Presentation on theme: "Allergic Rhinitis in Children"— Presentation transcript:
1Allergic Rhinitis in Children Dr. KANUPRIYA CHATURVEDI
2Outline of Presentation What is allergic rhinitis?EpidemiologyPathophysiologyDiagnosis and differential diagnosisAssessment and classification of ARHealth effects of ARManagement of AR
3What is Allergic Rhinitis Allergic rhinitis involves inflammation of the mucous membranes of the nose, eyes, eustachian tubes, middle ear, sinuses, and pharynx.The nose invariably is involved, and the other organs are affected in certain individuals.Inflammation of the mucous membranes is characterized by a complex interaction of inflammatory mediators but ultimately is triggered by an immunoglobulin E (IgE)–mediated response to an extrinsic protein
4IgE mediated Rhinorhoea Nasal blockage Postnasal drip Itchiness SneezingAssociated health effectsIgE mediatedAllergic rhinitis 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 [1-3].The pathogenesis of allergic rhinitis is presented in this topic review. The clinical manifestations, diagnosis, and treatment of this condition are discussed separately. (See "Clinical manifestations and epidemiology of allergic rhinitis (rhinosinusitis)" and "Diagnosis of allergic rhinitis (rhinosinusitis)" and "Pharmacotherapy of allergic rhinitis".)
5PathophysiologyThe tendency to develop allergic, or IgE-mediated, reactions to extrinsic allergens has a genetic component.In susceptible individuals, exposure to certain foreign proteins leads to allergic sensitization, which is characterized by the production of specific IgE directed against these proteins.This specific IgE coats the surface of mast cells, which are present in the nasal mucosa.When the specific protein is inhaled into the nose, it can bind to the IgE on the mast cells, leading to immediate and delayed release of a number of mediators.
6PathophysiologyThe mediators that are immediately released include histamine, tryptase, chymase, kinins, and heparin.The mast cells quickly synthesize other mediators, including leukotrienes and prostaglandin D2.These mediators, via various interactions, ultimately lead to the symptoms of rhinorrhea (ie, nasal congestion, sneezing, itching, redness, tearing, swelling, ear pressure, postnasal drip).Mucous glands 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 of these events can occur in minutes; hence, this reaction is called the early, or immediate, phase of the reaction
7PathophysiologyOver 4-8 hours, these mediators, through a complex interplay of events, lead to the recruitment of other inflammatory cells to the mucosa, such as neutrophils, eosinophils, lymphocytes, and macrophages.This results in continued inflammation, termed the late-phase response.The symptoms of the late-phase response are similar to those of the early phase, but less sneezing and itching and more congestion and mucus production tend to occur.The late phase may persist for hours or days.
8EpidemiologyFrequency: Allergic rhinitis affects approximately 40 million people in the United States. Recent US figures suggest a 20% cumulative prevalence rate. Scandinavian studies have demonstrated a cumulative prevalence rate of 15% in men and 14% in women. The prevalence of allergic rhinitis may vary within and among countries. This may be due to geographic differences in the types and potency of different allergens and the overall aeroallergen burden.Mortality/Morbidity- While allergic rhinitis itself is not life-threatening (unless accompanied by severe asthma or anaphylaxis), morbidity from the condition can be significant. Allergic rhinitis often coexists with other disorders, such as asthma, and may be associated with asthma exacerbations.
9EpidemiologyRace: Allergic rhinitis occurs in persons of all races. Prevalence of allergic rhinitis seems to vary among different populations and cultures, which may be due to genetic differences, geographic factors or environmental differences, or other population-based factors.Sex: In childhood, allergic rhinitis is more common in boys than in girls, but in adulthood, the prevalence is approximately equal between men and women.Age: Onset of allergic rhinitis is common in childhood, adolescence, and early adult years, with a mean age of onset 8-11 years, but allergic rhinitis may occur in persons of any age. In 80% of cases, allergic rhinitis develops by age 20 years.
