RHINITIS

Ricky Yue, M.D.

Department of ENT-HNS
Faculty of Medicine
Atmajaya Catholic University of Indonesia
The nose act as a “gate-keeper” or a
“security check-point” for the entire airway
Introduction
 Inflammation of the nasal cavity (nasal mucosa)
 AR >< NAR
 Cause enonomic burden in US .
 Direct cost  1.9 billion annually
 Cost of lost productivity  3.8 billion annually
Introduction
Non Allergi Rhinitis
A. Infective
a. Acute
b. Chronic
 Specific
 Non Specific: Immune deficiency, Clearance
abnormality
B. Non-Infective
a. Hyperreactivite (vasomotor rhinitis, drug induced
rhinitis)
b. Anatomical (and mechanical)
c. Tumours
Acute Rhinitis
 Definition : Acute viral or bacterial infection of
the nasal mucous membrane.
 Synonym : “ common colds”, influenza, flu
(selesma)
 Causative agents :
 Viral infection  most common
 Bacterial infection
Acute Rhinitis
 Predisposing factors :
 Climate changes
 Environment, temperature and humidity
 Immune status, chronic illness
 Nutritional and vitamin deficiency
 Viruses causing common colds :
 Rhinovirus ( 50%)
 Coronavirus (15-20%)
 Influenza, parainfluenza, adenovirus (15-20%)
 Others (10-20%)
Acute Rhinitis
 Mode of transmission :
 Most common droplet infection (air-borne
disease).
 Contact
 The incubation period of the pathogen : 3-7 days.
 Incidence :
 Children and young adult
 Women
 Men
Acute Rhinitis
 Clinical presentation :
1. Dry stage : malaise (lethargy, headache, fever) &
local discomfort in the nose and nasopharynx
(burning and soreness)
2. Catarrhal stage :
 watery- serous nasal discharge, nasal
obstruction due to mucosal swelling, headache
and febrile.
 Damages of the mucociliary clearance system
profuse nasal discharge and inflammatory
process in nasal vestibule.
 Damages of the epithelium promote a
secondary infection (bacterial infection) 
watery-serous nasal discharge becomes a
mucopurulent nasal discharge.
Acute Rhinitis
 Resolution phase usually happened after 7-10
days.
 Complications of the acute rhinitis :
 Sinusitis
 Nasopharyngitis and pharyngitis
 Otitis media
 Tonsillitis
Acute Rhinitis
 Treatment :
 Supportive treatment ( bed rest & symptomatic
treatment)
 Antibiotic is not recommended , EXCEPT in
case of super-infection and or secondary
infection.
 Humidification, steam inhalation relieve nasal
discomfort.
Specific Chronic Rhinitis
 Chronic Inflammation of the nasal mucosa
caused by a specific pathogen/organism :
 Atrophic Rhinitis
 Diptheria Rhinitis
 Tuberculosis
 Rhinoscleroma
 Syphilis
 Fungal Infection
 Nasal Myasis
Atrophic Rhinitis
 Chronic inflammation of the nasal mucosa, causes :
 Progressive atrophy of the nasal mucosa and turbinate
 Especially in female
 Related to socio-economic status and environmental
condition.
 Etiology  unknown (multifactorial) :
 Bacterial infection : Klebsiella ozaena
 Fe defisiency
 Vit A defisiency
 Chronic Sinusitis
 Hormonal imbalance
 Autoimmune disorder
Atrophic Rhinitis
 Pathologic findings :
 Metaplasia of the epithelium from columnar-ciliated
to squamous type
 Fibrosis of the tunica propria
Atrophic Rhinitis
 Clinical manifestations :
 Foul odour, greenish, mucopurulent nasal secretion
 Crusting formation
 Anosmia
 Nasal obstruction & headache
 Endoscopy examination :
 A dry, crusted mucosa
 Ancillary procedures :
 Histopathologic investigation middle turbinate
biopsy
 Culture and sensitivity test
 PNS CT-Scan
Atrophic Rhinitis
 Treatment : Conservative & Surgical
 Conservative treatment :
 AB based on the C&S test
 Nasal douche 2-3/ a day using hypertonic saline
solution
 Vit A 3X50.000 iu
 Ferrous sulphate for 2 weeks
All factors that considered has correlation to AR,
should also be treated.
