Rhinitis is inflammation of the nasal cavity that can be allergic or non-allergic in nature. Allergic rhinitis, also known as hay fever, is caused by an allergen triggering an immune response. Non-allergic rhinitis includes acute viral/bacterial rhinitis from infections as well as chronic rhinitis from long-term irritation or obstruction. Symptoms include sneezing, congestion, and rhinorrhea. Treatment focuses on environmental control, medications like antihistamines, nasal steroids, and immunotherapy for allergies. Chronic rhinitis can lead to sinusitis if mucus is unable to drain properly from the sinuses.

1. RHINITIS
SASHA BONDI NURSING STUDENT
UZCHS NURSING SCIENCE DEPARTMENT

2. DEFINITION
 Rhinitis, also known as Coryza, is inflammation of the mucous lining of
the nasal cavity. Rhinitis is a non-specific term that covers infections,
allergies, and other disorders whose common feature is the location of
their symptoms.
 In rhinitis the mucous membranes become infected or irritated, common
symptoms being rhinorrhoea, congestion, swelling of the tissues,
sneezing and itching

3. CLASSIFICATION
 Rhinitis is classified as allergic or non-allergic, it can also be acute (short
lived) or chronic (long-standing). Acute rhinitis often results from viral
infections but may also be a result of allergies, bacteria or other causes.
Chronic rhinitis usually occurs with chronic sinusitis (chronic
rhinosinusitis).

4. ALLERGIC RHINITIS
 Also called hay fever.
 Caused when an allergen such as pollen, dust, animal dander,
is inhaled by an individual with a sensitised immune system,
triggering antibody production.

5. PATHOPHYSIOLOGY
 These antibodies, IgE, mostly bind to mast cells, which contain histamine.
 When the mast cells are stimulated by an allergen binding to the IgE, histamine is released, along with
prostaglandins leukotrienes, bradykinins, and heparin.
 This causes rhinorrhoea (sneezing, congestion, itching, redness, tearing, swelling, ear pressure, postnasal drip.).
 Mucous gland s are stimulated, leading to increased secretions.
 Vascular permeability is increased, leading to plasma exudation.
 Vasodilation occurs, leading to congestion and pressure. Sensory nerves are stimulated, leading to sneezing and
itching.
 All these events constitute the early phase or immediate phase of the reaction.
 Over 4-8 hours there is recruitment of other inflammatory cells of the mucosa i.e. neutrophils, eosinophils,
lymphocytes and macrophages. This results in continued inflammation, termed the late phase response.

6. PATHOPHYSIOLOGY CONT.
 Symptoms are similar to early phase.
 Less sneezing and itching and more congestion and mucous production
tend to occur.
 This late phase may persist for hours or days.
 The tendency to develop allergies has a genetic component.

7. CLINICAL FEATURES
 Sneezing
 Itching: nose, eyes, ears, palate
 Rhinorrhoea (runny nose)
 Postnasal drip
 Congestion
 Anosmia ( absence of sense of smell)
 Headache
 Earache
 Tearing
 Redeyes
 Eye swelling
 Fatigue
 Drowsiness
 Malaise

8. COMPLICATIONS
 include Acute or Chronic sinusitis
 Otitis media
 Sleep disturbances
 Dental problems (overbite): caused by excessive breathing through the
mouth
 Palatal abnormalities and Eustachian tube dysfunction

9. DIAGNOSIS
 Allergy skin test
 Fluorescent enzyme immune assay (FEIA): indirectly measures the
quantity of IgE
 total serum IgE: neither sensitive nor specific for the diagnosis but the
results can be helpful in some cases when combined with other factors.

10. INVESTIGATIONS
 Radiography can be helpful for evaluating structural abnormalities, detect
complication e.g. sinusitis or adenoid hypertrophy
 Coronal CT scan helpful to evaluate acute or chronic sinusitis

11. MANAGEMENT
 Environmental control measures and allergen avoidance: these include keeping
exposure to allergens such as pollen, dust mites and mould to a minimum
 Pharmacological management: nasal corticosteroid spray (phenylephrine,
oxymetazoline) or cromolyn sodium. They decrease inflammation, safe for long
term use.
 Antihistamines: diphenhydramine, loratadine, cetirizine.

