Allergic Rhinitis Treatment(K)
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Allergic rhinitis |
|---|
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Seasonal |
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Perennial |
| Perennial with seasonal exacerbations |
| Nonallergic rhinitis |
| Structural/mechanical factors |
| Deviated septum/septal wall anomalies |
| Hypertrophic turbinates |
| Adenoidal hypertrophy |
| Foreign bodies |
| Nasal tumors |
| Benign |
| Malignant |
| Choanal atresia |
| Infectious |
| Acute |
| Chronic |
| Inflammatory/immunologic |
| Wegerner granulomatosis |
| Sarcoidosis |
| Midline granuloma |
| Systemic lupus erythematosus |
| Sjogren syndrome |
| Nasal polyposis |
| Physiologic |
| Ciliary dyskinesia syndrome |
| Atrophic rhinitis |
| Hormonally induced |
| Hypothyroidism |
| Pregnancy |
| Oral contraceptives |
| Menstrual cycle |
| Exercise |
| Atrophic |
| Drug-induced |
| Rhinitis medicamentosa |
| Oral contraceptives |
| Antihypertensive therapy |
| Aspirin |
| Nonsteroidal anti-inflammatory drugs |
| Reflex-induced |
| Gustatory rhinitis |
| Chemical or irritant-induced |
| Posture reflexes |
| Nasal cycle |
| Environmental factors |
| Odors |
| Temperature |
| Weather/barometric pressure |
| Occupational |
| NARES (nonallergic rhinitis with eosinophilia syndrome) |
| Perennial nonallergic rhinitis (vasomotor rhinitis) |
| Emotional factors |
On the basis of timing and duration of allergen exposure, and thus the allergen pathogeneses, AR is classified as seasonal or perennial. Overall, approximately 20% of all cases are strictly seasonal, 40% perennial, and 40% mixed (perennial with seasonal exacerbations).
Tree, grass, and weed pollens and outdoor mold spores are common seasonal allergens. The symptoms typically appear during a defined season in which aeroallergens are abundant in the outdoor air. The length of seasonal exposure to these allergens is dependent on geographic location. Therefore, familiarity with the pollinating season of the major trees, grasses, and weeds of the locale makes the syndrome easier to diagnose.[28] Certain outdoor mold spores also display seasonal variation, with highest levels in the summer and fall months.[29]
Typical symptoms during pollen exposure include the explosive onset of profuse watery rhinorrhea, itching, and sneezing, along with frequent allergic symptoms of the eye. Congestion also occurs but usually is not the most troubling symptom. The onset and offset of symptoms usually track the seasonal pollen counts. However, hyperresponsiveness to irritant triggers, which develops from the inflammatory reaction of the late phase and priming responses, often persists after cessation of the pollen season. Such triggers include tobacco smoke, noxious odors, changes in temperature, and exercise.
Year-round exposure to dust mites, cockroaches, indoor molds, and cat, dog, and other danders leads to persistent tissue edema and infiltration with eosinophils, mast cells, TH 2 lymphocytes, and macrophages.PAR can also be caused by pollen in areas where pollen is prevalent perennially.
A universally accepted definition of perennial rhinitis does not exist. Most often, it is defined as a disease that persists for longer than 9 months each year and produces two or more of the following symptoms: serous or seromucus hypersecretion, nasal blockage caused by a swollen nasal mucosa, or sneezing paroxysms. Nasal congestion and mucous production (postnasal drip) symptoms predominate in most patients, and sneezing, itching, and watery rhinorrhea may be minimal.
Symptoms of AR may also be perennial with seasonal exacerbation, depending on the spectrum of allergen sensitivities.
A careful history and physical examination are the most effective diagnostic maneuvers for the identification of AR in children.[The key to accurate and timely diagnosis in children is a heightened awareness of the condition and its potential comorbidities. AR in children is often undiagnosed or misdiagnosed as other disorders such as recurrent colds. When cough is predominant, especially at night, AR may be misdiagnosed as "cough-variant" asthma. To make a correct diagnosis with appropriate accuracy and timeliness, the clinician must be knowledgeable and attentive of the symptoms and signs of rhinitis, ask specific questions directed at the presence and cause of rhinitis symptoms at each well-child visit, and understand the differential diagnosis of AR in children[. One must be aware of the comorbidities of AR (asthma, sinusitis, otitis media), pursue specific diagnostic testing when indicated, and often administer therapeutic trials of anti-inflammatory medications.