Atrophic Rhinitis
 Surgical Treatment : To reduce a nasal volume
 Implants to fill nasal volume
 Closure of the nostrils
 BSEF can be applied in atrophic rhinitis to
eradicate infection and to restore the normal
function of the sinuses
Diphtheria Rhinitis
 Etiology : Corynebacterium diphtetiae
 Nose can be a primary or secondary infection
from pharynx
 Acute & Chronic
 Slow 3 months into recovery phase
 Prevalence ↓ due to immunization
 Clinical manifestations : Fever, lymphadenitis,
paralysis respiratory muscles in severe cases
Diphtheria Rhinitis
 Local manifestations :
 Nasal obstruction & congestion
 Nasal discharge : watery bloodstained
mucopurulent
 Whistish pseudo-membranous adherent to
nasal mucosa easily bleed
 Ancillary procedure : Bacteriologic examination
from nasal secretions
 Treatment :
 Isolation room
 ADS
 AB Penicillin ( local or intramuscular)
Tuberculosis
 Extra pulmonary infection of the mycobacterium
tuberculoses and a primary infection caused by
inhalation of infectious droplets, forming a primary
complex + 6 weeks post infection
 Nodular >< Ulcerative
 Site of infection : cartilagenous nasal septum 
perforation
 Clinical manifestations :
 Nasal obstruction  mucopurulent nasal discharge + crusts
 Slightly pain
 Lupus vulgaris most common post primary form of the
cutaneous tuberculosis
 Dx : Bacteriologic examination of the nasal
discharge
 Treatment :
 Anti-TB drug
 Nasal douche
Rhinoscleroma
 Chronic granulomatous disease who manifest in
the nose, oral mucosa and upper respiratory
tract.
 Klebsiella rhinoscleromatis
 Endemic in the East part of Indonesia
 Clinical manifestations almost similar to atrophic
rhinitis
Rhinoscleroma
 3 stages of rhinoscleroma :
 Atrophic stage : crust formation & foul-smelling
discharge
 Granulation or nodular stage : inflammation mucosa
granulation formation  cause destruction of the
cartilage and bone (nasal deformity)
 Cicatrizing stage : transformation of the granulation
 fibrotic tissue & sclerotic formation (nasal
obstruction)
 Dx : biopsy  pathological characteristics :
presence of the plasma cells, lymphocytes, and
eosinophil, scattered large foam cells ( Mikulicz
cell)
Rhinoscleroma
 Treatments :
 AB for minimal 4 weeks :
 Tetracycline, Chloramphenicol,
Trimetrophrime- Sulfametoksazole,
Ciprofloxacin, Clyndamicin, Cephalosporin.
 2 consecutive biopsy after treatment showed (-)
 Surgery : to remove the granulation tissue and
cicatrix.
 Plastic surgery
Syphilis
 Etiology : Treponema pallidum
 Very rare
 3 classes of syphilis :
 Primary : a hard, non tender ulcerated papul on the external
nose/ nasal vestibule. Disappears spontaneously in 6-10
weeks
 Secondary : most infectious stage (6-10 weeks after
innoculation)  Simple catarrhal rhinitis
 Tertiary : mainly in the nose.
 Characteristic : isolated gummata or diffuse gummatous
infiltration of the nasal cavity( septum) destruction septal
perforation.
 Dx : microbiologic & biopsy examination
 Treatment :
 Antisphilitic treatment : Penicillin
 Nasal douche
 Regular nasal cleaning to remove the crust formation
Fungal infection
 Invasive >< Non-Invasive
 Close relation to sinusitis
 Invasive : Present of the fungal hifa in lamina propria
(submucosal layer) Perforation & Saddle nose
deformity.
 Non-Invasive : present of rhinolith + severe inflammation
process of the nasal mucosa.
 Etiology :
 Aspergillosis sp : most common
 Candida, histoplasmosis, Fussarium sp, Mucormycosis,
Rhinosporidium sp
 Treatment :
 Non-Invasive : Removal of the fungus ball (rhinolith)
 Invasive : Systemic & local Anti-Fungal
Nasal Douche
Nasal Reconstruction if needed
Nasal Myasis
 Common in tropical countries
 Etiology : infestation of larvae (chrysomia
bezzina)
 Related to :
 Bad hygiene conditions
 Have source of offensive decaying material :
 Atrophic rhinitis
 Chronic rhinosinusitis
 CSOM
Provide a suitable environment for egg of the fly
 larvae.
