Wasps are members of the order Hymenoptera, suborder Apocrita. Members of this order, which includes bees, yellow jackets, hornets, and ants, are found in all 50 states.
See the image below.
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Western paper wasp (Mischocyttarus flavitarsis) building a nest. By Sanjay Acharya (self-made at Sunnyvale, California, USA). Courtesy of Wikimedia Co....
Wasps can be further divided into social wasps and solitary wasps. Social wasps include the aggressive wasps found in northern temperate regions, such as the yellow jacket (black and yellow bands on abdomen) and the hornet (mostly black with yellow markings on the face and thorax). Social wasps live in colonies that may contain from a dozen to many hundred mature insects. The colonies can range in size and position from the underground nest of the yellow jacket, which is found in rotted tree stumps and mammal burrows, to the hornet's paper nest that hangs from shrubbery, trees, or is plastered to the side of a shed or house.
Solitary wasps act as predators, feeding on smaller insects and bringing the paralyzed prey back to the nest for their young. Solitary wasps include the mud wasp, which makes its nest in crevices of windows.
More than 25,000 species of wasps exist worldwide. They include yellow jackets, which are members of the genus Vespula and are large and aggressive. The female yellow jacket begins to construct her nest in the springtime. The nest is composed of a paperlike substance that wasps regurgitate from chewed wood or plant material. The nest consists of multiple vertically oriented cells, with the opening on the bottom of the nest.
Envenomation or stinging by members of the order Hymenoptera is a major cause of morbidity and mortality and accounts for more fatalities than any other venomous animal. The skin is the most commonly affected organ system. The result of a wasp sting can vary from a single area of localized inflammation to a generalized urticarial rash.
See the image below.
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Yellow jacket. By Richard Bartz, Munich aka Makro Freak (Own work). Courtesy of Wikimedia Commons.
Upon penetration of the skin, the muscles around the wasp's venom sac begin to inject the venom. Wasp venom contains up to 13 different antigens. The wasp sting first causes an intense stinging sensation that is believed to be mediated by the presence of acetylcholine and serotonin, which make up to 5% of the dry weight of the venom. The acetylcholine causes an intense depolarization of the nociceptors within the dermis. The serotonin causes multiple effects through the 5-hydroxytryptamine (5-HT) receptors, including an intense localized vascular spasm.
In addition, the wasp venom also contains phospholipase A, phospholipase B, as well as mastoparan peptide, which can cause direct mast cell degranulation with the release of histamine. The resultant localized ischemia increases the inflammatory response with subsequent vasodilation. This produces increased capillary permeability and localized swelling and redness at the site of the wasp sting. For most individuals who are stung and who have not been sensitized previously to the various antigens within the venom, this reaction is the extent of the injury, and the swelling and pain resolve in several hours. On the 4-point Star Sting Pain Scale for Hymenoptera stings, the wasp sting is a level 2, with level 4 being the most painful.[1]
Systemic reaction
For individuals who have been sensitized to the venom by a past exposure to Hymenoptera venom, symptoms may progress. This progression involves elements of both cellular and humoral immunity. The cellular components consist of lymphocytes, both T cells (CD4+ and CD8+) and B cells, macrophages, and mast cells. The humoral factors include immunoglobulin E (IgE) and cytokines. The process begins with sensitization. This occurs after the protein peptide moieties in the wasp venom, the allergen or immunogen, are processed by antigen-presenting cells, such as macrophages, to form major histocompatibility complex molecules located on the cell wall. This complex is then presented to the T-cell receptor (TCR) on the CD4+ cells. This is followed by the production of IgE and ends with the binding of IgE to the high-affinity receptor, designated FcRI, on the mast cells.
An immediate type of hypersensitivity occurs when the sensitized mast cells contact the offending immunogen. The mast cells become activated, causing solubilization and enlargement of the crystalline granules within their cytoplasm. This is followed by degranulation with the release of these chemical mediators, which include histamine, heparin, and tumor necrosis factor (TNF), into the surrounding tissue. In addition to degranulation, mast cell activation also initiates generation of bioactive products through lipid metabolism of arachidonic acid and the production of cytokines such as TNF, interleukin (IL)–6, IL-4, and IL-5. The nature and degree of the immediate hypersensitivity reaction depends on the location and the degree of activation of the mast cells. Mast cells are located in the connective tissue of the dermis, GI tract, airway, and lungs and around the vascular system, thus producing the symptoms discussed below.
Urticaria, which has also been termed "anaphylaxis of the skin", typically presents as raised pruritic erythematous wheals. Urticaria develops because of the presence of activated mast cells in the connective tissue of the dermis with the production of chemical mediators, such as histamine, that increase local vascular permeability. In general, localized vasculitis is thought to be caused by several factors. IgE triggers the release of vasoactive amines (eg, histamine, bradykinin, leukotrienes) from platelets or from mast cells, increasing vessel wall permeability. The antigen-antibody complexes also result in the activation of complement components, particularly plasmin-activated complement 5 (C5a). The C5a then causes neutrophilic infiltration of the vessel wall to phagocytose the immune complexes. The release of intracytoplasmic enzymes further damages the vessel wall.