12. RECOMMENDED
Fluticasone, adults 50µg 2 sprays each nostril total of 200µg daily, below 12
years 50µgeach nostril, a nasal corticosteroid spay;
fexofenadine,12years and above 60mg bd or 180mg once daily with a lot of
water, below 12 years 30 mg bd, antihistamine;
Montelukast, 15 years and over 10mg PO OD, 6-14 years 5mg PO
chewable tablet OD, 2-5years 4mg granules PO OD, 12-23 months 4mg
granules PO OD, in the evening, Leukotriene modifier.
Prednisone, 5-60mg PO maintenance dose then adjust to maintain
satisfactory response. Decrease gradually. Glucocorticoid
Ipratropium Bromide 0.06% Nasal spray to treat runny nose, adult 2 sprays
per nostril qid, 5-12 years 2 sprays per nostril qid, anticholinergic
Desensitising Immunotherapy (allergy shots); desensitising injections
that contain small amounts of the substance that triggers the allergy help
build long term tolerance to specific environmental triggers, but they may
take months to become fully effective.

13. NON-ALLERGIC RHINITIS
 There are 4 types of Non-Allergic Rhinitis; Acute (Viral/Bacterial) Rhinitis, Chronic
Rhinitis, Atrophic Rhinitis and Vasomotor Rhinitis

14. ACUTE (VIRAL/BACTERIAL) RHINITIS
 It is usually caused by a viral or bacterial infection, including the common
cold, which is caused by Rhinoviruses, Coronaviruses and Influenza
viruses, other viral causes include adenoviruses, human parainfluenza
viruses, human respiratory syncytial virus, enteroviruses.
 Bacterial causes include Streptococcus pneumonia, Haemophilus
influenza and Moraxella catarrhalis.

15. PATHOPHYSIOLOGY
 Acute Rhinitis (Viral) possesses various transmission modes and can infect a huge population at any given time.
 Transmitted to susceptible individuals through direct contact or via aerosol particles.
 The virus attaches to the respiratory epithelium and spreads locally
 On the epithelium they use the same receptors that bind leukocytes to enter and infect the cells. Symptoms
develop 1-2 days later after viral infection, peaking 2-4 days inoculation.
 As the viruses attach to the epithelial cells, natural killer T cells recognise the virus as foreign and initiates attempts
to remove them, along with the infected cells.
 The NK cells release chemical messengers that dilate surrounding blood vessels and attract additional immune cells
(neutrophils, antibody producing B cells).
 These cells release their own chemical messengers, and soon a full blown inflammatory response has been
generated.

16. PATHOPHYSIOLOGY CONT.
 This causes a local inflammatory response which causes swelling, increased
mucous production and leakiness these account for the nasal congestion and
runny nose that characterise a cold.
 Infected cells release interleukin (IL)-8, a chemo attractant of leukocytes
 The more the IL-8 secretions the more severe the cold symptoms
 In the most common presentation, symptoms develop and resolve over a course
of 10 days
 acute bacterial rhinosinusitis is preceded by an acute viral rhinitis.
 When this happens the cold symptoms get worse. At this point it is appropriate to
start antibiotic therapy.

17. CLINICAL MANIFESTATION
 Nasal dryness or irritation-may be first symptom
 Nasal Discharge
 Nasal congestion, sneezing
 Headache
 Facial and ear pressure
 Loss of sense of smell and taste
 Cough
 Hoarseness
 Posttussive vomiting
 Irritability or restlessness
 Fever (unusual, when present typically low-grade)

18. COMPLICATIONS
 Otitis media
 Sinusitis
 Chronic Bronchitis
 Exacerbations of reactive airway disease

19. DIAGNOSIS
 Through History Taking and Physical examination (findings of pharyngitis,
bronchitis, nasal congestion).
 Sputum test
 Broncho-alveolar lavage (fluid squirted into a small part of lung and then collected
for examination)
 Endotracheal aspirates (method of obtaining tracheal secretions for culture and
microbiological diagnosis)
 Sinus aspirates
 Tympanocentesis (drainage of fluid from middle ear)

