RHINITIS(ALLERGIC AND

VASOMOTOR)
BY
DR CHUKS .P.NWOSE
SR ENT HNS,UBTH,DEC 2023
 ALLERGIC RHINITIS
• Allergic rhinitis (AR) is defined as a
symptomatic disorder of the nose
induced by an IgE – mediated
inflammation of the nasal mucosa.
 Contd
It is an antigen-mediated inflammation of the
nasal mucosa that may extend into the
paranasal sinuses.

• Allergic rhinitis (AR) refers to two

significant clinical areas:

1. Rhinitis – inflammation of the nasal mucous

membranes;
2. Allergy - the specific cause of the rhinitis.
 PREVALENCE OF ALLERGIC RHINITIS.

• Allergic rhinitis is a global health problem

and the prevalence has been noted to be on
the increase.

• Patients from all countries, all ethnic groups

and all ages suffer from AR.

• However, the prevalence is higher in

children with a peak among the 6 – 7yr olds.
 Causes of Allergic Rhinitis

• Genetic predisposition (family history of allergic

rhinitis is often present)
• Environment (exposure to allergens such as pet
dander,house dust mite such Dermatophagoides
pteronyssinus)
• Some medications may cause symptoms that can be
confused with allergic rhinitis
– α- or β-blockers
– ASA
– NSAIDs
– ACE inhibitors
 OVERVIEW OF PATHOPHYSIOLOGY

There are 3 phases

1. Sensitization
2. Early / Immediate reaction
3. Late / delayed reaction

Sensitization
For allergy to exist, allergen sensitization must first occur.
Antigen-presenting cells, such as macrophages and
dendritic cells that are present in the mucosal surfaces ,
detect the allergen.
 .

• The antigen-presenting cells come into contact with

the allergen which, in people predisposed to atopy,
is perceived to be an invader.

• The allergen is then absorbed, processed and

displayed on the surface of the antigen-presenting
cell.

• This cell then migrates to the T-lymphocyte (T-cell)

and presents the allergen, which then stimulates
the B-cell to produce antibodies specific to the
allergen.
 .

• These specific antibodies, IgE, are then released, and

attach themselves to high-affinity receptors on the
surfaces of mast cells in the mucosal surfaces
SENSITIZATION.

Early Reaction Phase

Thereafter there is a period of latency, and on
subsequent re-exposure to the allergen the early
allergic response is triggered.

The allergen cross-links with the IgE on the surfaces of

the mast cell or basophil, causing the cell to
 .

• These include largely histamine, cysteinyl

leukotrienes, prostaglandins and kinins.

• They have different actions in terms of symptoms in

different organs.

• The late phase is promoted by factors generated in

the early phase, which encourage release of
inflammatory mediators and the activation and
recruitment of cells to the nasal mucosa.
 .

Allergen-specific IgE binds to the high affinity

receptor for IgE (FcεRI) on the surface of mast
cells.

IgE SENSITIZATION
• Genetic factors and immunologic change
reactions ??
.
 EARLY PHASE (IMMEDIATE)
RESPONSE

• The early or immediate phase response occurs in IgE-

sensitized individuals within minutes of exposure to
the allergen and lasts for about 2-4 hours.

• Mast cell degranulation is the main occurrence in the

early phase response.

• Mast cells are abundant in the epithelial

compartment of the nasal mucosa and can be easily
activated upon re-exposure to the allergens.
 Effects of the Mediators

• They are responsible for allergic reactions, by

causing mucosal edema, increased vascular
permeability and nasal discharge in AR.

• Histamine, the major mediator of AR, stimulates the

sensory nerve endings of the trigeminal nerve and
induces sneezing and itching.
 Contd.

• Histamine also directly stimulates the mucous

glands to cause secretion of mucous and nasal
discharge.

• The leukotrienes and prostaglandins act on the

blood vessels causing vasodilatation nasal
congestion.
 LATE PHASE RESPONSE

• 4-6 hours after allergen stimulation, the early phase

response is usually followed by the late phase
response.

