1. Rhinosinusitis
• By Dr Amit Jha ,
•PG Resident , ENT-HNS

2. • Inflammation of the mucous membrane of nose and
paranasal sinuses
• It accounts for about 5% of visits to primary care
physicians.
• RS in children is a multifactorial disease and the
importance of predisposing factors changes with
increasing age.
• There is almost always involvement of nose in all
the inflammatory sinus condition.
• Therefore Task force of the Rhinology and
Paranasal Sinus Committee in 1997 suggested the
term rhinosinusitis (RS), instead of sinusitis.

4. o It is an inflammatory condition of one or more
of the para-nasal cavities
o Lasts up to 4 weeks
o Can range from acute viral rhinitis (common
cold) to acute bacterial rhino-sinusitis

5. • lasts 4-12 weeks
• Sub-acute rhino-sinusitis usually involves one
or two pairs of the paranasal cavities.

6. • It is the inflammatory and infection that
concurrently affects the nose and para-nasal
sinuses
• Lasts for longer than 12 weeks

7. • 4 or more recurrences of acute disease within a 12-
month period,
• With resolution of symptoms between each episode
lasts greater than 2 months .
• In most cases, each episode lasts for at least 7 days

8. • URTI
• Cold weather
• Day care attendance
• Smoking in the home
• Anatomic abnormalities (nasal polyps, ciliary disorder, septal deviation,
concha bullosa, turbinate hypertrophy, tumors, congenital abnormalities i.e.
cleft palate)
• Immunesupressed
• Direct extension: dental infection, facial fractures
• Inflammatory disorder:
– Wegener's Granulomatosis
– Sarcoidosis
• Mucosal disorder
– CF
– Allergic Rhinitis and other hyperreactivity
– Samter syndrome
• Asthma
• Nasal Polyps
• Aspirin intolerance .

9. • Viral (10-15%) - Rhinovirus (most common viral sinusitis cause),
Influenza, Parainfluenza,Adenovirus
• Bacterial
– Acute Sinusitis: S.Pneumoniae, H.Influenzae, Moraxella,
Streptococcus Pyogenes
– Chronic Sinusitis:
• Anaerobes (>50%)
– Bacteroides,Anaerobic Gram Positive Cocci, Fusobacterium
species
• Other less common causes
– Staphylococcus aureus, Hemophilus Influenzae, Pseudomonas
aeruginosa, Escherichia coli, Beta-hemolytic Streptococcus,
Neisseria causes
• Fungal (Immunocompromised or DM)
Aspergillus, Mucormycosis…

11. Allergic Rhinitis
 Allergic rhinitis involves inflammation of the mucous
membranes of the nose, eyes, eustachian tubes, middleear,
sinuses, and pharynx.
 Rhinitisdue to IgE mediated inflammation following
exposure to allergen.
 Affects 10-25% of global population .
 The nose invariably is involved, and theotherorgans are
affected in certain individuals.

12. Classification based on ARIA guidelines
Intermittent
. < 4 daysperweek
. or < 4 weeks
Persistent
. > 4 days perweek
. and > 4 weeks
Mild
-normalsleep
- no impairmentof daily
activities, sport,
leisure
- normal work and
school
- no troublesome
symptoms
Moderate-
severe
one or more of
following
. abnormal sleep
. impairmentof daily
activities, sport,
leisure
. abnormal work and
school
. troublesome
symptoms

13. 2 Types:
• Seasonal (summer, spring, early autumn)
– Tree pollens, grass pollens, mold spores
– Lasts several weeks
– Disappears and recurs following year at the same time
• Perennial
– Inhaled: house dust, wool, feathers, foods, tobacco, hair
– Ingested: wheat, eggs, milk, nuts
 occurs intermittently for years with no pattern or may be
constantly present
Causes :

14. Risk factors
Geneticsand family history
 The bestestablished risk factor forallergic rhinitis is a
family historyof allergy, especiallyof allergic rhinitis.
 Genes which appear to be involved in atopy includean
area on the 5q chromosome.

15. Environment-
Lifestylechanges, increased exposure toallergen, pollution
and irritants, dietary modifications leading to a reduction
in Th 1-type immune responseand stress.
 Pollution increases symptomatic rhinitis.
 Living in developed countries, pollution, climate
interaction and good hygieneall seem to be risk factors.
Co-morbidities-
Conditions associated with allergic rhinitis are asthma,
sinusitis, otitis media, sleep disorders, LRTI & dental
occlusion.