Parents must also be aware of signs and symptoms and report them to physicians, because the more subtle case presentations may otherwise go undiagnosed. Such underdiagnosis may be responsible for substantial morbidity in children, who often do not report their symptoms. Unfortunately, children who live with allergic symptoms on a daily basis for prolonged periods of time may mistakenly assume that their altered state is normal.
Typical symptoms of AR include sneezing, itching, clear rhinorrhea, and congestion. Congestion may be bilateral or unilateral or may alternate from side to side. It is generally more pronounced at night. With nasal obstruction, the patient is likely to be a mouth-breather, and snoring can be a nocturnal symptom. As such, sleep disturbances may indicate the presence of an allergic disorder. With chronic disease, abnormalities of facial development, dental malocclusion, and the allergic facies may ensue, with an open mouth and gaping habitus.
Whereas older children blow their noses frequently, younger children do not. Instead, they sniff, snort, and repetitively clear their throats. Nasal pruritus may stimulate grimacing and twitching and picking of the nose. The latter may result in epistaxis. Children often have the allergic salute, an upward rubbing of the nose with the palm of the hand. This often produces an allergic nasal crease, an accentuated, horizontal skin fold over the lower third of the nose. Children with AR also may have recurrent sinusitis or otitis media, eczema, or asthma.
Patients may also complain of red, itchy eyes, along with itchy throat and ears. They may also lose their senses of smell and taste. Increased symptoms are frequently noted with increased exposure to the responsible allergen, such as after cutting grass or sleeping on a feather pillow.
With development of the allergic reaction, clear nasal secretions will be evident, and the nasal mucous membranes will become edematous without much erythema. The mucosa appears boggy and blue-gray. With continued exposure to the allergen, the turbinates will appear swollen and can obstruct the nasal airway. Conjunctival edema, itching, tearing, and hyperemia are frequent findings in patients with associated allergic conjunctivitis. AR patients, particularly children with significant nasal obstruction and venous congestion, may also demonstrate edema and darkening of the tissues beneath the eyes. These so-called "shiners" are not pathognomonic for AR because they also can be seen in patients with chronic rhinitis and/or sinusitis. Thick, purulent nasal secretions generally indicate the presence of infection, including the possibility of sinusitis.
In severe cases, especially during the peak pollen season, mucous membranes of the eyes, eustachian tube, middle ear, and paranasal sinuses may be involved. This produces conjunctival irritation (itchy, watery eyes), redness and tearing, ear fullness and popping, itchy throat, and pressure over the cheeks and forehead. Malaise, weakness, and fatigue may also be present. The coincidence of other allergic syndromes, such as atopic eczema or asthma, and a positive family history of atopy point toward an allergic pathology. Approximately 20% of cases are accompanied by symptoms of asthma.[4]
When a clear relation between onset of pollenation and the typical rhinitis symptoms is present, the diagnosis of AR is relatively simple. However, when all of the typical rhinitis symptoms are not expressed, the diagnosis is more difficult. Chronic nasal obstruction alone may be the major symptom of PAR as a result of ongoing inflammation and late phase allergic reactions.[24]
Distinct temporal patterns of symptom production may aid diagnosis. Symptoms of rhinitis, which occur each time that the patient is exposed to a furry pet, suggest IgE-mediated sensitivity to that pet. Furthermore, patients who are sensitive to animal proteins may develop symptoms of rhinitis and asthma when entering a house, even though the animal was removed several hours earlier. Exposure to airborne allergens in the school or work environment may produce symptoms only during the week, with a symptom-free period at weekends. Likewise, vacations may be notably symptom-free.
Several processes and anomalies in presentation may complicate the diagnosis of AR. For example, the symptoms on any particular day of pollen exposure will be influenced by exposure on that day but also on previous days because of the priming phenomenon. As a consequence, at the end of the pollen season, the decline in symptoms usually takes place more slowly than the decline of pollen counts themselves.[32] In cases of perennial rhinitis, the symptoms are chronic and persistent, and patients may have secondary complaints of mouth-breathing, snoring, sinusitis, otitis media, or "a permanent cold."[33]
The most common form of nonallergic rhinitis in children is infectious rhinitis. Infectious rhinitis may be acute or chronic. Acute infectious rhinitis, such as the common cold, is usually caused by one of a large number of viruses, but secondary bacterial infection with sinus involvement may be a complication. Symptoms of chronic infectious rhinosinusitis include mucopurulent nasal discharge, facial pain and pressure, olfactory disturbance, and postnasal drainage with cough.