10Diagnosis of Allergic Rhinitis History & symptoms of recurrent or persistent rhinitis and/or associated health effectsSigns of atopy and recurrent or persistent rhinitisDemonstration of IgE allergyExclusion of other causes of rhinitis— The diagnosis of allergic rhinitis is made on clinical grounds based upon the characteristic history (including presence of risk factors), symptoms and signs on physical examination, and (if indicated) the confirmed presence of allergen-specific IgE. Symptoms should also be reproducible on exposure to allergens to which the patient has been sensitized. (See "Clinical manifestations and epidemiology of allergic rhinitis (rhinosinusitis)".)A positive response to a therapeutic trial of either topical nasal steroids or topical antihistamines does not establish a diagnosis of allergic rhinitis . These two therapies, which are often useful in the treatment of allergic rhinitis, are also effective in the treatment of perennial nonallergic rhinitis .
11Diagnosis of Allergic Rhinitis History & clinical symptoms of recurrent or persistent rhinitis and/or associated health effectsRhinorhoeaNasal blockagePostnasal dripItchinessSneezingOthers: conjunctivitis, eczema, asthma, chronic rhinosinusitis, otitis media with effusion, sleep obstruction…
12HistoryImportant elements in history include an evaluation of the nature, duration, and time course of symptoms; possible triggers for symptoms; response to medications; comorbid conditions; family history of allergic diseases; environmental exposures; occupational exposures; and effects on quality of life.Symptoms that can be associated with allergic rhinitis include sneezing, itching (of nose, eyes, ears, palate), rhinorrhea, postnasal drip, congestion, headache, earache, tearing, red eyes, eye swelling, fatigue, drowsiness, and malaise.Some forms of allergic rhinitis can be readily diagnosed by history alone. Seasonal allergic rhinitis caused by tree and grass pollen typically occurs in the spring (rose fever), and symptoms caused by ragweed pollen exposure in the fall (hay fever), although there are regional variations (figure 1). Symptoms of seasonal allergic rhinitis are predictable and reproducible from year to year.By comparison, classic perennial allergic rhinitis is associated with nasal symptoms which occur for more than two hours per day and for more than nine months of the year. Perennial allergic rhinitis usually reflects allergy to indoor allergens like dust mites, cockroaches, or animal dander, although aeroallergens may cause perennial rhinitis in tropical or subtropical climates.The presence of consensus risk factors for atopy provides additional support for the diagnosis of allergic disease. This is particularly true for those with a personal or family history of atopic disease, as well as a clear history of animal and pollen triggers of allergic rhinitis symptoms. A review of multiple studies proposed symptomatic classification of allergic rhinosinusitis by frequency ("intermittent" or "persistent") and severity ("mild" or "moderate-severe"). The WHO had targeted allergic rhinitis because of its impact on asthma, and the classification is strikingly similar to consensus asthma guidelines .
13Symptoms and chronicity Determine the age of onset of symptoms and whether symptoms have been present continuously since onset.Determine the time pattern of symptoms and whether symptoms occur at a consistent level throughout the year (ie, perennial rhinitis), only occur in specific seasons (ie, seasonal rhinitis), or a combination of the two.During periods of exacerbation, determine whether symptoms occur on a daily basis or only on an episodic basis. Determine whether the symptoms are present all day or only at specific times during the day.Determine which organ systems are affected and the specific symptoms.
14Trigger factorsDetermine whether symptoms are related temporally to specific trigger factors. This might include exposure to pollens outdoors, mold spores, specific animals, or dust while cleaning the house.Irritant triggers such as smoke, pollution, and strong smells can aggravate symptoms in a patient with allergic rhinitis. These are also common triggers of vasomotor rhinitis.Other patients may describe year-round symptoms that do not appear to be associated with specific triggers. This could be consistent with nonallergic rhinitis, but perennial allergens, such as dust mite or animal exposure, should also be considered in this situation.
