Food allergy management
Food Diaries
Ask the patient to prospectively keep a detailed listing of all ingested foods (and medications) and any APR and AFR-associated events (e.g., exercise) for a few weeks. This is most useful if manifestations are intermittent. It is also more objective than relying on the patient’s recollection of previous events. Analysis of food diaries often reveals unexpected associations and helps to interpret skin tests and EAST assays in the proper context
Diet Elimination
This technique is useful’in chronic nonintermittent manifestations of suspected food allergies. It involves switching the patient to a diet consisting of foods believed to be the least allergenic in most people (e.g., rice and lamb). Resolution of symptoms suggests a food-related etiology. Reintroduction of selected foods over time Cone new food item every 8-4 days) may help identify culprit foods. This approach ia contraindicated in suspected food-induced anapbylaxis. Care should be taken to avoid malnutrition, vitamin deficiencies, and dehydration.
With more prolonged exposure to an allergenic food, allergic rhinoconjunctivitis and bronchial asthma may manifest, especially in patients with AD.
In a few cases, IgE-mediated food allergy can present as infantile colic, eosinophilic gastroenteritis, and infantile gastroesophageal reflux disease. Diagnosis of the latter group requires a high index of suspicion and endoscopic biopsy.
Food-associated exercise-induced anaphylaxis is a recently established class of food allergy. In this interesting disease, anaphylaxis occurs only if vigorous exercise occurs 1-2 hrs after ingestion of certain foods (or less commonly any food).
Non-lgE-Medlated Immune Reactions to Food
Types II and III of non-IgE-mediated immune reactions as well as cell-mediated food reactions have been implicated in rare cases of AFRs.
Food-induced thrombocytopenia (type II reaction to cow’s milk) has been reported (but is exceedingly rare).
A rare syndrome known as Heiner’s syndrome, first described in 1966, is believed to result from hypersensitivity to cow’s milk. Early aspiration and sequestration of milk in the lungs initiates an immune reaction manifesting as a pneumonia-like disease with pulmonary infiltrates associated with iron-deficiency anemia and pulmonary hemosiderosia. In addition to IgE, patient’s serum contains high levels of a precipitating IgG antibody to cow’s milk. Disease pathology is likely mediated via immune complex and cell-mediated hypersensitivity-type reactions. This rare disease has also been described in breast-fed infanta.
Celiac disease, or gluten enteropathy, is possibly mediated in part by a type IV hypersensitivity to gluten in addition to direct gluten toxicity.
Nonimmunologic Reactions to Food
A variety of mechanisms are involved in several AFRs.
Scombroid fish poisoning is an anaphylactoid type reaction resulting from the action of bacterial decarboxylase on histidine-rich fish meat (tuna, mackerel, bonito, mahi mahi). Histamine is generated enzymatically, and when the fish is ingested, the patient complains of burning mouth sensation, pruritus, flushing, nausea, vomiting, headache, and even vascular collapse.
Similar symptoms can occur as a result of ingestion of histamine-rich foods such as Roquefort and Parmesan cheeses, eggplant, spinach, and red wine. Ingestion of foods rich in serotonin (tomato, pineapple, avocado, and banana) or tyramine (cheese and wine) can be associated with “pharmacologlc” symptoms such as flushing, headaches, and palpitation. These symptoms are much more pronounced in individuals on MAOIs.
Idiosyncratic Intolerance is exemplified by lactose intolerance, which is frequently indistinguishable from GI presentations of IgE-mediated milk allergy. Careful history taking usually resolves the confusion. Asian, Arab, or black ethnic background; later age of onset (over 7 yrs); and occasional association with recent gastroenteritis are associated with lactose intolerance.
Several food-induced GI syndromes are identified that are similar to IgE-mediated syndromes with no evidence of food-specific IgE. These include: gastroenteritis, proctocolitis, enteropathy {e.g., gluten enteropathy), and gastroesophageal reflux diaease. Gluten enteropathy is frequently associated with an intensely pru-ritic vesicular condition known as dermatitis herpetiformis, which affects extensor surfaces and buttocks.
Food-induced migraine is a poorly understood entity that has been reported in some patients with positive DBPCFC. The mechanism is unknown.
Hereditary angioedema
DIAGNOSIS. Diagnosis is made by an initial screening C4 level that is always low and can drop to undetectable levels during an attack. IF the C4 level is low, obtain a C1 inhibitor level. In approximately 15-20% of patients, the level is normal, but the protein is not functional and a functional assay must be performed.