16. PATHOPHYSIOLOGY
 Allergic reactionoccurs in fourphases-
1. Sensitization
2. Subsequentreaction toallergen-early phase.
3. Late phasereaction.
4. Systemicactivation.

17. Sensitization
 In atopies, allergen molecules are inhaled and
presumably notcompletelycleared by the mucociliary
system.
 They reach antigen presenting cells in the nose, the
most importantof which are dendriticcells /
Langerhanscells.
 Theycaptureantigen, process itand present it to naive
T cells in the local lymph nodes.
 If noadditional signal is present then a T-cell response
will notensue.
 In atopic individuals, Th2 cells predominateat the
sitesof allergic response.

18. Sensitization
 In the secondary immuneresponse, anycell expressing
surface MHC class 2 may serve as an antigen-
presenting cell, including the nasal epithelium.
 Activated, Th2 cells secretecytokines, (IL-4, IL- 13 , IL-
5).
 They also activate B lymphocytes in the local
lymphoid tissues, encouraging them to proliferate,
migrate to the nasal lining and produce IgE antibody.
 Once produced, the IgE isvery rapidly taken up by
mastcells.
 Thus mastcellsareable specifically torespond to
subsequentallergen contact.

19. Subsequent reaction to allergen: early
phase
 Mastcellsare encouraged todegranulateonce their
cell-bound IgE has been cross-linked byallergen.
 Secretionof histamine, leukotriene C4 &
prostaglandin D2 in nasal mucus.
 Histamine & cytokines are preformed while
leukotriene and PGs are manufactured from
membranearachidonicacid.

20.  Histaminecauses
 Rhinorrhoea, sneezing, pruritisand nasal obstruction.
(The response is of short duration)
 Action on sensory nerves induces itching and sneezing.
 Prostaglandins induces
 Sustained nasal obstruction and is ten times more
potent than histamine.
 Leukotrienes induce
 Vascularpermeabilityand oedema in the nose
 Involved in eosinophil and neutrophil recruitment.
 Cytokinesare important in regulationof IgE response.

21. Late phase response
 This is inflammatory in nature.
 Involves the ingress of cells such as eosinophils, basophils,
mast cells, T lymphocytes, neutrophils and macrophages
into the local reaction site.
 The main symptomsare nasal obstruction and hyper-
reactivity.
 Eosinophil products increase local vascular permeability
and mucus secretion and cause further inflammatorycell
influx

22. Systemic activation
 Upregulation of production and release of eosinophil
and basophil precursors from the bone marrow occurs
in response toallergen contact in the noseor lung.
 The resultantcirculating precursorsare attracted to
the reaction site & otherpartsof respiratory tract.

23. The four phases o f the
allergic reaction in the
nose.

24. Diagnosis of Allergic Rhinitis
 Mostallergic rhinitis patientscan bediagnosed bya
combinationof
 History,
 Examination
 SPT (Skin Prick Test )
 Radioallergoabsorbent tests (RAST) forspecific IgE.

25.  Importantelements in history includean evaluationof
 the nature, duration, and timecourse of symptoms;
 possible triggers forsymptoms;
 response to medications;
 comorbid conditions;
 family historyof allergic diseases;
 environmental exposures;
 occupational exposures;
 effects on qualityof life.

26.  Symptoms thatcan beassociated with allergic rhinitis
include
 sneezing,
 itching (of nose, eyes, ears, palate),
 rhinorrhea,
 postnasal drip,
 congestion,
 headache,
 earache,
 tearing, red eyes, eyeswelling,
 fatigue, drowsiness, and malaise.

27. Examination
 Look at the pt toassessanyobviousexternal features,
such as an ” allergiccreaseorallergicsalute.”
 Atopicdermatitisorconjunctivitisshould noted.
 A full ENT examination should then becarried out
with particularemphasis on the nose.
 Allergic nasal mucosa is usually bilaterallyswollen pale
or bluish in colour, oedematous and covered with
waterysecretions.

28. Allergic salute

29. Allergic Rhinitis

30. Diagnostic tests
 Demonstrationof IgE allergy

31. SPT(SKIN PRICK TEST)
 Allergen introduced into the
skin causes degranulation of
IgE-sensitized mast cells with
mediator release and
formationof awheal and flare.
 Simple ,cheap & safe.
 Low risk of systemic reactions.
 Always undertaken where
emergency equipments and
resuscitationcapablestaff is
available

32.  Should not be performed in ptson antihistaminesor
with severeeczema, previousanaphylaxis
 Positiveresults- reaction >2mm in under fives
>3mm in adults.