• The late phase response lasts for about 18-24 hours

and is characterized by influx of T lymphocytes,
basophils and eosinophils in the nasal submucosa.
 Contd

• Several mediators released by these cells include

leukotrienes, kinins, histamine, chemokines and
cytokines, which result in the continuation of the
symptoms.

• The production and release of a variety of cytokines

such as IL-4, IL-5, IL-9 and IL-13 from mast cells, ILC,
basophils and Th2 cells play a role in the
prolongation of the late phase response.
 .

• The late phase response is characterized by a

prolongation of symptoms of sneezing, rhinorrhea
and sustained nasal congestion.

• AR also triggers a systemic inflammation besides

local inflammation, which can in turn augment
inflammation in both the upper and lower airways.

• This explains the link to asthma.

 Clinical Phases of Allergic Response.
• ACUTE OR EARLY PHASE.
• Occurs within 5-30min, after exposure to allergen.
– Sneezing, rhinorrhoea, nasal blockage / bronchospasm.
– Due to vasoactive amines eg Histamine.

• LATE OR DELAYED PHASE.

Occurs 2-8hrs after exposure.
– Due to infiltration of inflammatory cells.
– Marked by congestion and thick secretion
 Chemical Mediators
Preformed Newly Synthesized
• Histamine • PGD2

• ECF-A • Leukotrienes eg SRS-A

• NCF-A • PAF

• Heparin • Thromboxane

• TNF
 CLINICAL EVALUATION
• History
 Onset, timing, duration, seasonality, severity,
 Associated symptoms, aggravating/alleviating
factors
 Thorough environmental history
 Family history of atopy
 Suspected allergens
 Nasal trauma
 EXAMINATION
• General:
• ENT: nasal salute,transverse nasal crease on dorsum ,pale
bluish nasal mucosa,watery rhinorrhea.Tympanic
membrane maybe dull and retracted{OME).
• EYE:Watery red eyes,Dennie morgan flods or
lines,allergic shiners(dark/grey circles under the lower
eye lid)
• CHEST: Rhochi
• Skin: ezcematous changes,Dermatographism(raised
inflammed skin lines after scratching)
 Differential Diagnosis
• Non-allergic rhinitis
– Infectious, NARES, vasomotor rhinitis, atrophic rhinitis,
drug induced, hormonally induced, exercise, reflex

• Structural/mechanical factors
– Septal deviation, turbinate hypertrophy, adenoid
– hypertrophy, foreign body, tumors

• Inflammatory/immunologic
– Wegener’s, sarcoidosis, midline granuloma, SLE, Sjogren’s
• CSF rhinorrhea
 ARIA Differential Diagnosis for Symptoms of Allergic
Rhinitis:
• Symptoms suggestive of Allergic Rhinitis
– 2 or more of the following symptoms for > 1 hour on
most days:
• SOIRE
• Sneezing
• Obstruction (nasal)
• Itchy nose
• Rhinorrhea
• Eye symptoms – Itchy, watery, redness etc
 .

Symptoms usually not associated with allergic

rhinitis
• Unilateral symptoms
• Nasal obstruction without other symptoms
• Mucopurulent rhinorrhea
• Post nasal drip with thick mucus
• Facial pain
• Recurrent epistaxis
• Anosmia
 INVESTIGATIONS
• Allergy Testing
– Nasal smear
– Skin testing
– In vitro testing
Nasal provocation tests

• Radiology
• Endoscopy
• Lung function tests
 Nasal smear

• Looks at nasal secretion component cells

• Can help differentiate allergic rhinitis and NARES

(non allergic rhinitis with eosinophilia) from other
forms of rhinitis
 Skin testing

• The goal of testing is to identify antigens to which

patients are symptomatically reactive and to
quantify the sensitivity if immunotherapy is
planned.