Treatment
Acute reactions presenting to the ER should be treated immediately and aggressively (nee Chap. 13, Anaphylaxis). Other causes of collapse and shock should not be ignored either. If food ingestion is recent, gastric lavage may help reduce allergen load. Oropharyngeal laryngeal angioedema may benefit from aerosolized epinephrine and may require endotracheal intubation. All treated cases should be observed for a minimum of 4 hrs (preferably 8-10 hrs, and for up to 24 hrs in the case of severe reactions) in the ER before discharge with referral to an allergist/immunologist.
The only long-term control measure for food allergy Is strict elimination from the diet.
In children, but not adults, many foods can be reintroduced after a few years of elimination without reactivation of allergic reactions. With certain foods, such as peanuts (see Natural History), however, life-long elimination is required. Patient education is the most important component of the management plan. The patient’s family and caregivers of young children and infants also need education. This includes careful checking of food labels, education about alternative food names and “hidden” foods (e.g., casein for milk), heightened awareness in restaurants (only the cook knows!), and elimination of foods with unidentified ingredients. Avoiding situations where cross-contamination of foods is frequent (e.g., open buffets and salad bars) may make the difference between life and death in patients with history of food-induced anaphylaxis.
History of anaphylaxis or other IgE-mediated reactions warrants the prescription of preloaded epinephrine kits (e.g., Ana-Kit, EpiPen, and EpiPeu Jr autoinjectors).
Emphasize the absolute need to
have injectable epinephrine within reach at all times (no exceptions). The prescription should be refilled every 6 mos, and the kit should be protected from extreme temperature (avoid automobile glove compartments or freezing weather). The patient should use epinephrine at the earliest sign or symptoms of a reaction. The patient should also he instructed to call 911 to’be transported to the ER (and not to drive him-or herself) as soon as the epinephrine is administered, regardless of how good he or she feels. Risk factors for fatal anaphylaxis include poorly controlled bronchial asthma, older age with compromised cardiovascular health, use of beta-adrenergic hlockers, being away from home, and a delay of epinephrine injection >1 hr after appearance of symptoms. Patients should wear a medical alert bracelet all the time.
Children with milk allergy can he managed with formula substitutes: soy-based (e.g., Isomil, ProSoyBee), casein protein hydrolysate (e.g., Nutramigen, Carnation Good Start) or, in cases of extreme intolerance, elemental amino acid-based formula (Neocate).
Antihistamines, cromolyn, corticosteroids, and ketotifen (not available hi the United States) are of no proven value in long-term management of food allergies. Immunotherapy with food antigens has not been proved beneficial and are likely to he unacceptably risky.
Recent studies evaluating the benefits of maternal avoidance of allergenic foods during the last trimester of pregnancy and during lactation, as well as exclusive breast-feeding in the first year of life, remain to be validated.
Further patient information and support can be obtained from Food Allergy Network, Fairfax, VA (phone: 1-800-929-4040; Web address: www.foodallargy.org).
SPECIAL TOPICS
Allergies to Food Additives
Over the years, many case reports have blamed food dyes, preservatives, and additives, such as aspartame and monosodlum glutamate (MSG), for a variety of allergic or pseudoallergic reactions. Reactions range from acute or chronic urticaria and induction or exacerbation of bronchial asthma to migraine headaches and behavioral disorders, such as hyperactivity and attention deficit disorders. Larger-scale trials and DBPCFC have not substantiated most of these associations.
MSG was reported to cause the “Chinese restaurant syndrome” rarely in individuals consuming large amounts of MSG. Symptoms start 30 mins after ingestion and manifest with anxiety, headache, sweating, flushing, palpitation, tightness, a burning sensation in the face and chest, and a crawling sensation of the akin. The condition is self-limited and subsides over 1-2 hrs.
Food preservatives, such as benzoate, butylated hydroxyzole, and butylated hydrox-ytoluene, were not associated with APR in well-designed studies. Sulfites, on the other hand, were found to exacerbate asthma in a small percentage of asthmatics (<5%), particularly in patients with severe asthma. The mechanism behind the reaction is not clear, but the exposure occurs in part by inhalation of SO, gas that evolves from metabisulfite-preaerved foods (especially at salad bars) during mgestion. Certain individuals with inherent sulfite oxidase deficiency may be more at risk for AFR.