The symptoms of AR are frequently confused with infectious rhinitis when patients complain of a constant cold. Symptoms persisting longer than 2 weeks should prompt a search for a cause other than infection. If tests for atopy or airway disease (eg, asthma) are negative, foreign body rhinitis should be considered in the differential diagnosis. In such cases, symptoms may be acute or chronic, unilateral or bilateral, and the nasal discharge may be bloodstained or foul-smelling.
Exacerbations of rhinitis symptoms with predominant clear rhinorrhea in patients with a known history of AR may be difficult to diagnose. The difference between active infection and allergy should be made. When the history or physical examination is not diagnostic, a nasal smear should be obtained to aid in differentiation.
Allergy, mucociliary disturbance, and immune deficiency may predispose certain individuals to the development of chronic infection. Mucociliary abnormalities may be congenital, as in primary ciliary dyskinesia,Young syndrome, or cystic fibrosis, or they may be secondary to infection. Similarly, immune deficiency may be congenital or acquired.
Tumors or nasal polyps as well as other conditions (eg, nasal septal deviation, adenoidal hypertrophy, hypertrophy of the nasal turbinates) can produce nasal airway obstruction. Nasal polyps are common in children with cystic fibrosis but not in children with AR. Tumors as a cause of rhinitis are very uncommon in children. Other anatomic anomalies are more common in children. Nasal septal deviation and nasal turbinate or adenoidal hypertrophy may block the flow of nasal secretions, leading to rhinorrhea or postnasal drip, as well as causing nasal blockage. The most common acquired anatomic cause of nasal obstruction in infants and children is adenoidal hypertrophy.
Children with rhinitis should also be assessed for congenital and acquired anatomic causes of nasal obstruction.Reduced air flow through the nasal passages in infants may be caused by congenital choanal atresia.
Refractory clear rhinorrhea may be caused by cerebrospinal fluid leak, even in the absence of trauma or recent surgery. Any case of suspected tumor should be promptly referred to an otolaryngologist for a complete examination of the upper respiratory tract.
Nonspecific allergy tests
Laboratory confirmation of the presence of IgE antibodies to specific allergens, such as dust mites, pollens, or animal dander, is helpful in establishing a specific allergic diagnosis, especially if the history of specific allergen exposure is not clear-cut. In many patients, it is necessary to test for specific allergens to convince the family and patient of allergic diagnosis and reinforce the importance of environmental control measures.
Although skin testing might be performed on any child of any age, children younger than l year of age may not display a positive reaction. Often the child with seasonal respiratory allergy will not have a positive test until after two seasons of exposure. Clinicians should be selective in the use of allergens for skin testing and should use only common allergens of potential clinical importance. The most useful allergens for testing in the child with perennial inhalant allergy are house dust mite (Dermatophygoides), animal danders, and fungi (molds). Allergens important in the diagnosis of seasonal AR are weed, grass, and tree pollens. Because there is significant geographic specificity with regard to pollens, the importance of these seasonal allergens varies not only by season of year but by geographic distribution. Therefore, allergens used for skin testing must be individualized and should be selected on the basis of prevalence in the patient's geographic area of the country and the home and school environment in which they live and play.
Although the presence of the signs of allergic rhinitis in a child is a vital diagnostic clue, it is also a nonspecific 1. The classic signs of allergic shiners and an allergic crease (with or without the physical findings of a high, arched palate and a constantly open mouth) only identify children with nasal obstruction; they do not necessarily indicate an underlying allergic cause.
To establish the diagnosis of allergic rhinitis with certainty, allergy testing is recommended. As in adults, inhalant allergens are the most frequent trigger of allergic rhinitis in children; however, food allergy should not be ignored in infancy or early childhood. Foods are a significant source of allergic reactions until about the age of 2 years. Because two or more seasons of pollen exposure are required for sensitization, allergy testing for seasonal allergens such as trees, grasses, and weeds is typically requested after 2 or 3 years of age. However, allergy to perennial inhalant allergens such as house dust mite, dog, cat, cockroach, and feathers can manifest after several months or even weeks of daily exposure. In these instances, allergy testing to perennial inhalant allergens as well as potential food allergens may be performed in children less than 2 years of age if clinically indicated. However, these children will exhibit a smaller wheal-and-flare in the event of a positive allergy skin test than will older children and adults.
