Allergic Rhinitis and Rhinosinusitis
Allergic rhinitis is a common chronic disease affecting about 60 million people in the United States. In sensitized individuals, allergens cause release of chemical mediators from mast cells in the nasal mucosa. These mediators may cause rhinorrhea, sinus congestion, sneezing, and eye, palate, and nasal pruritis. In addition, rhinitis may result in postnasal drip, which, in turn, may lead to a cough, sleep disturbance, and fatigue. In allergic individuals, rhinitis is often seasonal and may worsen significantly during the pollen seasons (spring and fall).
Acute rhinosinusitis is a symptomatic inflammatory and infectious process of the paranasal sinuses and nasal cavity that typically lasts less than 4 weeks. The most common cause is viral upper airway infection. Acute rhinosinusitis can be divided into acute viral rhinosinusitis and acute bacterial rhinosinusitis. Acute bacterial rhinosinusitis is a secondary event occurring in up to 2% of cases of viral infection.
Rhinosinusitis can be classified as subacute (lasting 4-12 weeks) or chronic (lasting more than 12 weeks). Common causes of subacute and chronic rhinosinusitis are unresolved upper respiratory infections or untreated acute sinusitis.
- History of atopy in patient or family.
- Sex. In childhood, the condition is more common in males; the reverse is true in adulthood.
- Firstborn child. Having multiple siblings decreases this risk.
- Birth during spring or summer.
- Early introduction of infant formula and food. Breastfeeding for 3 to 6 months appears to be protective.
- Exposure to second-hand smoke during childhood.
- Maternal smoking during pregnancy.
Regular early childhood exposure to cats and dogs in the home or living on a farm may decrease the risk of developing allergic rhinitis in adolescence. The “hygiene hypothesis” postulates that being “desensitized” with early and repeated antigen exposure can help prevent mounting an allergic reaction years later when exposed to the same allergen.
The role of air pollution as it relates to the development of allergic rhinitis remains somewhat controversial.
- Upper respiratory viral infection, most commonly because of rhinovirus, influenza virus, respiratory syncytial virus, coronavirus, parainfluenza virus, and adenovirus.
- Bacterial secondary infection, typically with group A beta-hemolytic streptococci, Streptococcus pneumoniae or Haemophilus influenzae.
- Maxillary dental infection.
- Local trauma.
- Barotrauma (prolonged ventilation).
- Cigarette smoking or second-hand smoke exposure.
- Cocaine use.
- Cystic fibrosis or other ciliary abnormalities (Kartagener’s syndrome).
- Chemical irritation (occupational gas fumes; bleach).
- Obstruction: nasal septum deviation, tumor, or foreign body.
- Vasculitis (Wegener’s granulomatosis, also called granulomatosis with polyangiitis).
- Nasogastric intubation.
The diagnosis of allergic rhinitis is based on consistent findings in the history and physical examination, including a seasonal or perennial pattern of rhinorrhea, congestion, and pruritis, as well as positive skin tests for sensitivity to aeroallergens.
On examination, a clinician may observe pale or bluish nasal mucosa, edematous turbinates (with or without drainage), and “cobblestoning” of the oropharynx. A transverse nasal crease (the “allergic salute”), puffy eyes, and mouth breathing may be signs of allergic rhinitis in the pediatric population. Young children may also make a clicking sound while rubbing their soft palates with their tongues due to chronic irritation or a postnasal drip. Rhinoscopy will allow visualization of nasal polyps (caused by chronic inflammation), septal deviation (cocaine use or Wegener’s), foreign bodies, or tumors.
The diagnosis may be confirmed by prick skin testing, which consists of placing a series of liquid extracts containing various allergens on a patient’s forearms and gently pricking the skin. A positive response consists of erythema and a wheal ≥ 3 mm in diameter in the designated area after 20 minutes of observation. Negative skin tests usually exclude an “allergic” or IgE-mediated origin, yet they may not reflect a “nonallergic”/irritant or “vasomotor” reaction.
Other tests, such as blood eosinophils and serum IgE are not necessary in most clinical situations. The radioallergosorbent (RAST) test is sometimes used as an alternative to skin testing when there is widespread skin disease or medications that have antihistaminic properties that cannot be stopped for skin testing.