15Co-morbid conditionsPatients with allergic rhinitis may have other atopic conditions such as asthma or atopic dermatitis.Look for conditions that can occur as complications of allergic rhinitis. Sinusitis occurs quite frequentlyOther possible complications include otitis media, sleep disturbance or apnea, dental problems (overbite), and palatal abnormalities.Nasal polyps occur in association with allergic rhinitis, although whether allergic rhinitis actually causes polyps remains unclear.Investigate past medical history, including other current medical conditions. Diseases such as hypothyroidism or sarcoidosis can cause nonallergic rhinitis.
16Family historyBecause allergic rhinitis has a significant genetic component, a positive family history for atopy makes the diagnosis more likely.A greater risk of allergic rhinitis exists if both parents are atopic than if one parent is atopic.However, the cause of allergic rhinitis appears to be multifactorial, and a person with no family history of allergic rhinitis can develop allergic rhinitis.
17Environmental exposure A thorough history of environmental exposures helps to identify specific allergic triggers.This should include investigation of risk factors for exposure to perennial allergens (eg, dust mites, mold, pets).Risk factors for dust mite exposure include carpeting, heat, humidity, and bedding that does not have dust mite–proof covers.Chronic dampness is a risk factor for mold exposure.A history of hobbies and recreational activities helps determine risk and a time pattern of pollen exposure.
18Diagnosis of Allergic Rhinitis Signs of atopy and recurrent or persistent rhinitisAtopic individuals respond to allergen exposure by producing allergen-specific IgE. IgE antibodies bind to IgE receptors on mast cells throughout the respiratory mucosa and to basophils in the peripheral blood. When the same allergen is subsequently inhaled, the allergen binds to and crosslinks IgE on the mast cell surface, resulting in activation and release of inflammatory mediators.Nasal mast cells release histamine, prostaglandins, leukotrienes, PAF, and bradykinin, among other mediators. These result in the signs and symptoms of allergic rhinitis. Tissue eosinophilia is also a feature of allergic rhinitis, and eosinophil-derived mediators are associated with nasal epithelial injury and desquamation, subepithelial fibrosis, and hyperresponsiveness.The allergic nasal response consists of an immediate phase, which peaks at 15 to 30 minutes after allergen exposure and corresponds to mast cell degranulation and mediator release, and a late phase, which peaks at 6 to 12 hours after exposure and corresponds to infiltration of the nasal tissues by eosinophils, basophils, and other inflammatory cells. Patients with allergic rhinitis usually have similar inflammatory changes in the linings of the paranasal sinuses.
20Diagnosis of Allergic Rhinitis Demonstration of IgE allergyAllergic rhinitis is associated with a symptom complex characterized by paroxysms of sneezing, rhinorrhea, nasal obstruction, post nasal drainage, and itching of the eyes, nose, and palate. (See 'Introduction' above.)Identification of the specific allergens to which the patient is sensitive is not necessary for successful treatment in many cases. However, patients whose symptoms are severe or refractory to therapy should be referred to an allergy specialist for a more definitive evaluation. Properly performed skin testing is the best method for determining allergic sensitization.The differential diagnosis of allergic rhinitis includes acute and chronic rhinosinusitis, chronic nonallergic rhinitis, rhinitis medicamentosa, atrophic rhinitis, and rhinitis due to systemic medications.
