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Emergency and Acute Medicine - Serum Sickness
Serum sickness is a type III hypersensitivity reaction that occurs when the immune system forms antigen–antibody complexes in response to a foreign protein or drug. These immune complexes deposit in tissues and activate the complement system, leading to inflammation and tissue damage. Complement components such as C3a and C5a act as anaphylatoxins, with C5a strongly attracting neutrophils. These neutrophils infiltrate vessel walls and release enzymes like collagenase and elastase, resulting in vascular injury. Symptoms typically develop 6–21 days after initial exposure to the antigen, but may occur sooner (1–4 days) if there has been prior sensitization. The condition is usually self-limited, resolving within 1–2 weeks.
Serum sickness can be triggered by exposure to foreign proteins such as vaccines (e.g., pneumococcal or rabies vaccines), antivenoms, and tetanus immunizations derived from animal serum. It may also occur with monoclonal antibodies. A related condition, serum sickness–like reaction, is more commonly caused by nonprotein drugs, especially antibiotics such as penicillins, amoxicillin, cephalosporins (e.g., cefaclor), and sulfonamides. Other implicated medications include thiazides, aspirin, gold, thiouracils, hydantoins, and certain antimicrobials.
The classic clinical presentation includes fever, rash, arthralgias, and lymphadenopathy. Patients may also report myalgias, facial or neck edema, chest pain, and shortness of breath. The rash is often urticarial, morbilliform, or scarlatiniform. On examination, findings may include fever, lymphadenopathy, arthritis, edema, splenomegaly, and, in severe cases, peripheral neuritis, myocarditis, pericarditis, or even anaphylaxis. A key diagnostic clue is the timing of symptoms following exposure to a potential offending agent.
Diagnosis is primarily clinical, based on history and physical findings. Laboratory studies may support the diagnosis and include decreased complement levels, elevated erythrocyte sedimentation rate (ESR), hypergammaglobulinemia, and possible eosinophilia. Urinalysis may reveal proteinuria or hematuria, indicating renal involvement. Imaging such as chest radiography may be considered in selected cases. A biopsy can confirm the diagnosis but is rarely required in routine practice.
The differential diagnosis includes other vasculitides such as polyarteritis nodosa, Goodpasture syndrome, and granulomatosis with polyangiitis, as well as dermatologic conditions like erythema multiforme or toxic epidermal necrolysis. Immunologic diseases such as systemic lupus erythematosus and infectious conditions like tick-borne illnesses or mononucleosis should also be considered.
Management is largely supportive, as the condition is usually self-limited. The most important step is identification and discontinuation of the offending agent. Treatment focuses on symptom relief using antihistamines, antipyretics, and nonsteroidal anti-inflammatory drugs. Corticosteroids such as prednisone may be used in more severe cases, although their use remains somewhat controversial. In cases involving airway compromise or anaphylaxis, standard emergency management with airway support and resuscitation is required.
Most patients can be discharged once stable, as symptoms typically resolve spontaneously. Hospital admission may be necessary for patients with severe systemic involvement, airway compromise, immunosuppression, or significant comorbid conditions. Follow-up with a primary care physician is recommended, and future exposure to the offending antigen should be avoided. Early recognition and removal of the causative agent are essential to prevent complications and ensure recovery.
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