Systemic symptoms can include nausea, vomiting, abdominal cramping, and diarrhea due to mast cell activation in the GI tract. Coughing, dyspnea, and wheezing can occur after mast cell activation in the airway.
Severe systemic or anaphylactic reaction
Anaphylactic shock is an immediate-type hypersensitivity reaction that occurs when mast cells are activated within multiple organ systems and vascular collapse occurs. This is an IgE-mediated reaction to the sting. Six percent of blood donors are estimated to have elevated IgE levels to Hymenoptera venom. In one study of postmortem sera from patients with sudden death, 23% had elevated levels to Hymenoptera venom. As a rule, the severity of the response can be estimated by how quickly it occurs after the sting. Most fatalities occur within 1 hour, with most severe reactions occurring within 10 minutes of the wasp sting.[2] This is more related to the existing level of circulating IgE than to the number of wasp stings or the amount of venom injected.
Potential risk factors include outdoor activities (recreational or occupational) during the mild-to-warm months of the year. The disturbance of an established wasp nest, which can occur during routine yard work, raking, or trimming bushes that may contain a concealed nest, can result in multiple wasp stings.
The wearing of any scented material (eg, perfume, hairspray, soaps, deodorants, sunscreen) or brightly colored clothing, especially floral designs, may attract wasps and insects.
Odors near the home environment (eg, open garbage pails, rotting fruit from fruit trees) may also attract wasps.
Partially closed or protected areas (eg, in a wood shed, under a car hood) may harbor a wasp nest, and an attack may result if the nest is disturbed.
In addition, a noted increase of Hymenoptera stings have occurred following environmental disturbances of their customary habitat such as after hurricanes or floods.[3]
Ninety-four percent of individuals will be stung by a member of the Hymenoptera order sometime during his or her lifetime.[4]
United States
Hymenoptera stings and wasp stings have increased over the last 60 years and now account for over 79 deaths each year.[5] This may be an underestimation because sudden death syndrome is usually attributed to cardiac causes. In one series of 2606 patients, the frequency of the various presentations was as follows:
Local reaction - 16% (This may be an underestimation because many patients with a single wasp sting and only a local reaction do not seek medical attention.)
Severe systemic reaction - 24%
Systemic reaction - 40%
In the general population, 3% of adults and less than 1% of children have systemic reactions. This is probably because adults are more likely to have developed sensitization from a prior wasp sting.
Sex
Wasp stings are more common in males than in females, likely because of increased occupational and recreational exposure in men.
Age
More reported wasp stings occur in adults than in children. Children tend not to have reactions as severe as those in adults, possibly because adults tend to have had more opportunity to have developed sensitization to the allergens in the venom. However, a recent article also suggests that serum tryptase is a risk factor for severe anaphylactic reactions. Serum tryptase levels increase with age and seem to correlate with mast cell load or reactivity.[6] When a child develops an allergic reaction to a wasp sting, it tends to be worse than an adult’s reaction because of the higher ratio of venom quantity to body mass.
Mastocytosis or clonal mast cell disorders[14, 15]
Severe atopic diseases such as allergic rhinitis[16]
Medications such as beta-blockers and ACE inhibitors[17, 18]
The anaphylactic reaction begins with the onset of symptoms distal to the wasp sting. The patient frequently feels increased anxiety, lightheadedness, headache, nausea, abdominal cramps, and palpitations. This is followed by objective findings of the patient appearing flushed, hypotensive, and tachycardic. This is due to the circulating levels of histamine and kinins that cause decreased systemic vascular resistance, increased capillary permeability, and resulting reduction of intravascular volume. The resulting reduction in perfusion pressure causes the neurologic symptoms of lightheadedness, syncope, and seizures.
Sensitization to Hymenoptera or wasp venom occurs in almost 1% of all stings. Each year, 90-100 deaths occur. Risk factors that tend to increase morbidity and mortality include age, cardiopulmonary risk factors, medication, and prior history of an allergic reaction to a Hymenoptera or wasp sting. Factors that favor a systemic reaction include multiple simultaneous wasp stings or single sequential wasp stings within several weeks. In most cases of Hymenoptera stings, death is the result of airway and respiratory compromise. Edema of the larynx, epiglottis, and supraglottic area is found in 69% of fatal cases. These structures are particularly vulnerable target areas because of their rich vascular supply. Prior history of sensitivity or an allergic reaction to a Hymenoptera sting places the patient at higher risk for another reaction.