In European studies, artificial food colors have been blamed for S 15% of chronic urticaria cases, whereas in the Unites States this high percentage has never been substantiated. Tartrazine (food dye yelZow 5) has been reported to cross-react with aspirin in aspirin-sensitive asthmatics, a finding that could not be validated in DBPCFC in aspirin-sensitive individuals. However, yellow 5 is implicated in rare cases of asthma independent of aspirin.
The sugar substitute aspartame has been implicated in very few cases of chronic urticaria. A multi-center study using DBPCFC was unable to confirm this association. Sugar allergy, a term coined in the mid-1980s, was believed to contribute to attention deficit disorder and juvenile delinquency behavior, an assumption completely refuted by controlled studies.
KEY POINTS
More patients believe they have food allergies than what could be found using blinded food challenges.
Pood “allergy” is a subset of a larger group of adverse food reactions (AFRs). AFRs include idiosyncratic, toxic, and pharmacologic, as well as allergic, reactions to food.
Young children have more food allergies than adults but tend to outgrow their allergies, especially after a period of strict elimination.
Milk, egg, wheat, soybean, and peanut cause more than 90% of food allergies in children.
Oral allergy syndrome results from cross-reactivity of food allergen with certain pollen aeroallergens.
Detailed history and skin tests are the most valuable diagnostic tools of food allergies.
There is no role for Immunotherapy in the treatment of food allergy. Patient (and parent) education and anaphylaxls kits are the most powerful life-saving measures in severe food allergy.
The only long-term control measure for food allergy Is strict elimination from the diet in children, but not adults, many foods can be reintroduced after a few years of elimination without reactivation of allergic reactions. With certain foods, such as peanuts (see Natural History), however, life-long elimination is required. Patient education is the most important component of the management plan. The patient’s family and caregivers of young children and infants also need education. This includes careful checking of food labels, education about alternative food names and “hidden” foods (e.g., casein for milk), heightened awareness in restaurants (only the cook knows!), and elimination of foods with unidentified ingredients. Avoiding situations where cross-contamination of foods is frequent (e.g., open buffets and salad bars) may make the difference between life and death in patients with history of food-induced anaphylaxis.
History of anaphylaxis or other IgE-mediated reactions warrants the prescription of preloaded epinephrine kits (e.g., Ana-Kit, EpiPen, and EpiPeu Jr autoinjectors).
TREATMENT
Acute Attacks. Provide supportive care in acute attacks. Isolated limb swelling can be observed. Laryngeal swelling may lead to asphyxiation and is the leading cause of mortality and morbidity in patients with this disorder. Intubation must be considered electively before laryngeal swelling makes this difficult or impossible. Appropriate personnel and equipment for a tracheotomy should be available.
Long Term Therapy. Synthetic androgenic steroids (danazol [danocrine] or stanozolol [Winstrol] have attenuated virilizing side effects and can improve occur symptoms in patients with frequent occurrences. However side effects do still occur. Conseling to women of childbearing age is necessary because of interference with gonadal development. Fibrinolytic agents (such as E-aminocaptroic acid) have also been shown to ameliorate symptoms. Unfortunalty this therapy also carries the risk of numerous side effects. Decision for therapy must be made on an individual basis.
Prophylaxis. The use of agents for allergic urticaria and corticosteroids are of little value. Adrogens are also ineffective in the acute setting but may be given 4-5 days before scheduled surgery. Other agents that may be used prophylactically are antifibrinolytics and fresh frozen plasma.
Acquired Angloedema
Findings for acquired angioedema are similar to those for hereditary angloedema. Symptoms are the result of a C1q autoantibody. A low C1q level combined with low C1 inhibitor and C4 levels warrants an investigation for an occult malignancy, because this disorder is associated with lymphproliferative disorders. It is also rarely associated with connective tissue disease.
Urticarial Vasculitis
Exam usually reveals lesions in dependent areas. Other signs of vascultis, such as petechiae and palpable purpura, are often evident. Lesions tend last >24hrs and be more painful than pruritic. A punch blopsy is necessary to make the diagnosis and will show necrotizing vasculities.
Physical Exam
Physical exam is frequently negative.
In emergency situations, ascertain the cardiovascular and respiratory condition of the patient to rule out anaphylaxis.
If in doubt about the etiology in a patient with cardiovascular collapse and suspicious history or suggestive signs (e.g., hives, wheezes in patient without history of bronchial asthma, protracted or nonresponsive shock state), consider and possibly treat as anaphylaxis. Obtain blood for serum tryptase level (within 4 hrs) for later confirmation.
