitis,
but true tissue hypertrophy in chronic hyperplastic rhinitis does not.
In the later stages, the mucosa over the turbinates develops a slightly
granular surface, which gradually becomes nodular and demonstrates
micropolyps. These edematous processes can develop into single or
multiple nasal polyps, especially around the inferior turbinate. Often, this
true tissue hypertrophy begins at the posterior ends of the turbinates,
usually of the inferior turbinate. The choanae are then blocked by
mulberry-shaped masses, which can be seen only on endoscopic
examination of the nasopharynx or on indirect examination with a mirror.
48
•Differential diagnosis. This includes sinusitis, foreign bodies, specific infections
of the nasal mucosa , adenoidal hypertrophy, allergy, Wegener granulomatosis,
and tumors. Biopsy should be performed if appropriate.
•Treatment. Conservative: Any known or suspected etiologic agents should be
dealt with. Some medicines may need to be curtailed, drug overuse controlled,
and the patient may need endocrinology studies by a specialist physician.
Attention to the environment and occupation may prove valuable.
Symptomatic medical treatment by decongestant nose drops is only of short-term
benefit .
In the long term, uncritical symptomatic treatment is not only valueless but may
be damaging. Topical steroids (e. g., triamcinolone, mometasone, fluticasone)are
the treatment of choice in chronic hyperplastic rhinitis. These drugs are suitable
for long-term use.
Surgical treatment, in increasing order of extent:
1. Reduction of the inferior turbinate is performed with the use of various lasers,
radiofrequency surgery (Coblation), and submucosal diathermy.
2. Turbinectomy includes a limiting resection of the lower edge of the inferior
turbinate, occasionally of the middle turbinate, and from the enlarged
posterior ends of the turbinate. The purpose is to reduce the volume of the
turbinate, but atrophic rhinitis can occur if too much tissue is removed
49
50
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.
51
52
Several common medications may induce
rhinitis when administered topically or
orally.
Drugs can be divided into pharmacologic
or aspiring hypersensitivity.
53












Cocaine
Topical nasal decongestants
phosphodiesterase type-5 inhibitors
(PDE-5)--Sildenafil
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
54
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.
55
Pharmacologic rhinitis is infrequent and a
predicable side effect.
Usually lead to nasal congestion, but watery
secretions and PND can be accompanying
symptoms.
56
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.
57
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.
58
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.
59
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.
60
61
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 nonallergic rhinitis.
62
63
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.
64
65
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.
66
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.
67
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.
68
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
69
Idiopathic Rhinitis (Nasal Hyperreactivity, Vasomotor Rhinitis)
The WHO’s ARIA guidelines recommend that the term
“idiopathic rhinitis” should be used instead of noninfectious
and vasomotor rhinitis. The synopsis of classifications in the
ARIA report and the consensus report on nasal
hyperreactivity defines idiopathic rhinitis as a group of nasal
oversensitivity syndromes due to unknown
pathomechanisms.
Idiopathic rhinitis is a diagnosis of exclusion; it is considered
present if the forms of rhinitis and differential diagnoses can
be ruled out.
•Clinical Features. The International Consensus Report on the
Diagnosis and Management of Rhinitis (1994)requires at least
two symptoms from the
group urge to sneeze, runny nose, nasal obstruction, and/or
itching, lasting for more than 1 h per day.
Healthy individuals may sneeze or wipe their noses up to four
times daily.
70
Idiopathic rhinitis (IR) is usually diagnosis of exclusion.
Therefore, it is solely diagnosed on patient complaints.
•



Pathogenesis. There are three pathomechanisms:
1. Neuronal dysfunction : Neurogenic inflammation is mediated by
neurotransmitters and interacts in many ways with the immune
system. Activation of neurokinine-1 receptors in the airways causes
contraction of smooth muscles, dilation of blood vessels, glandular
secretion, and extravasation of plasma proteins. Activation of
neurokinine-2 receptors causes bronchoconstriction and stimulates
afferent nerves. Hyposympathicotonia or hyperparasympathicotonia
leads to obstruction and hypersecretion.