Individuals who are atopic, individuals with a history of multiple allergies, and individuals who have had a prior anaphylactic reaction to a different allergen may be at increased risk for sensitization to their first Hymenoptera sting. The following factors also increase the risk of sensitization:
Age
Children and elderly people are at increased risk. Infants and small children are at risk after multiple wasp stings because of the relatively large amount of venom per body mass. The smaller-diameter pediatric airway may also occlude more readily from edema. Elderly people may have poor cardiac reserves to compensate for the allergic reaction.
Cardiopulmonary risk factors
People with coronary artery disease, a history of ischemia, prior myocardial infarctions, or reduced cardiac ejection fractions may not be able to compensate for the increased insult to their circulatory system from circulating vasoactive peptides or from the catecholamines administered to resuscitate them. People with pulmonary disease (eg, asthma, chronic bronchitis, emphysema) may experience acute decompensation of the respiratory system because of increased bronchospasm or pulmonary edema.
Medication
Beta-blockers may increase morbidity and mortality because they inhibit attempts to improve cardiac output by either endogenously produced or exogenously administered catecholamines.
Calcium channel blockers may exacerbate the reduced systemic vascular resistance caused by circulating vasoactive peptides. The vasodilating antihypertensive agents may blunt the body's physiologic response to hypotension. As the circulating vasoactive chemical mediators of anaphylaxis cause vasodilation, the systemic vascular resistance falls. This causes a subsequent drop in the glomerular filtration rate, resulting in increased activation of the renin-angiotensinogen-angiotensin system.
ACE inhibitors and ACE receptor blockers, which may inhibit the degradation of tryptase, histamine, and bradykinin,[19] as well as other vasodilators, can interfere with the body's ability to increase vasoconstriction and increase the systemic vascular resistance and the blood pressure (BP). The effect that nonsteroidal anti-inflammatory drugs (NSAIDs) and leukotriene inhibitors may have in modulating the severity or the morbidity and mortality of Hymenoptera-induced allergic reactions is unclear.
Symptoms can vary depending on the reaction of the patient to the wasp sting.
A localized reaction causes symptoms of redness, swelling, and pain over the site of the wasp sting. The pain begins immediately and gradually worsens as the redness and edema gradually worsen. The localized reaction may last 6-12 hours.
A patient with a mild allergic reaction may experience itching and hives.
Severe allergic reactions and anaphylaxis may present in patients as symptoms of a throat-closing sensation, dyspnea, chest tightness, lightheadedness, increased anxiety, headache, nausea, abdominal cramps, and palpitations.
Physical signs vary in severity, depending on host sensitivity to the protein allergens in the venom. This can vary from a local reaction at the site of the wasp sting to a more generalized pruritic urticarial reaction to angioedema, laryngeal spasm, bronchial spasm, and vasomotor collapse of anaphylactic shock.
Local reaction
A raised, painful, erythematous inflammatory reaction may be observed at the site of each wasp sting, usually developing several minutes after the sting.
A minute punctate lesion is visible at the center of the lesion where the wasp sting occurred.
Generalized urticarial reaction
A generalized, allergic, immunoglobulin E (IgE)–mediated reaction that involves only the skin can occur within minutes to hours of the wasp sting.
Patients present with multiple pruritic hives.
Angioedema
Patients may present with signs of airway obstruction with stridor and dyspnea. The voice may be muffled or hoarse. Patients may not be able to process their own secretions and may be drooling or appear to have odynophagia.
Inspection of the oral pharynx may show soft tissue swelling of the mucosa or of the tongue. Normal results on examination of the oral pharynx do not preclude edema and impending obstruction of the larynx.
Anaphylaxis
Impending vasomotor collapse may be associated with the appearance of restlessness or anxiety in patients.
Vital signs include tachycardia, tachypnea, and thready pulses. In the early phase, the BP may be maintained because of increased cardiac output until the patient decompensates.
Skin appearance may vary from a warm flushed appearance shortly after the wasp sting (due to increased vasodilation caused by circulating vasoactive amides) to a cold, pale, diaphoretic appearance late in the event.
Auscultation of the chest may reveal variable results, from wheezing due to bronchospasm and prolongation of the expiratory phase to poor air movement or coarse crackles due to pulmonary edema.
Anaphylaxis is highly likely when any one of the following three criteria is fulfilled:
The acute onset of illness (minutes to several hours), with involvement of the skin, mucosal tissue, or both (eg, generalized hives; pruritus or flushing; swollen lips, tongue, or uvula) and at least one of the following: Respiratory compromise (eg, dyspnea, wheeze or bronchospasm, stridor, reduced peak expiratory flow [PEF], hypoxemia) or reduced BP or associated symptoms of end-organ dysfunction (eg, hypotonia [collapse], syncope, incontinence)
Two or more of the following that occur rapidly after exposure to a likely allergen for that patient (minutes to several hours):
Involvement of the skin or mucosal tissue (eg, generalized hives; itch or flush; swollen lips, tongue, or uvula)
Reduced BP or associated symptoms (eg, hypotonia [collapse], syncope, incontinence)
Persistent GI symptoms (eg, crampy abdominal pain, vomiting)
Reduced BP after exposure to a known allergen for that patient (minutes to several hours), as follows:
Infants and children - Low systolic BP (age specific) or greater than 30% decrease in systolic BP (Low systolic BP in children is defined as less than 70 mm Hg in those aged 1 mo to 1 y, less than 70 mm Hg + [2 X age] in those aged 1-10 y, and less than 90 mm Hg in those aged 11-17 y.)