There are two methods for specific IgE antibody testing:
in vivo skin testing and in vitro serum testing[
At the present time, properly performed skin tests are the best available method
for detecting the presence of allergenspecific IgE. The skin prick, also called
the puncture or epicutaneous skin test, is the preferred method of IgE antibody
testing. Scratch testing has been abandoned as too traumatic. If skin prick
tests are negative and allergy is highly suspected, then intradermal testing,
which is more sensitive but less specific, may be used if indicated.
In vitro tests are acceptable substitutes for skin tests in the following circumstances: (1) the patient has abnormal skin, such as dermatographism or extensive dermatitis, (2) the patient cannot or did not discontinue antihistamines or other interfering medications, (3) the patient is very allergic by history and anaphylaxis is a possible risk, and (4) the patient is noncompliant for skin testing.
To avoid false-negative skin tests, short-acting antihistamine medications should be withheld for 36 to 48 hours, and long-acting antihistamines, for example, astemizole, should be withheld for 4 to 6 weeks before skin tests are performed because antihistamines suppress the skin test results.
Physicians must remember that positive tests for allergen-specific IgE themselves are not sufficient for a diagnosis of allergic disease. These tests only indicate the presence of IgE molecules with a particular immunologic specificity. A decision whether the specific IgE antibodies are responsible for clinically apparent disease must be based on the physician's assessment of the entire clinical picture. The ultimate standard for the diagnosis of allergic disease remains the combination of (1) positive history, (2) the presence of specific IgE antibodies, and (3) demonstration that the symptoms are the results of IgE-mediated inflammation.
Nonspecific allergy tests
Blood eosinophilia and total serum IgE level have been proposed as screening tests for allergies, but they have relatively low sensitivity and should not be used routinely for diagnosis of AR. The nasal secretions or sputum of patients with respiratory allergy contain increased numbers of eosinophils, which forms the basis of a useful nonspecific test (nasal smear for eosinophils), but one that will not identify any specific allergen etiology. Nasal smears for eosinophil/neutrophil counts can be useful in differential diagnosis when the diagnosis is unclear.
Local irritation is the most frequently observed adverse effect with intranasal steroids, with approximately 10% of patients having some form of nasal irritation, nasal burning, or sneezing after administration. Bloody nasal discharge occurs in approximately 2% of patients treated with intranasal steroids, and there have been a few reports of septal perforations and delayed hypersensitivity reactions
There has been some concern about the serious side effects associated with systemic corticosteroids, such as growth retardation, hypothalamic-pituitary-adrenal suppression, and behavioral disturbances. However, the intranasal corticosteroids, which act locally on the nasal mucosa, are rapidly metabolized, have a long duration of action, are not associated with the same side effects as the systemic agents, and do not produce clinically important side effects. In fact, a review of more than 200 studies demonstrates that beclomethasone, 1 of these agents, does not produce systemic side effects, even with prolonged use of up to 6 years.
There have been several case reports of children who were treated with systemic corticosteroids or with inhaled corticosteroids and pulse systemic corticosteroids who had poor clinical outcomes after contracting chicken pox. Therefore current thinking is that children who are on low-dose corticosteroids and/or receiving inhaled corticosteroids should be vaccinated against the varicella virus.
Mast cell stabilizers, such as cromolyn sodium, can be useful in relieving nasal pruritus, rhinorrhea, sneezing, and obstruction; however, they have minimal effect on congestion. Cromolyn sodium is generally well tolerated and is most efficacious when taken prophylactically, well in advance of allergen exposure. In addition, because of its short duration of action, it should be taken 4 times a day; as a result, compliance is difficult for many families.
Profile of Patients With Allergic Rhinitis Who Are
Candidates for Allergen Immunotherapy
Allergen immunotherapy is another proven treatment for children with allergic rhinitis and should be considered when other treatments are inadequate in controlling symptoms. However, in making the decision to prescribe this therapy, the clinician should consider the positive and potentially negative effects of regular office visits for the administration of injections.[20] If the decision is made to prescribe immunotherapy, it must be administered by a physician who is experienced in its use and whose office is set up for dealing with the management of adverse allergic reactions, including anaphylaxis should this rare untoward event occur