33. BLOOD TESTS FOR ALLERGY
 Thiscan be undertaken by RASTs
(radioallergosorbent test) or by fluorescent assays and
enzyme-linked immunosorbent assays (ELISA).
 RAST involves
 allergen bound toasolid phase, &
 incubated with the patient'sserum and
 IgE molecules bind to theallergen.
 Afterdetailed washing, radio labelled anti-IgE is added
 the radioactivity is measured.

34.  CAP RAST is a recent improvement in which
 theallergen iscoupled toacellulose carrier
 anti-IgE is enzyme-labelled with a fluorescent substrate
acting as thedeveloping agent.
 This system has a highersensitivityand specificity than
RAST test
 ELISA test
 allergen is in the fluid phase
 IgE isenzyme-labelled.
 The substrate for theenzyme isadded and
 the resulted colourchange isdetected photometrically.

35. Immunoassay vs Skin Test for Diagnosis of Allergy
Immunoassay
 Not influenced by
medication
 Not inf luenced by skin
disease
 Does not require
expertise
 Qualitycontrol possible
 Expensive
Skin test
 Highersensitivity
 Immediate results
 Requiresexpertise
 Cheaper

36. NASAL ALLERGEN CHALLENGE
 Allergen is introduced into the noseand any reaction
is measured and compared to placebo.
 This is thegold standard of allergy diagnosis, but is
rarely necessary.
 The allergen should be applied in gradually increasing
concentrationswith careful monitoring.
 Nasal challenge testing is time-consuming, difficult
and requires extensive laboratory facilities.

37. Management of allergic rhinitis
The managementof allergic rhinitis involves the
following
components:
 Allergen avoidance
 Pharmacotherapy.
 Allergen immunotherapy
 Surgery is rarely needed

38. Globally important sources of
allergens
 House dust mites
 Grass, tree and weed pollen
 Pets
 Cockroaches
 Molds

39. Basic treatment plan for allergic
rhinitis according to severity and duration.

40. 1. Identification and avoidance of allergen
2. During the acute attack:
1. Antihistamine (systemic or intranasal)
2. Local steroids
3. Decongestant (ephedrine)
3. Sodium cromoglycate (mast cell stabilizer
used as prophyaxis)
4. Desensitization (we keep exposing the body to
gradually increased amounts of allergen until the
body fails to produce IgE as a result to exposure).
Treatment

41. Allergen Avoidance
 Pets
 Remove pets from bedroomsand, even better, from theentire home
 Vacuum carpets, mattresses and upholsteryregularly
 Wash petsregularly (±)
 Molds
 Ensuredry indoorconditions
 Useammonia to remove mold from bathrooms and otherwet spaces
 Cockroaches
 Eradicate cockroacheswith appropriate gel-type, non-volatile, insecticides
 Eliminate dampness, cracks in floors, ceilings, cover food; wash surfaces, fabrics to
removeallergen
 Pollen
 Remain indoorswith windows closed at peak pollen times
 Wearsunglasses
 Useair-conditioning, where possible
 Install carpollen filter

42. Newer Generation Oral Antihistamines
 First line treatment for mild allergicrhinitis
 Effective for
 Rhinorrhea
 Nasal pruritus
 Sneezing
 Less effective for
 Nasal blockage
 Possibleadditional anti-allergicand anti-inflammatory effect
 In-vitroeffect > in-vivoeffect
 Minimal or nosedative effects
 Oncedailyadministration
 Rapid onsetand 24 hourduration of action

43. Nasal Corticosteroids
 Beclomethasonedipropionate
 Budesonide
 Ciclesonide
 Flunisolide
 Fluticasonepropionate
 Mometasone furoate
 Triamcinoloneacetonide

44. Nasal Corticosteroids
• Most potent anti-inflammatory agents
• Effective in treatmentof all nasal symptoms including
obstruction
• Superior toanti-histaminesand anti-leukotienes
• First line pharmacotherapy forpersistentallergic rhinitis

45. IMMUNOTHERAPY
 Repeated administration of an allergen extract in order to
induce immunological tolerance,with a reduction in
clinical symptoms & requirements for medication during
subsequent natural allergen exposure.
 Indicated in those pts of AR who fail to respond adequately
to usual t/twith antihistamines & topical corticosteroids.
 The sublingual route involves application of allergen as
drops or tablets under the tongue where theyare retained
forseveral minutes.