21Immunoassay vs Skin Test for Diagnosis of Allergy Not influenced by medicationNot influenced by skin diseaseDoes not require expertiseQuality control possibleExpensiveSkin testHigher sensitivityImmediate resultsRequires expertiseCheaperSerum tests for allergy — Immunoassays to detect allergen-specific IgE antibodies in the serum have limited utility in the diagnosis of allergic rhinitis. (These tests are sometimes referred to as radioallergosorbent tests, or RASTs, because earlier methods utilized radioactive reagents. The methods currently in use are more correctly referred to as immunoassays for allergen-specific IgE).Skin testing — Carefully performed immediate hypersensitivity skin testing (prick skin tests) is a quick, relatively inexpensive, and safe way to identify the presence of allergen specific IgE. These tests are usually performed by allergy specialists. In sensitive patients, testing with selected diagnostic vaccines of tree, grass, or weed pollen, mold, house dust mite, and/or animal allergens results in a wheal and flare reaction at the skin test site within 20 minutes.Skin testing is particularly useful among patients with:An unclear diagnosis based upon the history and physical examinationPoorly controlled symptoms, such as persistent nasal symptoms and/or an inadequate clinical response to nasal glucocorticoidsCoexisting persistent asthma and/or recurrent sinusitis/otitis
22Other Causes of Rhinitis in Children InfectionViral, bacterial,RhinosinusitisForeign body in the noseRhinitis associated with physical or chemical factorsDrug, food induced rhinitisNARES, aspirin sensitivityVasomotor rhinitisUnderlying causes of nonallergic rhinitis include vasomotor rhinitis, rhinitis medicamentosa, nonallergic rhinitis with nasal eosinophilia syndrome, and miscellaneous other disorders. Additional diseases to consider include acute infectious rhinitis, atrophic rhinitis, and rhinitis that occurs in association with systemic diseases.Except for patients with mixed rhinitis, all nonallergic syndromes are distinguished from allergic rhinitis by negative skin tests, and a history that supports the alternative diagnosis— Symptoms of the common cold vary from patient to patient, with rhinitis and nasal congestion being the most common. Nasal obstruction, rhinorrhea, and sneezing are usually present early in the course of the cold, although a sore or "scratchy" throat is frequently the most bothersome symptom on the first day of illness. The sore throat is usually short lived, and nasal symptoms predominate by the second and third day. Cough typically becomes troublesome on the fourth or fifth day of illness, by which time the nasal symptoms are less severe.Chronic nonallergic rhinitis — Chronic nonallergic rhinitis is characterized by perennial symptoms, an older average age than in patients with allergic rhinitis, and mild or absent nasal itching and sneezing. Patients with this disorder complain of chronic nasal congestion intensified by rapid changes in temperature and relative humidity, odors, or alcohol. They have little nasal itching or sneezing; however, headaches, anosmia, and sinusitis are common. A family history of allergy or allergic symptom triggers is uncommon. Negative skin tests to inhalant allergens are essentially diagnostic for a nonallergic rhinitis syndrome. Vasomotor rhinitis is sometimes considered a subset of chronic nonallergic rhinitis. The various clinical syndromes that can be included under the more general term chronic nonallergic rhinitis are reviewed separately.
23Health Effects of Allergic Rhinitis Social inconvenienceSleep disturbances/obstructionLearning difficultiesImpaired maxillary growthDental problemsInfection: nose and sinusesCo-morbidities: conjunctivitis, asthma, rhinosinusitis, otitis media
26In Patients with Rhinitis: Routinely ask for symptoms suggestive of asthmaPerform chest examinationConsider lung function testingConsider tests for bronchial hyperresponsiveness in selected cases
27AR Classification Intermittent Persistent . < 4 days per week. or < 4 weeksPersistent. > 4 days per week. and > 4 weeksMildnormal sleep& no impairment of daily activities, sport, leisure& normal work and school& no troublesome symptomsModerate-severeone or more items. abnormal sleep. impairment of daily activities, sport, leisure. abnormal work and school. troublesome symptomsin untreated patients
29Management of allergic rhinitis The management of allergic rhinitis involves the followingcomponents:Allergen avoidancePharmacotherapy.Allergen immunotherapy. Of note, immunotherapy helps prevent the development of asthma in children with allergic rhinitis, and thus should be given special consideration in the pediatric population.