• There are a variety of acceptable techniques:

– Prick testing, intradermal testing, intradermal
dilutional testing, and in vitro testing
 Skin prick/scratch

• Superficial skin reaction, does not penetrate dermis.

• Highly specific, sensitive, convenient and safe

• Requires positive (histamine) and negative (saline)

control
 Skin prick

• Droplet of antigen is introduced about 1 mm deep

into the skin.
• Correlates with RAST, and set endpoint dilutional
testing (81-89%). Gungor et al Grade A

• Disadvantages
– Patient discomfort
– Intertester variability
– Non-standardized allergen extracts, and different
interpretation scales
 Intradermal testing

• A dilute antigen extract is injected into the dermis,

and a superficial wheal forms.

• Causes relatively minimal patient discomfort

• Disadvantages
– higher risk of anaphylaxis
– Time intensive
– Possible false positive
 In vitro testing

• RAST (radioallergosorbent assay) measures antigen

specific IgE

• Safe and highly sensitive

• Better for patients taking beta-blockers.

• Patients on antihistamines (skin testing is unreliable)

• Patients with dermatographism, and children that cannot

tolerate skin testing
 RAST
RAST is a radioimmunoassay test developed in the late
60's for the detection of specific serum IgE antibodies.

• Initial studies demonstrated a 96% efficiency, sensitivity

and specificity.

• The modified RAST is the form now used.

• It was introduced by Fadal and Nalebuff in 1977 with

the advantages of increased test sensitivity without a
loss in specificity.
 CLASSIFICATION OF AR

• In 2001, a group of experts, the “Allergic Rhinitis and

its Impact on Asthma (ARIA) Workshop Expert Panel”,
met to develop guidelines on the diagnosis and
treatment of rhinitis.

• The panel also dealt with other inflammatory

processes interrelated/associated with asthma.

• The acronym “ARIA” comes from “Allergic Rhinitis and

 ARIA New Classification of AR

Intermittent symptoms Persistent symptoms

•<4days per week •>4days/week
•Or <4 weeks •And >4 weeks

Mild Moderate-severe
all of the following One or more items
•Normal sleep •Abnormal sleep
•No impairment of daily activities, •Impairment of daily activities,
sports, leisure sports, leisure
•No impairment of work & school •Impaired work and school
•No troublesome symptoms •Troublesome symptoms
The ARIA recommendations led to a
shift in the management of AR from

Opinion – based practice

Evidence – based practice

Patient focused care.

 TREATMENT METHODS

• Allergen avoidance
– Environmental control measures

• Pharmacotherapy

• Immunotherapy

• Surgery
 Morbidities associated with AR
.Sleep Disturbances (Difficulty falling asleep
snoring,Day time
sleepiness,Fatigue,Irritability,Poor
concentration,Psychomotor
impairments,Cognitive impairments
ring,Sleep fragmentation,Sleep apnoea).
• Decreased productivity,Absenteeism,Loss of
man hours,Poor school performance.
 complications
 Asthma
 Conjunctivitis
 Sinusitis
 Nasal Polyposis
 Aspirin intolerance and nasal polyps.
 Otitis media
 Atopic dermatitis
 VASOMOTOR RHINITIS
• Is a non allergic rhinitis(NAR) described as non
infectious and non allergic. It’s the most common
type of NAR.
• Its etiology is not well understood but thought to
be associated with dysregulation of
sympathetic,parasympathetic and nociceptive
nerves innervating the nasal mucosa.Imbalance in
the mediators leads to increased vascular
permeability and mucosal secretions from the
submucosal nasal glands.
• Acetylcholine is the main parasym NT that
regulates mucus secretion and
rhinorhea,norepinephrine and neuropeptide Y
are symp NTs that regulate the vascular tone of
nasal mucosa blood vessels and also modulate
the parasym system initiated secretions.
Nciceptive type C fibers of the trigeminal nerve
contribute to mast cell degranulation as well as
itching/ sneezing reflexes.
THANKS