20. INVESTIGATIONS
 Then these samples are taken for virus culture,
antigen or antibody detection (not rhinovirus), PCR.

21. MANAGEMENT
 Treatment is supportive with decongestants, analgesics and antipyretics as need.
 Analgesics and antipyretics can include acetaminophen (paracetamol) 2.5 ml syrup
for 3-6 months, 5ml for 6-24 months, 7.5ml for 2-4 years, 500mg from 6-12 years,
500mg-1g 12 years and above, and ASA (aspirin). Avoid ASA in children due to
Reyes syndrome
 Dextromethorphan 4-5 years2.5-5 mg Po q4h max 30mg/day,5-10mg PO q4h max
60mg/day,10-20mg PO q4h max 120mg/day or codeine 12 years and older 12-
30mg PO q4-6h prn can be used for cough suppression
 Decongestants

22. CHRONIC RHINITIS
 It is generally a prolongation of sub-acute inflammatory or
infectious viral rhinitis
 It may also rarely occur in syphilis, TB, rhinoscleroma,
rhinosporidiosis, leishmaniasis, blastomycosis, histoplasmosis
and leprosy- all of which are characterised by granuloma
formation and destruction of soft tissue, cartilage and bone

23. CAUSES
 Persistence of nasal infection due to sinusitis, tonsillitis and adenoids.
 Chronic irritation from dust, smoke, cigarette smoking, snuff.
 Nasal obstruction, vasomotor rhinitis
 Anatomical Obstruction (Nasal polyps, Deviated septum, Nasal tumour)
 Endocrinal or metabolic factors e.g. hypothyroidism
 Dryness (rhinitis sicca, impairs cilia movement an mucous flow)
 Certain medications (rhinitis medicamentosa)
 Foreign bodies (NGT, nasotracheal tube)
 Diseases (Cystic Fibrosis, Asthma, Kartegener’s [defective cilia])
 The epithelium that covers the nasal passages is contiguous with the epithelium of the sinuses, maxillary,
sphenoidal, frontal and ethmoidal sinuses
 When the nasal epithelium is affected this also affects the paranasal sinuses and the condition is best known as
Rhinosinusitis.

24. PATHOPHYSIOLOGY
 Different causes of rhinitis cause excess production of mucus causing nasal congestion, paralysis or destruction of cilia.
 The paranasal sinuses also produce mucous and cilia propel the mucous into the nasal cavity via ostia (openings into the nasal
cavity/meatus).
 Front ethmoidal sinuses, frontal sinuses, maxillary sinuses empty their mucous in the middle meatus creating a congested area
called the osteomeatal complex.
 The posterior ethmoidal sinuses and the sphenoidal sinuses open into the superior meatus.
 Clearing of mucous from the sinuses keeps them healthy and sterile, this depends on functioning cilia, thin fluid mucous and
unobstructed ostia.
 Insufficient air circulation and build-up of mucous cause pain and pressure, sinus infection and inflammation, and in response
the immune system causes more secretion of mucous as the preceding environment produces a conducive climate for
pathogen growth and multiplication, all this causing obstruction of the ostia.
 The cycle continues and thus leads to chronic rhinosinusitis.

25. CLINICAL MANIFESTATION
 Symptoms divided into major and minor
 Major; facial pain/pressure/fullness, nasal congestion, discharge,
diminished sense of smell, fever
 Minor; Headache, Halitosis, Fatigue, Tooth pain, Cough, Ear
pain/pressure/fullness.

26. COMPLICATIONS
 These are rare if managed properly
 Rhinosinusitis can spread to the facial bones or to the meninges, which could
cause brain damage due to inflammation and compression of surrounding tissue.
 It can spread to the eye socket and cause reduced vision or even blindness
 It can also sometimes spread to the neighbouring veins and cause aneurysms or
blood clots.
 Rhinosinusitis can also increase the symptoms of asthma and other chronic lung
diseases.

27. DIAGNOSIS
 Comprehensive history taking and physical assessment.
 For the condition to be classified as chronic symptoms must persist for 12
weeks or more,
 and there must be a presence of 2 or more major symptoms, one major
symptom and 2 minor symptoms or just nasal purulence.