30Medications for Allergic Rhinitis - ARIA sneezing rhinorrhea nasal nasal eye obstruction itch symptomsH1-antihistaminesoral tointranasalintraocularCorticosteroidsCromonesintranasalintraocularDecongestantsintranasaloralAnti-cholinergicsAnti-leukotrienesManagement combines allergen avoidance and pharmacologic therapy, with allergen immunotherapy added for refractory or severe cases.Intranasal glucocorticoids (INGCs) are the most effective single therapy for allergic rhinitis in most patients with significant or persistent symptoms.With this in mind, we favor the following approaches for specific patient groups:Children <3 years — For children <3 years, initial treatment depends upon both of the child's symptoms and the concerns of the parents/caregivers.For children <3 years with mild symptoms, we suggest a second generation antihistamines (Grade 2B). Cetirizine (approved for children ≥6 months), loratadine, and fexofenadine (both approved for children ≥2 years) are similarly efficacious and are available in syrups.If this is not effective or the child has prominent congestion, we suggest changing to an INGC with minimal systemic bioavailability and once-daily dosing (Grade 2B). Mometasone furoate and fluticasone furoate are approved for children ≥2 years of age.Intranasal cromolyn may be helpful for children with mild or episodic symptoms, whose parents are especially concerned about possible side effects, although the need for frequent dosing (one to two sprays three to four times daily) limits compliance.
31Oral Antihistamines Newer agents First generation agents Acrivastine ChlorpheniramineBrompheniramine DiphenydraminePromethazineTripolidineHydroxyzineAzatadineNewer agentsAcrivastineAzelastineCetirizineDesloratadine Fexofenadine Levocetirizine LoratadineMizolastineFirst generation agents — First generation antihistamines include diphenhydramine, chlorpheniramine, hydroxyzine, brompheniramine, and others. These are available over-the-counter, both as single agents and in combination with other drugs. They are similarly efficacious compared to each other, with minor differencesAdverse effects and safety — First generation antihistamines cause significant sedation because they are lipophilic and easily cross the blood brain barrier Central nervous system symptoms are reported by 20 percent or more of patients, and adverse effects on intellectual and motor function are well-documented, even in the absence of subjective awareness of sedationSecond and third generation antihistamines — The second generation antihistamines include loratadine, cetirizine, azelastine, and olopatadine. These lipophobic agents were developed primarily to avoid the unwanted central nervous system effects of the first generation drugs Onset of action is within one hour for most agents, and peak serum levels are attained in two to three hours . They are also longer-acting, and are dosed once or twice daily. Like older H1 antihistamines, they have less impact on nasal congestion compared to intranasal glucocorticoids (INGCs). The oral second generation agents appear to be similarly efficacious to each other .
32Nasal Antihistamines Azelastine Levocabastine Olopatadine Antihistamine nasal sprays — Azelastine and olopatadine are available as prescription nasal sprays. These agents appear to have some antiinflammatory effect and can improve nasal congestion They are similarly effective . Antihistamine nasal sprays have a rapid onset of action (less than 15 minutes) and can be administered "on demand" . Azelastine has a bitter taste that can be bothersome to some patients, although this has been corrected in newer preparations [93. Azelastine can be sedating if it is inadvertently swallowed.