Sinusitis is diagnosed from signs and symptoms which may include purulent nasal discharge, nasal congestion or blockage, persistent cough, headache, sinus pressure (especially with forward flexion of the head), fever, maxillary tooth pain, and facial pain from bacterial infiltration. Although sinusitis may be asymptomatic, it often causes a decreased sense of smell (anosmia) and halitosis (especially in pediatric patients), and may exacerbate asthma due to mucosal inflammation of the nasal and paranasal sinus cavities.
In cases of complicated acute, refractory (chronic), or recurrent sinusitis, a non-contrast CT scan of the head may help to determine the presence of fluid, anatomical abnormalities, tumors, or varying degrees of mucosal disease.
Differentiating acute bacterial rhinosinusitis from acute viral rhinosinusitis is typically based on symptom duration and severity. While acute viral rhinosinusitis symptoms peak around day 2-3 and disappear by day 10-14, symptoms of acute bacterial rhinosinusitis persist longer than 10 days, tend to be more severe, and may include fever. A pattern of initial improvement followed by a worsening of symptoms—called double sickening—between days 5 and 10 of the illness is consistent with acute bacterial rhinosinusitis.,,
Avoidance of inciting factors is the most effective treatment. The following measures are also helpful:
Nasal irrigation with hypertonic saline solution may improve symptoms.
Antihistamines, oral or intranasal, improve allergic rhinitis symptoms and are most effective when taken prior to allergen exposure. Antihistamines are ideal for individuals with mild and intermittent symptoms. Common side effects include sedation and dry mouth and eyes. Second-generation antihistamines (H2 blockers) generally have a better sedation profile.
Intranasal steroids are highly effective and reduce nasal congestion more effectively than antihistamines. They are often recommended as the initial therapy option for moderate to severe symptoms. They need to be used regularly as effects start about a week after initiation. They are also available in combination with intranasal antihistamines.
Leukotriene antagonists (zileuton) and leukotriene receptor antagonists (montelukast, zafirlukast) help decrease nasal and ocular inflammation. They are not as often prescribed early in treatment due to side effects.
Nasal cromolyn inhibits mast cell mediator release. It is most effective when taken before allergen exposure and is less effective than nasal steroids in preventing nasal symptoms. It can be used during pregnancy.
Nasal decongestant sprays (e.g., phenylephrine) constrict intranasal blood vessels. They are effective prior to elevation gain (e.g., on mountains, in airplanes) or before initiating nasal steroid use. They should only be used temporarily (< 3 days), as prolonged use may result in rebound symptoms, in which nasal congestion worsens upon withdrawal of medication.
Oral decongestants, such as pseudoephedrine, are effective in relieving acute nasal congestion. Caution should be taken in hypertensive patients. Distribution over the counter is limited due to the use in producing illicit substances.
Nasal ipratropium bromide may be most helpful in children needing an alternative to steroids, and it is highly effective in treating rhinorrhea without nasal congestion.
Nonsteroidal anti-inflammatory drugs (NSAIDs) can be administered for short-term use to improve systemic sequelae.
Symptomatic treatment with antihistamines, decongestants, and NSAIDs for systemic sequelae, such as cough, congestion, and fatigue, may be helpful over the short term. Most cases of rhinosinusitis resolve spontaneously within 10 days.
Nasal irrigation with hypertonic saline solution may improve symptoms.
Intranasal steroids may be used for refractory cases.
In presumed cases of acute bacterial sinusitis, antibiotics may be effective but are not necessary for initial therapy. To decrease resistance, antibiotics should only be prescribed when a patient presents after 10 days of worsening symptoms despite other treatment.
Amoxicillin, trimethoprim-sulfamethoxazole, and doxycycline are initial options for acute bacterial sinusitis. Amoxicillin-clavulanate and select cephalosporins/fluoroquinolones are sometimes needed to cover resistant bacteria. Treatment should last for 10 to 14 days.
Recurrent/chronic disease requires aggressive treatment with daily intranasal steroids and/or nasal saline flushes. A CT scan of the sinuses may be indicated, as mentioned above.