In nonemergency situations (e.g., elective office visit), look for the following signs:
Cutaneous: urticaria, angioedema, AD/eczema, dermatitis herpetiformis
Respiratory: distress, wheezing
Evidence of upper respiratory allergies (e.g., pale enlarged nasal turbinates, postna-
sal drip, pharyngeal cobblestoning, and pretonsillar throat erythema)
General: dehydration, anemia, malnutrition, failure to thrive (in children)
MANAGEMENT
Diagnosis
The history usually elicits a cause or underlying condition; thus the workup should be directed specifically. Resist the shotgun approach to obtaining labs. Occasionally, it is necessary to challenge the patient with a suspected agent. Drug allergy and Desensitization, and Food Allergy and other adverse food reactions, for specifies regarding drug and food testing. These tests should only be performed by physicians trained to interpret the results. If no cause is apparent, consider:
Lab studies: OBC, urinalysis, sedimentation rate, liver function tests, antithyroid antibodies.
Removal of exacerbating agents such as NSAIDs, opiates, and alcohol; may aid in the diagnosis.
Elimination diet: some advocate an elimination diet of rice, lamb and water when a food is suspected as the cause. New foods are introduced one at a time as they are tolerated. Compliance is the main hurdle with this endeavor. Food diaries can help direct specific IgE test.
Treatment
Choice of treatment depend on the lesions. It may involve avoidance (as in NSAIDs or opiates), specific therapy(some physical urticarias respond to antihistamines) or tratement of an underlying condition (such as thyroid replacement for autoimmune thyroiditis)
Hi-blocking antihistamines can be added if symptoms are not controlled.
If pruritus is not controlled with traditional antihistamines, doxepin (Sinequam) can be added, because it acts as a more potent antihistamine than H1 blockers. The typical dose is 10mg at bedtime. Doxepin can be very sedating; thus, the same caution regarding daytime somnolence and slowed reaction times applies.
A short burst of prednisone (deltasone) can often eradicate symptoms but has numerous, well-documented side effects. Therefore steroids should be used in severe cases or in cases refractory to antihistamines. The dose and course should be high enough and long enough to control symptoms. Tapering steroids is not necessary to prevent adrenal suppression for courses shorter than 3 wks but can be helpful to determine if symptoms have remitted and to achieve the lowest effective dose. Typical doses are 40-60 mg/day for severe exacerbations. Patients should be adequately counseled regarding side effects associated with steroids (irritability/euphoria, water retention, glucose introlerance, appetite stimulation, and sleep disturbance.
Treatment
The pillars of effective AD treatment are skin hydration, topical corticosteroids, and trigger avoidance. Education is crucial for effective participation of patients in their own care.
Education
AD is a potentially chronic and difficult to manage disease with unpleasant and stressful symptoms (pruritus and skin lesions). Poor sleep, frequent, aggravations by many normal daily activities, and disfiguring facial and hand lesions all contribute to emotional stress in patients and their families. The nutral history of AD, the value of skin hydration and environmental control, and the importance of itch-scratch cycle control should be the initial objectives of patient education. Adequate education is essential for the formation of a good therapeutic alliance.
Environmental and Trigger Control
Avoid extreme temperatures and humidity
Use dust mite control measures: dust mite covers on pillows and mattresses, wash bedding in hot water (1300F) weekly, and maintain relative humidity <50%.
Avoid contact with animal dander.
Avoid tight, nonbreathing clothes and excessive exposure to sunlight without protective creams.
Avoid wool, acrylic, ad coarse fabrics. Cotton is the preferred fabric for clothes.
Skin care and Hydration
Use unscented laundry detergents without bleach. Double rinsing is recommended.
Avoid skin exposure to solvents and irritating vapors.
Maintain skin hydration by bathing with tepid water (30 mins once or twice daily, depending on severity of disease), using oatmeal or baking soda bath unscented mild soaps (e.g., Neutrogena, Dove Basis). Showering is usually not adequate for good skin hydration. Avoid excessive or vigorous toweling.
Apply emollients such as Eucerin, Nutraderm, Aquaphor, or petroleum jelly generously within 3 mins after bathing to “lock in” skin moisture.
Trim nails short to minimize skin trauma. Wearing gloves and socks during sleep helps limit scratching.