Adults - Systolic BP of less than 90 mm Hg or greater than 30% decrease from that person's baseline
Consider local wound infection in any wasp sting site that worsens, persists, or partially resolves only to swell up with increased redness, swelling, or pain. Other symptoms and signs that should be elicited include fever, chills, red streaks extending proximally from the site, and purulent drainage from the site.
Wasp stings have also been associated with acute renal failure in children[20] as well as the Kounis syndrome or allergic myocardial ischemia and infarction.[21, 22]
Laboratory data usually are not helpful in patients with mild symptoms. Patients who present with anaphylaxis resulting from a wasp sting may benefit from studies such as arterial blood gas assessment, CBC count, electrolytes, BUN and creatinine, glucose, serum alpha/beta tryptases (which elevate within 15 min to 3 h from the onset of symptoms), histamine levels (which elevate from 15 min to 1 h from the onset of symptoms),[7] and liver function studies in order to provide their baseline values as part of the admission profile.
Patients may have mild leukocytosis related to demargination from catecholamine release.
Arterial blood gas values reflect the pathophysiology of the illness progression. The initial pH level should be normal or may be slightly elevated to reflect a respiratory alkalosis due to anxiety-produced hyperventilation with the corresponding decrease in the partial pressure of carbon dioxide (PCO2). As the patient becomes more hypotensive, the pH level may begin to fall. Conversely, this fall may also be due to increased respiratory distress with bronchospasm. This can be due to several factors. A respiratory acidosis can be caused by carbon dioxide retention from the respiratory bronchospasm and the development of pulmonary edema. At this point, the partial pressure of oxygen (PO2) level begins to fall. The decreased pH level can also be due to the development of a metabolic acidosis as the patient becomes more hypotensive and tissue perfusion decreases.
Lateral neck radiography to evaluate for soft tissue swelling may be helpful in patients who experience throat tightness after a wasp sting, although direct fiberoptic visualization of the airway (eg, with a Machida scope) is optimal.
Perform chest radiography in patients who present with dyspnea or chest tightness or who have an anaphylactic episode after a wasp sting. Chest radiography should be obtained by using a portable machine in the emergency department (ED) with equipment for aggressively managing the airway close to the bedside.
Perform an ECG on patients who experience palpitations, chest tightness, dyspnea, or lightheadedness after a wasp sting.
A baseline peak flow measurement helps to assess the progression of distress in patients who present with wheezing, dyspnea, or prolongation of the expiratory phase of respiration after a wasp sting.
Flexible fiberoptic visualization of the larynx and vocal chords may be useful to exclude laryngeal edema or spasm. This should be performed by a clinician experienced in emergency airway management; use caution to avoid precipitating laryngospasm.
The "ABCs" (airway, breathing, circulation) of patient resuscitation and care take precedent. Airway patency and security is the prime concern, especially if there is any evidence of potential airway obstruction from angioedema manifested by stridor, hoarseness of voice, difficulty swallowing, or pooling of secretions. Breathing should be assessed for the rate, depth and adequacy of ventilation with pulse oximetry and auscultation of the chest to determine air movement, and the presence of wheezing from bronchial constriction and spasm. The patient's circulatory status should be evaluated for presence of distributive shock, assessing the blood pressure, nail bed capillary refill, and the patient's mental status.
Apply ice to keep the area comfortably cool and to reduce swelling. Unlike honeybee stings, members of the wasp family (including hornets and yellow jackets) generally do not lose their stinging apparatus in the wound. Consider a secondary bacterial infection at the site in patients who present several days after the sting with fever or continued redness, warmth, swelling, and tenderness over the site or progression of the redness—red streaks that progress proximally.
Urticaria
Antihistamines remain the mainstay of therapy. H1 blockers such as oral diphenhydramine (Benadryl) or hydroxyzine (Atarax) have proven useful in reducing the severity of the itching and rash. Oral steroids (eg, prednisone, methylprednisolone [Medrol]) can be added to the regimen if needed, depending on the extent and severity of the patient's symptoms. Epinephrine, 0.3-0.5 mL subcutaneously in a 1:1000 solution, can also be used. Although it reverses the extent and itching of the urticaria, its benefit-to-risk ratio must be considered. The alpha effect of epinephrine increases the systemic vascular resistance, while its beta effect has a positive inotropic and chronotropic effect on the heart. This produces an increase in the heart's work and increases the myocardial oxygen demand. This may have a deleterious effect in patients with preexisting heart disease or coronary artery disease.