2. Immune inflammatory disorders: Among others, CD3+ , CD25+
,CD8+, CD45RA+ , and T cells, eosinophils, and mast cells are
increased.
3. Mucosal damage, with increased permeability for irritants.
71
Exclusion criteria for IR
Positive allergy test
Smoking
Nasal polyps
Pregnancy
Medications affecting nasal function
Beneficial effects of nasal corticosteroid
spray (NARES)
72
Studies have suggested autonomic
dysregulation, neuropeptide or nitric oxide
hyperactivity.
However, non of these studies have been
conclusive
73
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 Wegener’s
granulomatosis, sarcoidosis, and
polychondritis.
74
Atrophic Rhinitis and Ozena
Atrophic rhinitis is sometimes accompanied by a foul smell from
the nose, and in these cases it is known as ozena.
•Clinical Features. This disease occurs mainly (but not only) in
women, often beginning at puberty.
The face is typically flattened and broad.
The nasal cavity usually is filled completely with greenish-yellow
or brownish-black crusts.
Once the crusts are removed, it can be seen that the cavity is very
spacious. The mucosa is atrophic and dry due to fibrosis of the
subepithelial layer, and the inferior turbinate is atrophic.
In ozena, a fetid secretion and crusts are present. The repulsive
smell considerably hinders social contact. The patients have
anosmia, making them unaware of the unpleasant smell that they
produce.
However, they do have a sensation of nasal obstruction. There are
often severe mucosal changes, including dryness and dry, thick
crusts affecting the entire pharynx, larynx, and trachea.
75
•Pathogenesis. This is not known with certainty, but it is
probably multifactorial. Important accepted etiological factors
are malnutrition, iron deficiency, vitamin A deficiency,
immunodeficiency, and low IgA. The disease is more
common among Asians than Caucasians, and more common
in Caucasians than in people of African origin. There are
geographic concentrations—e. g., in eastern Europe and
India.
•The nasal cavity is abnormally wide due to atrophy of the
mucosa and of the bony nasal skeleton. The mucosal glands
and the sensory nerve fibers degenerate, the respiratory
epithelium undergoes squamous metaplasia, and the
mucociliary cleansing system is destroyed. The thick, gluey
secretions are decomposed by bacterial proteolysis of
Klebsiella ozaenae, Staphylococcus aureus, Proteus
mirabilis.
76
•Secondary atrophic rhinitis is caused by trauma or excessively
extensive surgery of the nose and sinuses, as well as occupational
exposure to glass, wood, asbestos, or extensive cocaine
consumption.
•Treatment. Conservative: The nose is cleansed by irrigating it
several times a day with dilute salt water and by inserting large
cotton-wool tampons impregnated with greasy ointments. Local
applications include oily nose drops, emulsions, or ointments, and
possibly vitamin A supplements. Steam inhalations with saline
solution are given, and osmotically active powders—e. g.,
dextrose—are sniffed into the nose.
Surgical treatment can be used to prevent the nose from drying
out by narrowing the nasal cavity. Two main procedures are used:
1. Bolstering of the nasal mucosa with autologous or homologous
tissue (cartilage or bone chips)
2. Median displacement of the lateral nasal wall by mobilizing and
rotating it toward the midline, then fixing it in its new position to
produce narrowing of the nasal cavity.
77
78
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.
79
80
Medical
specific treatment
nonspecific treatment
surgical
81
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.
82
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.
83
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.
84
85
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
86
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.
87
Of the antihistamines, Azelastine
intranasally 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.
88
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.
89
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
90
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.
91
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.
92
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.
93
Submucosal resection, vidian neurectomy or
the combination of the two have been
shown to be efficacious in treatment of
symptoms.
94
95