ACUTE TREATMENT, Health care setting
LONG-TERM RISK REDUCTION, Community setting
TREATMENT, IF NEEDED  Allergen-specific –Immunotherapy with insect venom –Desensitization to ˜-lactam antibiotics, NSAIDs, other  Allergen non-specific –Idiopathic anaphylaxis: consider glucocorticoid treatment
EMERGENCY PREPAREDNESS Epinephrine autoinjector Anaphylaxis Emergency Action Plan (www.aaaai.com) Medical ID    ASSESS/TREAT COMORBIDITIES ALLERGEN AVOIDANCE www.foodallergy.org www.latexallergyresources.org www.aaaai.org www.acaai.org     ASSESS NEED FOR CO-MEDICATIONS Asthma Cardiovascular disease Mastocytosis Other     Nonselective ˜-blockers Other  
Figure 81-2 Summary of anaphylaxis management. Acute treatment is the same regardless of the mechanism or trigger involved in anaphylaxis. In contrast, for long-term risk reduction, avoidance measures and immunomodulation are trigger-specific; currently immunomodulation is available only for a minority of individuals with anaphylaxis. All at-risk individuals need to have comorbidities and comedications assessed, be taught the importance of emergency preparedness, and be instructed in the use of self-injectable epinephrine. ACLS, Advanced cardiac life support; CPR, cardiopulmonary resuscitation; CVS, cardiovascular; GI, gastrointestinal; ID, identification (e.g., bracelet, wallet card); IV, intravenous. (From Simon FER: Anaphylaxis, J Allergy Clin Immunol 121:S405, 2008.) *The skin should be inspected, and weight estimation is important, especially in infants and children, and also in overweight and obese teens and adults, in order to calculate an optimal dose of epinephrine and other medications needed in treatment and resuscitation.
†Supine position, as tolerated, to prevent empty ventricle syndrome.
‡Call 911/emergency medical services for anaphylaxis occurring in community health care facilities such as medical, dental, or infusion clinics, where optimal backup might not be available for resuscitation.
Serum sickness is a type III hypersensitivity reaction (see Table 77-1). The patient’s immune system recognizes the proteins in the drug or antiserum as foreign and produces antibodies against them. The newly formed antibodies bind with the foreign protein to form antigen-antibody or immune complexes, which may enter the circulation and be deposited in blood vessels and in filtering organs. These complexes cause tissue injury by activating the complement cascade and recruiting neutrophils, resulting in increased capillary permeability, toxic mediator release, and tissue damage.
Immune complexes were first described after administration of heterologous serum, such as horse serum for diphtheria. The availability of human-derived biologics, bioengineered antibodies, and alternative pharmacotherapies has greatly reduced the incidence of serum sickness. Common inciting agents include blood products and foreign proteins, such as antithymocyte globulin and antivenoms. Medications frequently implicated include penicillin, sulfonamides, minocycline, cefaclor, hydantoins, and thiazides.
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