46. Mech . Of immunotherapy
 Immunotherapy results in a blunting of seasonal
increases in allergen-specific IgE.
 Induces immune deviation from Th2- type T
lymphocyte response in favourof a protectiveTh1-type
response & also to induce a distinct population of T
regulatory cells which produce the inhibitory
cytokines IL-10, TGF B, both of which downregulate
Th2 responses toallergens.

47. Indications for immunotherapy in
AR
 INCLUSION CRITERIA
 IgE mediated
disease(+RAST)
 Inability toavoid
allergen.
 Inadequacyof drug
treatment.
 Ptswho understand risks
& limitationsof t/t.
 CONTRINDICATIONS
 Coexistentasthma.
 Pts taking beta-blockers.
 Other
medical/immunological
dis.
 Small children.(<5yrs)
 pregnancy

48. Anti IgE - omalizumab
 Could be considered in severe cases unresponsive to
conventional treatment
 Could be an adjunct to immunotherapy in severe cases
Nasal Surgery
 Nasal surgery may be needed where there is a marked
septal deviation or bony turbinate enlargement which
makes topical nasal sprays usagedifficult

50.  The term Nonallergic rhinitis' is commonlyapplied to
a diagnosis of any nasal condition in which the
symptoms are identical to those seen in Allergic
rhinitis butan allergicaetiology has been excluded.
 Occur more frequently in adults than in children
 More likely to be perennial than seasonal.

51. NON ALLERGIC PERENNIAL
RHINITIS
TYPES:
1.Vasomotorrhinitis
2.Infection
3.Rhinitisassociated with physical orchemical
factors
4.Drug, food induced rhinitis
5.NARES, aspirin sensitivity
6.Rhinitisof pregnancy
7.Atrophic rhinitis

52. • Very common
• Non-inflammatory, non-allergic rhinitis
• Characterized by a combination of symptoms that
includes nasal obstruction and rhinorrhea
• Vasomotor rhinitis is a diagnosis of exclusion reached
after taking a careful history, performing a physical
examination, and, in select cases, testing the patient with
known allergens
• 2 types ; eosinophilic & non-eosinophilic (according to
the number of eosinophils found in the nasal secretion)
Vasomotor Rhinitis

53. • Temperature change
• Alcohol, dust, smoke
• Stress, anxiety, neurosis
• Endocrine – hypothyroidism, pregnancy,
menopause
• Parasympathomimetic drugs
Causes

54. Symptoms:
• Chronic intermittent nasal obstruction
• Rihinorhea (thin, watery)
Signs:
• Mucosa & turbinates : swollen, pale between
exposure
Clinical features

55. • Elimination of irritant factor
• Symptomatic relief with exercise
• Parasympathetic blocker
• Steroids
• Surgery
Treatment

56. Vasomotor Rhinitis
Surgical Treatment
 Turbinate surgery --Electrocautery,cryosurgery,
laser
 Correction of anatomical deformity
 Conchotomy
Parasympathetic nasal fibers divisions
(vidian neurectomy)

57. Atrophic rhinitis
 Predominantly in women & is charaterised by
progressiveatrophyof the nasal mucosa & underlying
boneof the turbinates.
 Leads to formation of thick crusts, which leavea
constant foul smell ( ozaena) in nose.
 Nasal cavities areenlarged & there is sensationof nasal
congestion.
 Thought to bedue to infection with klebsiella
ozaenae.

58. Atrophic Rhinitis
clinical presentation
 Greenish–yellow or brownish-black crusts
 Wide nasal cavity
 Atrophic mucosa & dry
 Subepithelial layer fibrosis
 Fetid secretion &crusts (Ozena)
 Anosmia & social problem
 Nasal obstruction
 Mucosal changes

59. Atrophic Rhinitis
Diagnosis
 Gluey, dry, greenish-yellow secretions & crusts
 wide nasal cavity & very small turbinates
Foul-smelling crusts

60. Atrophic Rhinitis
Conservative Treatment
 Nasal douching
 Alkaline nasal lotion
 Greasy ointments
 Oily nasal drops, emulsions , orointments
 Steam inhalations
 Osmotic Powders :Dextrose

61. Atrophic Rhinitis
Operative Treatment
 Bolstering of the Nasal Mucosa
by submucous injections of paraffin . Teflon strips,
powdered teflon in glycerine, plastipore, boneand
cartilage Insertion submucosally.
 Median Displacement of the lateral nasal wall by
internal rotationof the mobilized lateral nasal wall.