Anaphylaxis
The patient may present with airway obstruction due to angioedema, respiratory compromise due to bronchospasm, or circulatory collapse or with a combination of these three conditions. Follow the ABCs of emergency medicine as expediently as possible. The airway must be secured. Intubate the patient with rapid sequence technique upon evidence of impending airway obstruction due to swelling or evidence of respiratory failure due to bronchospasm. It is easier to extubate a patient than to wait too long and try to pass a tube through an edematous larynx. Establish two large-bore intravenous lines to provide a route for medication administration and for fluid bolus in the event of circulatory collapse. Place the patient on both pulse oximetry and a cardiac monitor.
Angioedema
If intubation is impossible because of the degree of swelling, obtain a surgical airway through cricothyrotomy. Surgical cricothyrotomy is contraindicated in patients younger than 8 years. In these cases, perform needle cricothyrotomy using the largest-bore needle practical as a temporizing measure. Obtain an emergency consultation with an anesthesiologist and an otorhinolaryngologist (ENT) to prepare the child for the operating room for definitive angioedema/airway management if parenteral beta agonists, histamine 1 (H1) blockers, and glucocorticoids do not relieve the obstruction.
Bronchospasm
Treatment of bronchospasm without obstruction depends on the acuity of the patient's presentation. Treat mild-to-moderate distress with a combination of nebulized beta agonist (eg, albuterol 0.5 mL of 0.5% solution in 2.5 mL of normal saline nebulized q15min) and parenteral glucocorticoids (eg, methylprednisolone 125 mg IV). As the severity of the respiratory distress increases, weigh the benefit-to-risk ratio of using a parenteral beta agonist (eg, epinephrine). As bronchospasm worsens, a point of peaked expiratory flow and forced expiratory volume decrease occurs and the only area being ventilated with the nebulized beta agonist is the appropriately named dead space.
Epinephrine, 0.3-0.5 mL of a 1:1000 solution, may be administered intramuscularly. Its onset of action should be 3-5 minutes; however, impending circulatory collapse with peripheral vasoconstriction due to anaphylaxis may make this route ineffective. Intravenous epinephrine using 3-5 mL (0.3-0.5 mg) of the 1:10,000 solution (0.1 mg/mL) diluted in 10 mL of normal saline or distilled water should be administered slowly over a 1- to 2-minute period, depending on the patient's condition.[28] The primary cause of death in anaphylaxis is failure to administer epinephrine in a timely manner. Less than a quarter of patients with cardiac arrest from anaphylaxis receive epinephrine before the cardiac arrest.[23] Epinephrine is given in less than half of cases of true anaphylaxis.[8]
As an alternative, 3-5 mL of 1:10,000 solution can also be administered via the endotracheal tube. Administer this solution via a catheter with the tip placed below the end of the endotracheal tube and then flushed through with several milliliters of saline or distilled water. Several positive ventilations follow to force the epinephrine into the terminal bronchioles and alveoli.
Vasopressin 40 IU has also been used for refractory hypotension.
Hypotension
The cause of hypotension is multifactorial. Histamine, prostaglandin, and leukotriene can reduce the systemic vascular resistance by vasodilating the peripheral vessels and increase the capillary endothelial permeability, allowing extravasation of fluid into the third space. The net effect of both of these processes increases the vascular bed and decreases the amount of fluid in the vascular compartment. Begin treatment with the establishment of 2 large-bore intravenous lines and crystalloid fluid boluses. Vasopressors then can be added, depending on the patient's clinical appearance. Epinephrine can be administered via continuous infusion by mixing 1 mg in 250 mL of normal saline and infusing at a rate of 0.5-1 mL/min. Norepinephrine (Levophed) can also be used. It has the advantage of having more of an alpha effect and less of a beta effect than epinephrine.
Pregnancy
Envenomations can cause miscarriage, stillbirth, placenta abruptio, and preterm birth. Current literature suggests that the best approach to improve fetal output is to optimize the maternal health by treating hypotension and anaphylaxis in the mother. Observation and fetal monitoring are mandatory in severe envenomations with viable fetuses.[29]
All patients who present with a moderate-to-severe reaction to a wasp sting that required treatment should be observed. A rebound or biphasic reaction has been reported in 1-20% of patients as initial treatment wears off.
Proactively treat patients who experience throat tightness resulting from a wasp sting. A treatment spectrum progresses from the asymptomatic patient to the patient with symptoms of mild throat tightness to the patient in respiratory distress from angioedema.