 Can affect eye, ear, nose, oral cavity, vagina,
anus
Nasal Myasis
 Clinical manifestations:
 Diffuse swelling around nose and eyes
 Nasal obstruction
 Epistaxis & foul smelling nasal discharges
 Presence of maggots coming out of the nose
 Rhinoscopy shows : congested oedematous
mucosa, necrotic material with embedded
maggots, ulcerated mucosa or septal perfortion.
 Can have a PNS , Lacrimal, & intracranial
extension
 Treatment :
 Admit
 Broad spectrum AB or based on culture’s result
 Local/ topical mixture of Chloroform : terpentin oil = 1 : 4
 Regular nasal toilette
Non Allergic, Non Infectious
Rhinitis
Dr. Ricky Yue, Sp. THT-KL
Department of ENT-HNS
Faculty of Medicine, Atmajaya Catholic
University
Introduction
 Non infectious NAR inflammation of the nasal mucosa.
 3 primary causative factors:
 Hyperreactive :
 Autonomic imbalance
 Post-infective
 Hormonal
 Drug induced
 Emotional
 Anatomical (and mechanical)
 Choanal atresia
 Adenoids
 Septal deformities
 Hypertrophic turbinates
 Polyps
 Foreign bodies
 Tumours
Introduction
 In case hyperreactivity:
 Difficult to establish the diagnosis
 “Wastebasket diagnosis”
 Can be manifest as “Mixed Rhinitis”
 Anatomical & tumour  more simple
 Early Dx & treatment
Vasomotor Rhinitis
 Chronic rhinitis due to “idiopathic” condition in the
absence of :
 Allergy
 Infection
 Hormonal changes
 Exposure to drug
 Synonym : idiopathic rhinitis
 Similar to allergic rhinitis in some clinical
features.
Vasomotor Rhinitis
 A differences of VMR compare to AR :
 Adult onset (more on female)
 Not worsened by exposure to classic allergen such
pollen, house dust, dog, cat.
 (-) skin prick test or in vitro test for allergen-specific
IgE (radioallergosorbent test)
 Multifactorial
 Has several hypotheses pathophysiology of
VMR
Pathogenesis
 Autonomic dysfunction
 Trauma
 Neuropeptides
 Nitric oxide
 Acid reflux
Autonomic Dysfunction
 Hypoactive sympathetic nervous system
 sympathetic nerve  vasoconstriction &
decrease of the nasal secretion, thru noradrenalin
& neuropeptide Y release.
 Fluctuated of the sympathetic tonus is reflecting a
normal nasal cycle.
 Parasympathetic nerve  vasodilatation &
increase nasal secretion, thru acetylcholine &
vasoactive intestinal peptide release.
 The action mechanism of the complex nerve
system not yet fully understood
Trauma
 VMR has been reported as a long-term
complication of the surgical and non surgical
trauma, via neurogenic &/ neuropeptide action.
Neuropeptide
 Speculation on the role of the sensory nerve
endings and autonomic dysfuntion.
 Type C nociceptive nerves releases
neuropeptides including substance P & calcitonin
gene-related peptides ↑plasma extravasation
and glandular secretion nasal congestion.
Nitric Oxide
 ↑NO  necrosis & decreased viability of the
normal nasal mucosa (epithelial disruption) 
↑reactivity of the afferent trigeminal fibers &
recruitment of secretory & vascular reflexes in
nasal mucosa symptomatic VMR
Acid Reflux
 Based on autonomic dysfunction
 Pt with both VMR + esophageal reflux showed a
significant greater degree of the autonomic
dysfunction compared with pt with isolated VMR.
Diagnosis
 Rule out other rhinitis
 Symptoms :
 Nasal obstruction (change in position), watery nasal
discharge, sneezing
 Less itching, redness, watery eyes
 History related to a temperature changes,
consumptions of the hot liquid or alcohol, or less
specifically to “emotional stress”
 No family & personal history of atopi or allergies,
medications, ahnormal hormonal status, pregnancy.