Medications
CORTICOSTEROIDS. Topical Steroids are the mainstays of AD antinflammatory treatment. For mild cases, a low-potency steroids ointment or cream (hydrocortisone [Cortef, Hydrocortone] 1-2.5%, bid/qid) may be adequate. Medium-potency steroids (mometasone furoate [elocon] 0.1% qd or triamcinolone [Aristocort, Kenalog, Triacet] 0.025-0.1% tid/qid) are required for more severe forms of the disease.
Please not that recent clinical trial suggest that moderate and severe AD may initially e treated with the topical immunosupressants tacrolimus (protopic) and pimercrolimus (Elidel) instead of higher-potency topical steroids for several months, then maintaining disease control using lower potency topical steroids if necessary.
Ointments are more efficacious than creams and should be used whenever possible. Creams may be adequate for milder forms of AD. Topical steroids can be applied over emollients used to maintain skin hydration.
Localized flares may be treaded with high-potency topical steroidst, such as clobetasol propionate (Clobevate, Cormax, Embeline E, Olux, Temovate) (0.005% bid) or halobetasol [Ultravate] (0.05% bid/tid), for 10-14 days followed by medium-potency topical steroids. High-potency steroids should be used sparingly and never on the face. If used for longer periods, the adrenal cortex may be suppressed, and tapering of the topical steroids is necessary.
High-potency corticosteroids should never be used on the face, intertriginous areas, or genitals. These areas should be treated with low-potency topical steroids only (e.g.hydrocortisone 1%)
Systemic corticosteroids have no place in the long-term treatment of AD. Widespread severe flares may require moderate doses of prednisone (deltasone, Liquid pred, Meticorten, Orasone, Prednicen-M, Sterpred) (40-60 mg/day), tapered by 20 mg/day every 4-5 days, with adequate topical coverage to follow. Abrupt interruption of systemic corticosteroid treatment may be associated with an exacerbation of dermatitis. A recurrent need for systemic steroids is an indication for referral to a specialist to consider alternative therapies.
Treatment
Localized Reactions
Molst compresses minimize oozing and facilitate absorption of topical steroids.
Drying antipruritic lotions (e.g.calamine lotion) are simple and effective, Oral antihistamines may be necessary. Topical antihistamines and topical anesthetics should be avoided because of their sensitizing ability.
Topical corticosteroid creams, not ointments, should be used.
Widespread Reactions
Systemic corticosteroids, given at a dose of 40-60 mg initially, should be tapered slowly over 14 days to avoid flare-ups.
Oral antihistamines (as for localized reactions) may be needed during the first few days of a course of systemic corticosteroids, particularly for pruritus that interrupts sleep.
Recurrence
Prevention of recurrence is predicated on avoidance (when possible). Patients should be educated about all possible sources of the allergen and potential cross-reacting substances.
KEY POINTS
Allergic contact dermatitis is mediated by T lymphocytes
Rash distribution is the most helpful aid in identifying the causative allergen.
Allergic Conjunctivitis
Vernal Conjunctivitis
TREATMENT
As the potential for serious ocular sequelae exists with VKC, it is frequently necessary and appropriate to use a multifaceted treatment plan for controlling the disease. Controlling the itching is extremely important; children particularly tend to rub their eyes vigorously, which can induce mast cell degranulation and promulgate the disease process.
1.Identify and remove the offending allergen.
2.Topical antihistamines such as levocabastine, emedastine, or azelastine.
3.Topical antihistamine/mass cell stabilizers such as olopatadine or ketotifen.
4.NSAIDs, such as ketorolac, help relieve itching.
5.Mast cell stabilizers, such as cromolyn, lodoxamide, nedocromil, and pemirolast, have been useful as adjunctive therapy. These agents have been shown to improve the symptoms and associated corneal findings in patients treated for several weeks. Additionally, these drugs have been able to eliminate the need for or decrease the dependency on topical corticosteroid drops.
6.Pulsed therapy with topical corticosteroids, such as loteprednol (Alrex; Lotemax) or rimexolone (Vexol), is sometimes necessary to control inflammation.
7.Cool compresses, oral NSAIDs, and ASA have been shown to relieve the symptoms and signs of VKC.
Atopic Keratoconjunctives.
AKC is a chronic disease usually seen individuals in their fifth to sixth decade of life who have a long history of eczema or atopic dermatitis.
SYMPTOMS. Patients complain of chronic, year-round itching associated with burning, light sensitivity, tearing and chronic redness of the eyes. The symptoms may go undiagnosed for years.