Assess the airway as soon as possible in the patient who experiences throat tightness. Although cross-lateral neck radiography to assess soft tissue can be helpful to rule out gross swelling, it has several disadvantages. It may not reveal early swelling. If transferred to the radiology department for the radiograph, the patient should be accompanied by both an intubation tray and a physician capable of managing the airway.
The airway is best visualized by either an otorhinolaryngologist or an emergency department (ED) physician using a Machida scope or, if a flexible fiberoptic scope is not available, indirect laryngoscopy. An intubation tray must be available at the bedside.
Supplemental oxygen supplied by a humidified cool mist is often helpful in the patient with minimal inflammation who does not need immediate intubation and is being observed.
Breathing
Continually monitor patients with pulse oximetry. Peak flow measurement may help evaluate the progression of bronchial spasm.
Evidence of poor ventilation with decreasing oxygen saturations, poor air movement, wheezing, poor air exchange, prolongation of the expiratory phase, or increased work of breathing requires aggressive management.
A nebulized beta agonist (eg, albuterol) can reduce bronchial spasm and improve oxygenation.
Use methylprednisolone 125 mg IV to decrease the inflammatory response of the airways.
Circulation
The cardiac rate and rhythm and the intravascular fluid compartment are 2 components of circulation that must be monitored.
Put the patient on a cardiac monitor and observe in an area where the patient can be intubated if necessary.
The BP must be monitored continuously because of the release of multiple factors in anaphylaxis that can reduce capillary integrity, increase capillary permeability, and subsequently decrease the amount of fluid in the vascular compartment and, at the same time, decrease the systemic vascular resistance.
Consider a surgical airway in any patient with evidence of upper airway edema or laryngeal spasm who is experiencing respiratory deterioration. The equipment and expertise to perform a cricothyrotomy should be readily available if orotracheal or nasotracheal intubation cannot be achieved.
Transfer the patient to the nearest facility capable of providing critical care monitoring if critical care monitoring cannot be performed at the facility initially treating the patient (in accordance with the current standards established by the Emergency Medical Treatment and Labor Act [EMTALA]).
A person capable of aggressively managing the patient's airway and monitoring and managing the patient's cardiopulmonary function should accompany the patient.
The transporter should have all the equipment and medication necessary to resuscitate the patient.
Patients should be taught the use of the EpiPen 0.3 mg auto-injector or the EpiPen Jr 0.15 mg before they leave the ED. The patient should be taught the indications for the use of the EpiPen such as the signs and symptoms of a severe allergic or anaphylactic reaction. They should be taught to inject the EpiPen into the anterolateral aspect of the thigh and that once the auto-injector is triggered to maintain the auto-injector in place for several seconds until all the medication is injected. The patient should be advised to keep one EpiPen in the home and one on his or her person at all times. Epinephrine is light sensitive and should be stored between 15o -30o C (59o -86o F).[30] Placement of an EpiPen in the car where internal summer temperatures can be well over 100o F is not recommended.
Oral H1 blockers (eg, diphenhydramine, hydroxyzine) and corticosteroids (eg, prednisone, methylprednisolone) also may be helpful.
A consultation with an otorhinolaryngologist may be necessary to visualize the epiglottic and supraglottic regions with a flexible fiberoptic laryngoscope in patients who experience throat tightness or throat closing and who present with little or no objective signs of airway compromise.
In patients with symptoms of throat tightness or throat closing with mild-to-moderate signs of airway compromise or patients who have evidence of early airway obstruction on flexible fiberoptic laryngoscopy, consultation with an anesthesiologist may be necessary to assist in securing the airway.
Patients who have moderate-to-severe signs and symptoms of airway compromise, such as increasing dyspnea, hoarseness, dysphagia, inability to clear secretions, use of accessory muscles, or decreasing oxygen saturation on pulse oximetry, require emergent consultation with both an anesthesiologist and an otorhinolaryngologist to place a surgical airway if intubation is unsuccessful. Rapid sequence intubation in these patients should be used with caution. The airway may be maintained open only by the patient's laryngeal muscles. The use of paralytics may allow the airway to be completely occluded.
Advise patients who have experienced an allergic reaction to prior wasp stings or to any Hymenoptera stings to exercise caution while outdoors during mild-to-warm weather. Advise these patients to avoid wearing any scented material (eg, perfume, hairspray, soaps, deodorants, sunscreen). Brightly colored clothing, especially floral designs, should be avoided. Tell patients who have experienced a severe reaction to a wasp sting to curtail solitary outdoor activities. Advise that the patient should be accompanied when outdoors and away from populated areas (eg, hiking, fishing) in case help is needed.
Because odors tend to attract wasps, tell patients and their families to examine the home environment to decrease risks of attracting insects. Cover garbage pails. Remove rotting fruit on the vine or tree or after having fallen to the ground.
Encourage patients to carry EpiPen auto-injectors when outdoors and to have one device in the home. Advise the patient that auto-injectors left in the car for prolonged periods during hot days may not be effective. They should periodically review the expiration date of the auto-injectors.