Diagnosis
 Anterior Rhinoscopy
 Similar to allergic rhinitis
 Ancillary tests :
 (-) Skin allergic testing or in vitro tests for specific
IgE
 (-) nasal wash cytology or nasal brushings for
eosinophils
Treatment
 Principles of treatment :
 Avoid predisposing factors
 Medical treatment
 Surgical treatment
 Based on a dominant symptoms :
 Sneezers : AHS & topical GCS
 Runners : topical anti cholinergic
 Blockers : oral decongestant & topical GCS
Medical Treatment
 Nasal Corticosteroid
 First-line therapy
 Reduce inflammatory conditions
 Antihistamines
 First generation AHS anticholinergic actions
 Intranasal AHS reduce inflammatory effects
 Anticholinergic
 Best for rhinorrea predominant VMR variants
 Better compare to AHS based on the side effects
such as dry mouth, sedation and urinary hesitancy
limit
Medical Treatment
 Decongestants
 Reduce nasal congestion/blockage
 Side effects  neurogenic and cardiac stimulation,
palpitation and insomnia effect
 Contraindication : hypertension
 Other medical treatment
 Isotonic & Hypertonic saline nasal washing
 Application of capcaisin
 Botulinum toxin A injection to inferior & middle turbinates
 Antileucotrienes therapy
 Acupunture therapy
Surgical Treatment
 In case turbinate hypertrophy : surgical reduction
of the inferior turbinate
 In case septal deviation : septoplasty
 In case intractable VMR :
 Vidian nerve neurectomy
 Sphenopalatine ganglion block
Drug-Induced Rhinitis
 Synonym :Rhinitis medicamentosa, chemical
rhinitis, rebound rhinitis
 Drug-induced non allergic rhinitis associated with
prolonged use of topical nasal decongestant.
Introduction
 Incidence 1-9%
 Equal sex distribution
 More common in young to middle-aged adult and
pregnant women
 2 dominant factors :
 Nasal mucosa microcirculation
 Action mechanism of drugs
Nasal Mucosa Microcirculation

 The nasal mucosa has a rich microcirculation

 Innervated by :
 Sympathetic nerve (↑) epinephrine post
sinaptic receptors :
 Alpha-1 & alpha-2  vasoconstriction
 Beta receptor  vasodilatation
 Parasympathetic nerve acetylcholine, VIP
increase nasal secretions, vasodilatation
 Sensory C-fibre & NANC peptide nasal
congestion by reducing sympathetic tone
Topical Nasal Decongestant
 2 groups :
 Sympathomimetic amines, e.g.
Phenylephrine, efedrine,
pseudoephedrine alpha-1
 Imidazoline derivatives, e.g. Oxymetazoline,
xylometazoline alpha-2
 Act as vasoconstrictor by stimulating nor-
epinephrine alpha receptors.
Pathophysiology
 For sympathomimetic amines:
 Stimulation beta-receptor is masked by alpha-
receptor, but more longer than alpha-receptor
 Vasodilatation occur after vasoconstriction effect
has stopped “ rebound congestion “
 For imidazoline derivatives :
 Prolonged use of imidazoline derivatives may
reduce the production nor-epinephrine due to (-)
feedback mechanism.
 Leads to insufficient endogenous norepinephrine to
maintain sympathetic tone increase
parasympathetic activity “rebound congestion”
Diagnosis
 Symptoms :
 Nasal obstruction
 Rhinorhea
 History chronic used of vasoconstrictor drugs > 7-
10 days.( 3 days-2months)
 Anterior rhinoscopy :
 Mucosa edema
 Hypertrophy concha
 Excessive nasal secretions
 No effect using adrenaline topical
Treatment
 Stop the drugs that can cause rhinitis
 Intranasal steroid at least 6 weeks for maximum
effect
 High dose oral corticosteroid up to 40 mg/day and
tapered 5mg every day
 AHS
 Turbinate steroid injection
after 3 weeks without improvement ENT
referrals
Rhinitis of Pregnancy
 Extremely common
 20-30% of pregnant women
 Usually in the last trimester
 Resolves spontaneously within 2 weeks of
delivery
 Due to progesterone stimulation mucosal
congestion
 Allergic Rhinitis (ARIA Guideline 2007)

Intermittent Persistent
. < 4 days per week . ≥ 4 days per week
. or < 4 weeks . and ≥ 4 weeks

Mild Moderate-severe
normal sleep one or more items
& no impairment of daily . abnormal sleep
activities, sport, . impairment of daily
leisure activities, sport, leisure
& normal work and . abnormal work and
school school
& no troublesome . troublesome symptoms
symptoms