62.  Young’soperation
Both nostrilsare closed completely justwithin nasal
cavity by raising flaps. Opened 6 month or later.
 Modified Young’soperation
toavoid discomfortof bilateral nasal obstruction,
nostrilsare partiallyclosed.

63.  Hormonal rhinitis-a/w pregnancy.
Oestrogens cause vascular engorgement in the nose
leading to nasal obstruction and/or nasal hypersecretion.
 EMOTIONALLY INDUCED RHINITIS
Emotional factors such as stress and sexual arousal have
been documented toaffect the nose,as a result of
autonomicstimulation.
 Drug induced- aspirin, other nsaids,B blockers,ACE
inhibitors,methyldopa,OCPs, nasal topical decongestants
induce symptoms of rhinitis when administred either
topicallyor systemically.

64.  FOOD-INDUCED RHINITIS
Certain foodsand alcoholic beverages can induce
nonallergic rhinitis .
Underlying mechanismsare largely unknown.
Hotand spicy foods lead toawatery rhinorrhoea
termed 'gustatoryrhinitis', probablyas a resultof the
capsaicin stimulating the sensory nerves to release
neuropeptidesand tachykinins.
Alcoholic beverages are thought to induce symptoms
as a resultof vasodilation.

65. RHINITIS DUE TO PHYSICAL AND
CHEMICAL FACTORS
In individuals with sensitized nasal mucous membranes.
Cold, dry air has been shown to lead toacondition known
as skier's nose, in which rhinorrhoea features prominently.

66. Rhinitis medicamentosa
 Persistent overuse of the topical nasal vasoconstrictors
also leads to nasal decongestion
 by a mechanism involving a rebound effect following
withdrawal of thesedrugs,
 excessiveuseof theseagents mayalso lead to nasal
hyper-reactivity and hypertrophy of the nasal mucosa
known as rhinitis medicamentosa.

67.  NARES- condition where there is presence of >20%
eosinophils in nasal smears of symptomaticpts with
perennial sneezing attacks, profusewatery
rhinorrhoea, nasal pruritis, incomplete nasal
obstruction & often lossof smell.
Marked feature is lack of evidence of allergy, as
indicated by negative SPT &/orabsence of serum IgE
antibodies tospecific allergens.
Triad of nasal polyposis , intrinsicasthma, intolerance
toaspirin-sampter’s triad.

68. THERAPY FOR NONALLERGIC
PERENNIAL RHINITIS
 Topical steroids & antihistaminesare the two main
drugs used.
 Use of fluticasone propionate, budesonide,
beclomethasone & azelastine has been approved by
the FDA.
 Azelastine nasal spray is effective forcontrol of
rhinorrhoea, postnasal drip, sneezing nasal
congestion.

69. Ocupational rhinitis
 Episodicwork related symptomsof rhinitis which
usually manifest on weekdays & abate during
weekends & holidays.
 Risk factors fordeveloping occupational rhinitisare:
o Exposure{intensity & duration}
o Atopy
o Smoking.

70.  Pathological effects of various chemicals & organic
dustsare eitherdue toan allergic reactionor irritation
of nasal mucosa.
 Nose is the portal of entry & materials impacton the
mucous surface as a function of aerodynamic
equivalentdiameter(AED)
 Approx 80% of those that havean AED of more than 9
micrometre, 50% of thosewith 2-9 micrometre AED &
40% of material wth less than 2 micrometre stick to
the nasal wall.

71.  Occupational rhinitis frequentlycoexistswith asthma
& conjunctivitis.
 Prevention is the bestapproach .
 In medical therapyonly non sedating antihistamines
should be used.

72. References :
• Scott-Brown's Otorhinolaryngology-Head and Neck
Surgery. Ed by Gleeson, Browning, Burton et al (7th Ed
2008; Hodder Arnold).
• Cummings Otolaryngology-Head and Neck
Surgery. Flint, Haughey, Lund et al (5th Ed 2010; Mosby).
• Current Diagnosis & Treatment in Otolaryngology-Head
and Neck Surgery. Lalwani (3rd Ed 2011; McGraw-Hill
Medical).
• Otolaryngology and Head and Neck Surgery - Oxford
Specialist Handbooks in Surgery. Warner, Burgess,
Patel et al (1st Ed 2009; Oxford).
• Oxford Handbook of ENT and Head and Neck
Surgery. Corbridge

73. THANK YOU !