Teach the patient how to modify behavior, to dress, and to use toiletries and perfumes appropriately (see Activity).
Refer the patient to an allergist for desensitization to Hymenoptera venom. Desensitization by venom immunotherapy can be accomplished by the injection of depot extracts using a slow and conventional schedule, which minimizes local and systemic side effects, or it can be accomplished rapidly by using a rush protocol with aqueous extracts if protection needs to be achieved rapidly. However, the incidence of severe reactions makes the rush protocol less than ideal for an outpatient procedure and requires hospitalization.[31]
Venom immunotherapy can reduce the relative risk of a future severe reaction to 0.1 as well as reduce the severity of the local reaction. Unfortunately, health economic analysis shows that it is not cost effective because of the infrequency that people are stung. In patients who are at risk for frequent stings, such as beekeepers, venom immunotherapy improves the quality of their life and can be cost effective.[32]
Up to 25% of patients who are on venom immunotherapy will still develop a severe anaphylactic reaction when re-stung.[31]
Prescribe autoinjectors (eg, EpiPen) and oral H1 blockers (eg, diphenhydramine, hydroxyzine). Teach the patient and patient’s family that they need to hold the auto injector on the skin for 10 seconds to let all the medicine enter the muscle.
Delayed biphasic reactions can occur in 4% of severe allergic reactions and up to 72 hours after exposure. Risk factors include prior history of anaphylaxis, unknown trigger, and delay of epinephrine use more than 60 minutes from onset of symptoms.[33, 34]
Direct outpatient care at preventing any further reaction.
Provide patient education to reduce high-risk activities that may lead to exposure (see Activity).
Prescribe self-administered auto-injectors (eg, EpiPen) to patients who have the potential for a severe reaction or who may be away from readily available medical assistance.
Refer patients to an allergist for desensitization. This follow-up referral should be made expeditiously. The factors to consider are include initial reaction of the patient and the patient's risk of being stung again, such as the patient's occupation and time of year.
Medication use varies depending on the severity of the wasp sting.
Antihistamines are used to treat mild urticarial symptoms. In a Canadian study, the use of an antihistamine reduced the progression to anaphylaxis from 3.4% without the H1 blocker to 1.9% with the H1 blocker.[33, 35] H2 blockers were more effective in decreasing urticaria from 46% to 14%.[35]
Catecholamines are needed in extreme cases (eg, anaphylaxis).
H1-receptor antagonists block the effects of histamine. Diphenhydramine and hydroxyzine are two of the most widely used H1 blockers for oral and parenteral use in wasp stings.
Clinical Context:
Steroids ameliorate the delayed effects of anaphylactoid reactions and may limit biphasic anaphylaxis. In severe cases of serum sickness, parenteral steroids may be beneficial to reduce the inflammatory effects of this immune complex–mediated disease.
These agents modulate and decrease the inflammatory response to the sting. Onset of action is delayed for several hours; therefore, glucocorticoids have very little effect in the acute setting. Early administration continues to stabilize the patient.
Clinical Context:
Epinephrine is the drug of choice for treating anaphylactoid reactions. It has alpha-agonist effects that include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta-agonist effects of epinephrine include bronchodilatation, chronotropic cardiac activity, and positive inotropic effects.
Epinephrine can be administered subcutaneously for mild-to-moderate reactions and intravenously and via an endotracheal tube.
Clinical Context:
Albuterol is a beta-agonist for bronchospasm refractory to epinephrine. It relaxes bronchial smooth muscle by action on beta2 receptors, with little effect on cardiac muscle contractility.
Clinical Context:
Famotidine is an H2 antagonist that, when combined with an H1 type, may be useful in treating allergic reactions that do not respond to H1 antagonists alone.
Clinical Context:
Cimetidine is an H2 antagonist that, when combined with an H1 type, may be useful in treating allergic reactions that do not respond to H1 antagonists alone.
Clinical Context:
Ranitidine is a competitive, reversible inhibitor of histamine at the H2 receptor that may be used in conjunction with H1-blockers for severely symptomatic cases. It has fewer drug interactions than cimetidine and may be better for patients who take other medications metabolized by the cytochrome p450 system.
The combination of H1 and H2 antagonists may be useful in chronic idiopathic urticaria not responding to H1 antagonists alone. It may also be useful for itching and flushing in anaphylaxis, pruritus, urticaria, and contact dermatitis.
Clinical Context:
Vasopressin has vasopressor and antidiuretic hormone (ADH) activity. It increases water resorption at the distal renal tubular epithelium (ADH effect) and promotes smooth muscle contraction throughout the vascular bed of the renal tubular epithelium (vasopressor effects). However, vasoconstriction is also increased in splanchnic, portal, coronary, cerebral, peripheral, pulmonary, and intrahepatic vessels. Vasopressin decreases portal pressure in portal hypertension.