33Newer Generation Oral Antihistamines First line treatment for mild allergic rhinitisEffective forRhinorrheaNasal pruritusSneezingLess effective forNasal blockagePossible additional anti-allergic and anti-inflammatory effectIn-vitro effect > in-vivo effectMinimal or no sedative effectsOnce daily administrationRapid onset and 24 hour duration of action
34Decongestants: Alpha-2 Adrenergic Agonists OralPseudoephedrineNasalPhenylephrineOxymetazolineXylometazolineDecongestants are relatively contraindicated in patients with hypertension, and contraindicated in those receiving monoamine oxidase therapy, and should be used with caution in patients with closed angle glaucoma, cardiovascular or cerebrovascular disease, hyperthyroidism, or bladder neck obstruction
36Anti-Leukotriene Treatment in Allergic Rhinitis EfficacyEquipotent to H1 receptor antagonists but with onset of action after 2 daysReduce nasal and systemic eosinophiliaMay be used for simultaneous treatment of allergic rhinitis and asthmaSafetyDyspepsia (approx. 2%)
37Nasal Corticosteroids Beclomethasone dipropionateBudesonideCiclesonideFlunisolideFluticasone propionateMometasone furoateTriamcinolone acetonideNasal steroid sprays are highly efficacious in treating allergic rhinitis. They control the 4 major symptoms of rhinitis (ie, sneezing, itching, rhinorrhea, congestion). They are effective as monotherapy, although they do not significantly affect ocular symptoms. Studies have shown nasal steroids to be more effective than monotherapy with nasal cromolyn or antihistamines. Greater benefit may occur when nasal steroids are used with other classes of medication. They are safe to use and not associated with significant systemic adverse effects in adults . Glucocorticoids inhibit allergic inflammation in the nose at many levels. These agents downregulate inflammatory responses by binding to intracellular glucocorticoid receptors in the cytoplasm of inflammatory cells. The receptors undergo conformational changes upon activation, entering the cell nucleus where they bind with glucocorticoid response elements located on antiinflammatory genes. These activated genes transcribe messenger RNA for antiinflammatory proteins. At the same time, activated glucocorticoid receptors suppress the transcription of most cytokine and chemokine genes* Currently only approved for asthma
39Nasal Corticosteroids Most potent anti-inflammatory agentsEffective in treatment of all nasal symptoms including obstructionSuperior to anti-histamines and anti-leukotienesFirst line pharmacotherapy for persistent allergic rhinitisIntranasal corticosteroids may be divided into first, second, and third generation preparations. These products are equally efficacious, although the total bioavailability (oral and nasal) of second and third generation intranasal steroids is markedly lower than that of first generation agents, resulting in lower risk of systemic effectsFirst generation: beclomethasone (unknown bioavailability), and flunisolide (40 to 50 percent bioavailability).Second generation: budesonide (10 to 34 percent).Third generation: fluticasone propionate (<2 percent), mometasone furoate (undetectable), and fluticasone furoate (<1 percent).— Glucocorticoids inhibit allergic inflammation in the nose at many levels These agents downregulate inflammatory responses by binding to intracellular glucocorticoid receptors in the cytoplasm of inflammatory cells. The receptors undergo conformational changes upon activation, entering the cell nucleus where they bind with glucocorticoid response elements located on antiinflammatory genes. These activated genes transcribe messenger RNA for antiinflammatory proteins. At the same time, activated glucocorticoid receptors suppress the transcription of most cytokine and chemokine genes.
41Other Management Aspects Manage other co-morbidities:Allergic conjunctivitisAsthmaSinusitis…Environmental manipulations:allergen avoidancePollution treatmentNutritional supportActivities and sports
42Environmental Control 1. AllergensHouse dust mitesPetsCockroachesMoldsPollen2. Pollutants and Irritants
43House dust mite allergen avoidance Provide adequate ventilation to decrease humidityWash bedding regularly at 60°CEncase pillow, mattress and quilt in allergen impermeable coversUse vacuum cleaner with HEPA filterDispose of feather beddingRemove carpetsRemove curtains, pets and stuffed toys from bedroom
44Allergen Avoidance Pets Remove pets from bedrooms and, even better, from the entire homeVacuum carpets, mattresses and upholstery regularlyWash pets regularly (±)MoldsEnsure dry indoor conditionsUse ammonia to remove mold from bathrooms and other wet spacesCockroachesEradicate cockroaches with appropriate gel-type, non-volatile, insecticidesEliminate dampness, cracks in floors, ceilings, cover food; wash surfaces, fabrics to remove allergenPollenRemain indoors with windows closed at peak pollen timesWear sunglassesUse air-conditioning, where possibleInstall car pollen filter
45To Conclude…Allergic rhinitis is very common and causes considerable morbidityAdequate and appropriate treatment leads to significant improvement in quality of lifeCo-morbid conditions are common and warrants special attention and treatment for optimal resultsEnvironmental manipulations is also important in the control of disease