Dietary history should be evaluated, as nutritional factors such as dairy intake may contribute to the development or exacerbation of allergies.,, In addition, children with allergic rhinitis may be more likely to be vitamin D deficient. Mediterranean-style diets may be protective due to higher intake of antioxidant-rich vegetables, fruits, legumes, and whole grains and limited meat and refined grain intake.,
Limited evidence suggests that longer duration of breastfeeding and avoidance of early introduction of potentially allergenic foods may reduce the likelihood of allergic sensitization. In an Italian study, new mothers were advised to breastfeed their infants and to avoid introducing commonly allergic foods (whole cow’s milk, eggs, fish, nuts, and cocoa) during the first year of life. Mothers who did breastfeed were also asked to limit dairy products and avoid eggs in their own diets, as well as to avoid exposure to other sources of allergens (smoking, day care attendance prior to age 2) as much as possible. These interventions greatly reduced allergic symptoms, including allergic rhinitis. More studies with greater racial diversity are needed to determine if there is a relationship between varying durations of breastfeeding and its impact on the development of allergic rhinitis in childhood.
Allergists in the US, UK and other countries now introduce peanut products to high-risk infants around 6 months of age to reduce development of a peanut allergy. In infants with an egg allergy, eczema or strong family history of allergy, early introduction of peanuts may reduce the subsequent development of peanut allergy by 70-80%.
Some evidence suggests that children who eat less saturated fat and cholesterol and more omega-3 fatty acids are at lower risk of developing rhinitis. Consumption of butter by children and of liver by adolescents has been associated with greater frequency of allergic rhinitis., In contrast, use of an omega-3 fatty acid supplement, paired with a multiple vitamin-mineral formula containing selenium, was shown to decrease the number of episodes of sinus symptoms and acute sinusitis in children.
Limited evidence also suggests that blood levels of vitamins C and E are lower in children with chronic sinusitis than in controls. Intake of citrus fruit or kiwi fruit, both high in vitamin C, has been associated with lower frequency of rhinitis in children. A study with 4,554 Korean school-aged children found that vitamin C intake was associated with reduced symptoms of allergic rhinitis. The antioxidant capacity of vitamin C may suppress secretion of superoxide anions.
Vitamin E has immunologic effects that might improve rhinitis symptoms, including suppression of neutrophil migration and inhibition of immunoglobulin E (IgE) production. Vitamin E intake from foods was protective against hay fever in an adult population. Patients with hay fever taking vitamin E supplements during pollen season experienced lower nasal symptom scores than those of placebo takers. Adults with allergic rhinitis may also benefit from having higher plasma carotenoid levels from a diet rich in fruits and vegetables. Additional studies are needed to determine if food or supplemental sources of ascorbic acid and vitamin E benefit sufferers of allergic rhinitis.
Studies suggest that, among individuals with allergic rhinitis, dietary fatty acids and antioxidants may influence the production of allergic mediators, including histamine and leukotrienes, and may thereby play a role in the treatment (and possibly the prophylaxis) of allergic rhinitis and sinusitis., Studies with children have found allergic rhinitis positively correlates with high-fat and low-carbohydrate diets.
A botanical treatment called butterbur (Petasites hybridus) significantly reduces both histamine and leukotriene production in sufferers of allergic rhinitis. .Benefits have been shown to be similar to those of a prescription antihistamine (cetirizine), without causing cetirizine’s sedating side effects.,
See Basic Diet Orders chapter.
Avoidance of known triggers.
Reporting to clinic with persistent symptoms or the presence of facial pain or high-grade fevers.
What to Tell the Family
Allergic rhinitis and rhinosinusitis are common yet treatable illnesses. Dietary adjustments may play a role in prevention and, to some extent, in treatment. Women who plan to have children should be encouraged to breastfeed (and withhold any dairy products for at least the first 6 months of life) and not smoke, to decrease the risk of allergic rhinitis and sinusitis in their children. Families should adopt the same changes as the patient to improve their own health and to support the patient. Thorough dusting, rug/carpet cleaning, air purifiers and decreasing exposure to environmental pollution (urban settings) should also be considered.
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