Vasoconstrictors reduce portal blood flow and/or increase resistance to variceal blood flow inside the varices. Therefore, these drugs reduce blood flow in the gastroesophageal collaterals because of their vasoactive effects on the splanchnic vascular system. In general, this class of drugs provides hemodynamic support.
Clinical Context:
Norepinephrine is used in protracted hypotension after adequate fluid replacement. It stimulates beta1- and alpha-adrenergic receptors, which in turn increases cardiac muscle contractility and heart rate, as well as vasoconstriction. As a result, it increases systemic blood pressure and cardiac output. Adjust and maintain infusion to stabilize blood pressure (eg, 80-100 mm Hg systolic) sufficiently to perfuse vital organs.
Cardiovascular performance deteriorates and cardiac output falls if effective therapy is not administered. Adrenergic antagonists improve the patient’s hemodynamic status by increasing myocardial contractility and heart rate, resulting in increased cardiac output. They also increase peripheral resistance by causing vasoconstriction. Increased cardiac output and increased peripheral resistance lead to increased blood pressure.
Clinical Context:
Glucagon is the drug of choice for severe anaphylaxis in patients who take beta-blockers (should be used in addition to epinephrine, not as a substitute).
Pancreatic alpha cells of the islets of Langerhans produce glucagon, a polypeptide hormone. It exerts opposite effects of insulin on blood glucose. Glucagon elevates blood glucose levels by inhibiting glycogen synthesis and enhancing formation of glucose from noncarbohydrate sources, such as proteins and fats (gluconeogenesis). It increases the hydrolysis of glycogen to glucose (glycogenolysis) in the liver in addition to accelerating hepatic glycogenolysis and lipolysis in adipose tissue. Glucagon also increases the force of contractions in the heart and has a relaxant effect on the GI tract.
The dose used for anaphylaxis is higher than the usual dose of 1 mg (1 U) IV/IM/SC used to treat hypoglycemia.
Glucagon uses a different receptor than that used by sympathomimetics to stimulate intracellular cAMP production, increasing cardiac conduction and contractility. Glucagon has positive inotropic and chronotropic effects, which may be useful for treating bradycardia caused by calcium channel blockers.
Carl A Mealie, MD, FACEP, FAAEM, Assistant Professor, Department of Emergency Medicine, Donald and Barbara Zucker School of Medicine at Hofstra/Northwell; Chief of Operations, Department of Emergency Medicine, Long Island Jewish Medical Center
Disclosure: Nothing to disclose.
Coauthor(s)
Max Vernon Wisgerhof, II, MD, Fellowship Program Director, Department of Endocrinology and Metabolism, Henry Ford Hospital
Disclosure: Nothing to disclose.
Specialty Editors
Francisco Talavera, PharmD, PhD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference
Disclosure: Received salary from Medscape for employment. for: Medscape.
Chief Editor
Joe Alcock, MD, MS, Associate Professor, Department of Emergency Medicine, University of New Mexico Health Sciences Center
Disclosure: Nothing to disclose.
Additional Contributors
Lisa Kirkland, MD, FACP, FCCM, MSHA, Assistant Professor, Department of Internal Medicine, Division of Hospital Medicine, Mayo Clinic; Chair, Department of Critical Care, ANW Intensivists, Abbott Northwestern Hospital
Disclosure: Nothing to disclose.
Acknowledgements
Alan S Multz, MD Associate Professor of Clinical Medicine, Albert Einstein College of Medicine; Program Director, Internal Medicine Residency, Associate Chairman, Department of Medicine, Long Island Jewish Medical Center
Alan S Multz, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Chest Physicians, American College of Physicians, American Thoracic Society, and Society of Critical Care Medicine
Disclosure: Astellas Pharmaceutical Honoraria Consulting; Merck Pharmaceutical Honoraria Speaking and teaching; The Medicines Company Honoraria Consulting; Schering Plough Honoraria Speaking and teaching; Wyeth Pharmaceuticals Honoraria Speaking and teaching; Pfizer Honoraria Speaking and teaching
References
Starr CK. A simple pain scale for field comparison of Hymenoptera stings. J Entomol Sci. 1985 April. 20:225-31.
Western paper wasp (Mischocyttarus flavitarsis) building a nest. By Sanjay Acharya (self-made at Sunnyvale, California, USA). Courtesy of Wikimedia Commons.
Yellow jacket. By Richard Bartz, Munich aka Makro Freak (Own work). Courtesy of Wikimedia Commons.
Western paper wasp (Mischocyttarus flavitarsis) building a nest. By Sanjay Acharya (self-made at Sunnyvale, California, USA). Courtesy of Wikimedia Commons.
Yellow jacket. By Richard Bartz, Munich aka Makro Freak (Own work). Courtesy of Wikimedia Commons.
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