28. MANAGEMENT
 Avoiding Allergens.
 Surgery is a last resort to correct any structural issues in the sinuses.
 Use of antihistamines should be avoided as they could cause drying.
 Treated according to chief cause of rhinitis

29. INVESTIGATIONS
 Percutaneous skin test
 Allergen-specific immunoglobulin E antibody test
 Nasal provocation testing
 Nasal cytology
 Nasolaryngoscopy

30. VASOMOTOR RHINITIS (VMR)
 It is chronic rhinitis that is characterised by intermittent episodes of sneezing, watery nasal drainage (rhinorrhoea) and blood
vessel congestion of the nasal mucus membranes
 With VMR there is no history of allergies and an irritant may or may not be identified by the patient.
 There is no infection causing the symptoms. VMR can have a variable presentation. Most patients seem to be older than the
typical patients with hay fever
 Can sometimes present with a seasonal pattern due to changes in temperature and humidity
 Patients present with rhinorrhoea, frontal headaches and congested turbinates but usually no pruritus
 Some patients will find that eating (especially spicy foods) causes more nasal dripping or congestion
 It is important to note that VMR is a nonspecific response to virtually any change or impurity in the air as opposed to allergic
rhinitis, which involves a response to a specific protein in pollen, dust, mould or animal dander.
 VMR sufferers fall into 2 categories; runners, have wet rhinorrhoea; dry, have nasal congestion, blockage of airflow and minimal
rhinorrhoea.

31. CAUSES
 Changes in temperature or barometric pressure, turbulent air
 Perfumes, strong cooking odours, smoke
 Inorganic dust (separate from house dust mite), air pollution
 Spicy foods, alcohol
 Some medications, like some blood pressure tablets (beta blockers)
 Sexual arousal
 Stress, emotional or physical

32. PATHOPHYSIOLOGY
 It is characterised by IgE response
 Mucous secretion and blood flow in the nasal mucosal lining is controlled by autonomic nervous system
 Sympathetic nervous system controls diameter of nasal resistance vessels.
 The glandular secretions and the capacitance vessels in the nasal mucosa are primarily influenced by the parasympathetic
system. Increased parasympathetic activity or hypoactivity of the sympathetic system lead to engorgement of the vessels.
 This in turn causes swelling of the nasal mucosa that presents as nasal congestion.
 Parasympathetic hyperactivity also causes increased secretions from the nasal mucosa thus causing rhinorrhoea.
 Hyperactive allergen receptors may also contribute to the pathophysiology of VMR
 Autonomic stimulation by activities such as sexual intercourse and emotional exacerbation may also affect vasomotor control in
the nasal mucosa

33. CLINICAL MANIFESTATIONS
 Sneezing
 Rhinorrhoea
 Post-nasal drip
 Nasal congestion
 Oedematous mucous membranes

34. COMPLICATION
 Difficulty sleeping
 Drowsiness during daytime
 Irritability or problems concentrating
 Nasal polyps
 Sinusitis
 Middle ear infections

35. DIAGNOSIS
 First other causes of the symptoms are ruled out.
 VMR diagnosed after taking careful history and performing a thorough
exam of the nose and throat
 Skin prick test should be performed to rule out allergies, since this would
affect the treatment approach

36. INVESTIGATIONS
 CT scan to rule out polyps
 Allergy testing (skin prick test)
 Nasolaryngoscopy
 Full blood count
 White blood cell count

37. MANAGEMENT
 Stepwise treatment option employed based on patients symptoms
 If Rhinorrhoea is predominant, Anticholinergic agent used i.e. ipratropium bromide.
 In cases with nasal congestion topical corticosteroids are used, mometasone or decongestants i.e. Pseudoephedrine
contraindicated in labile or overt hypertension, in elderly males may cause nervousness, insomnia, irritability and difficulty
urinating; oxymetazoline nasal spray.
 Topical antihistamines are best initial therapy for patients with nasal congestion, rhinorrhoea, sneezing and post-nasal drip, and
azelastine or olopatidine hydrochloride
 Exercise may be a useful adjunct, it reduces airway resistance and enhances natural decongestion of nasal cavity, however it is
short lived but can be repeated given the other benefits of exercise.
 During pregnancy symptoms may be treated with intranasal saline instillation
 If drug therapy fails surgery is considered i.e.
 Disruption of parasympathetic and sympathetic innervation of the mucosa by vidian neurectomy for reducing rhinorrhoea
 Cryosurgery for a primary complaint of nasal congestion

38. ATROPHIC RHINITIS
o It is a form of chronic rhinitis in which the underlying bone, mucous membrane
thins (atrophies) and hardens, causing the nasal passages to widen and dry out.
o This often occurs in older people, thick crusts form.