PHYSICAL EXAM. Exams of the patients show ecsematoid changes of the upper and lower eyelids typified by induration, erythematic, and scaling. Slit lamp exam revelas marked plugging of the meibomian gland orifices with purulent secretions and a con-current poor precorneal tear film. The bulbar conjunctiva may show mild to moderate injection and changes consistent with keratoconjunctivitis sicca (dry eye). In severe cases, conjunctival subepithelial fibrosis and symblepharon may develop. The tarsal conjunctival surfaces usually reveal mild to moderate injection. Corneal involvement in AKC may vary according to the severity of disease. In mild forms, the cornea may only show minimal punctuate stain with fluorescein dye, whereas severe cases demonstrate marked surface irrengularity with epithelial desiccation associated with corneal neovascularization, keratinization, and scarring.
TREATMENT
Vernal Conjunctivitis
Treatment must control both the skin and ocular surface inflammation and protect the corneal surface from the side effects of a poor tear film.
To help open the plugged meibomian glands associated with severe blepharitis, hot compresses and oral antibiotics such as doxycycline, 100 mg bid, are used to help improve the meibomian gland dysfunction and subsequently improve the tear film. Antihiotics should have good coverage against staphylococcus bacteria.
Preservative-free ocular lubricant drops or ointments help improve the aqueous deficiency of keratoconjunctivitis sicca..
The lid scale component of blepharitis may be addressed with a combination of lid scrubs, using an over-the-counter preparation such as Eye-scrub or baby shampoo with water.
For severe eczematoid changes, patients amy benefit from topical 1% hydrocortisone cream or 0.03% tacrolimus ointment (protopic) applied to the skin of the eye-lids after using nondrying soap such as Dove. Unscented lubricant creams, such as Eucerin, may be applied after the hydrocortisone cream to help hydrate the skin.
MANAGEMENT
Workup
Skin Tests
Skin tests using purified venom (bee YJ, hornet, and wasp) or whole body extract 9fire ants) are the mainstay of diagnostic workup. After a major systemic reaction to suspected Hymenoptera sting, a 4- to 6- wk delay of skin testing is recommended to avoid a false negative skin test during the post-anaphylaxis refractory period. Epicutaneous tests should precede intradermal tests to minimize risk of systemic reactions in highly sensitive individuals. A maximum extract concentration of 1ug/mL is used, with sensitivity of 90-95%. This concentration unfortunately may result in 20% false-positive results. Lower concentrations, however, are associated with an unacceptable sensitivity <70%.
Practically, a patient with suspected insect sting allergy is tested for all stinging insects, even if the history may suggest that a particular insect is the likely culprit. This is justified by the life-threatening nature of the disease and possible fatal sequelae if the diagnosis is missed. Cross-reactivity of skin testing has been observed within the vespid family (YJs closer to hornets, whereas wasps are much less likely to cross-react). HOnebee skin test detects honebee allergy and is likely to be positive in humblebee allergy as well. Vespids do not cross-react with bees. Although the question of “cross-reactivity vs multiple hypersensitivity” can be resolved using RAST inhibition assays, this is seldom needed or used in clinical practice.
Radioallergosorbent Test
RAST is 80% sensitive compared to skin tests but detects an additional 10% of patients that are allergic with negative skin tests. Both tests are required if the history suggests sting allergy and skin tests are negative or contraindicated.
Severity of the reaction and the risk of future anaphyxis do not correlate with the intensity of the local reaction to skin test or to the RAST titer.
Sting Challenge
Sting challenge in the ICU setting is not used for diagnostic purposes.
Treatment
Immediate
If the stinger is still in the skin it should be removed immediately (without squeezing). However stinger removal is only useful in the first 3-5 mins after stinging. After that time, the stinger has usually emptied its contents in the sting site.
Small local reaction: Do not usually require treatment, but ASA and cold compresses may provide symptomatic relief.
Larger local reaction: May last up to 7-10 days and will benefit form antihistamine, Analgesics, cold compresses, and if symptoms are sever or constitutional, a 2-to 3 day course of moderate doses of prednisone (e.g. 40 mg/day for an average adult).
Systemic reaction and anaphylaxis: Treated according to standard protocols for respiratory and circulatory collapse
Long term Management: Avoidance and Prophylaxis for Sensitive individuals
Carry an anaphylaxis kit (e.g., Ana-Kit or EpiPen) at all times. Use the kit as soon you are stung without waiting for a reactionto manifest. Go immediately to the ER for evaluation and observation if you needed to use the anaphylaxis kit. Call 911 and don’t drive to the ER.
Avoid wearing bright colors or scents, which may attract insects.