39. CAUSES
o Has a hereditary factors; disease runs in the family
o It is often seen in females and tends to start at adolescence and worsens during pregnancy and tends to cease after
menopause suggesting a hormonal factor
o Vitamin A, Vitamin D and iron deficiency
o Prolonged infections of nasal cavity with bacteria such as Klebsiella ozaenae, Proteus vulgaris and E.coli.
o TB, Leprosy and syphilis also cause wasting and destruction of the nasal structures leading to atrophic rhinitis.
o Autoimmune factors; viral infection or some other unidentified insult may trigger antigenicity of nasal mucosa
o Trauma to the nose can cause changes to the mucous membrane as in sinus surgery.
o Radiation treatment of the nose and sinuses can cause progressive atrophy.

40. PATHOPHYSIOLOGY
o Vitamin A deficiency leads to poor immune responses to infections and impairs immunity
o Vitamin D deficiency plays a part in the reduction or total loss of production of certain antibodies, vitamin D is
important in that it has an inhibitory effect on certain components of the immune system reducing the amplitude of
inflammatory responses and inflammation, and it helps immune cells function properly reducing risk of an
autoimmune attack.
o K. ozaenae causes rhinoscleroma which causes lesion on the nasal mucosa and also affects levels of CD4 cells in the
lesion inducing a decreased T cell response
o Chronic lesions lead to atrophying of the nasal mucosa
o Radiation damages DNA in some instance impairing the mechanisms of the nasal mucosa from producing proteins
needed for tissue replacement and proliferation thereby causing atrophy

41. CLINICAL MANIFESTATIONS
o Most commonly seen in females
o Reported among patients from lower socioeconomic groups
o Nasal cavities become roomy, filled with foul smelling crusts which are black or
dark green and dry, making expiration painful and difficult
o Merciful anosmia (elements responsible for the perception of smell have
atrophied)
o Complaints of congestion despite roomy nasal cavity
o Epistaxis may occur when dried discharge are removed

42. COMPLICATIONS
o In extreme cases severe deformities of the nose may occur e.g. septal perforation and dermatitis of
nasal vestibule, saddles nose deformity.
o In rare cases, destruction of tissues can extend into the surrounding tissues of the brain and into the
brain itself.
o Eustachian tube blockage causing middle ear effusion, otitis media
o Secondary infection, nasal myiasis (maggot infestation)
o Atrophic Pharyngitis
o Chronic Dacrocystitis (Infection of the nasolacrimal duct secondary to obstruction of the duct at the
junction of the lacrimal sac

43. DIAGNOSIS
o Smell of the patient
o A finding of anosmia
o Patients report that others have informed them of the smell
o A finding of nasal crust, often extensive filling entire nasal cavity
o Removal of the crusts may induce bleeding
o Volume of nasal cavity may appear large

44. INVESTIGATIONS
o Smell test
o CT scan
o Culture test
o Nasolaryngoscopy

45. MANAGEMENT
 Management can either be medical or surgical.
 Nasal irrigation using normal saline
 Nasal irrigation and removal of crusts using alkaline nasal solutions prepared by dissolving a spoonful powder containing 1 part sodium
bicarbonate, 1 part sodium biborate and 2 parts sodium chloride
 25% glucose in glycerine can be applied to the nasal mucosa to inhibit the growth of proteolytic organisms which produce foul smell.
 Local antibiotics such as chloromycetine
 Vitamin D2
 Estradiol spray for regeneration of seromucinous glands and vascuralisation of mucosa
 Systemic streptomycin, 1g/day, against Klebsiella
 Oral KI for liquefaction of secretions
 Surgical Intervention:
 Youngs operation (closure of the nasal cavity by creating mucocutaneous flaps; opened after 6 months; mucosa may revert back to normal and
crusting reduced
 Narrowing of nasal cavities; submucosal injection of Teflon paste, section and medial displacement of the lateral wall of the nose

46. references
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