D3.307 - Chlorhexidine-triggered anaphylaxis in a child with multisystem allergy and sickle cell disease: a diagnostic pitfall
Case report
Background
Chlorhexidine is a universal hospital antiseptic and a recognised cause of immediate Drug Hypersensitivity Reactions (DHRs), including anaphylaxis. Its presence in multiple products, such as line-care wipes and skin preparations, can lead to increased skin sensitisation and undocumented reactions, increasing the risk of misattribution to concurrently administered medications.
Case Presentation
A 9-year-old child with sickle cell disease and multisystem atopy (asthma, atopic dermatitis, IgE-mediated allergy to peanuts & tree nuts) developed grade III anaphylaxis prior to anaesthesia, shortly after intravenous access and drug administration preparation. Surgery was postponed. A rescheduled procedure, using chlorhexidine-containing theatre skin preparation, was uneventful. Drug and food anaphylaxis were excluded.
During a subsequent admission for treatment of a suspected post-operative infection, she experienced three immediate reactions following the first doses of Cefotaxime (grade III), Piperacillin/Tazobactam (grade II), and Clindamycin (grade II). Clinical features included urticaria, angioedema, wheeze, oxygen desaturation, and, in the case of the Cefotaxime episode, hypotension. All episodes were treated with intramuscular adrenaline, oxygen, & supportive care.
Serum tryptase was measured at 0 and 2 hours post-onset on 2 occasions and was within the normal range. No shared excipients were identified across the antibiotics. A thorough review identified repeated use of chlorhexidine-containing line-care products during intravenous access and antibiotic administration. As such, Chlorhexidine-specific IgE was found to be positive (55.4 kAU/L).
Discussion
The pattern of reactivity to unrelated antibiotics with prior drug tolerance and positive chlorhexidine-specific IgE supported chlorhexidine anaphylaxis. A chlorhexidine avoidance protocol was implemented. Cefotaxime and piperacillin/tazobactam drug allergy were de-labelled following multi-professional reviews; clindamycin evaluation is ongoing.
Conclusion
DHRs, via venous access and aseptic technique products, may get attributed to concurrent medications like antibiotics. However, clinicians should consider non-antibiotic exposures, such as Chlorhexidine, when multiple unrelated reactions occur with no defined trigger. Structured anaphylaxis grading (I-IV), accurate documentation of drug and care product exposures, and timed tryptase sampling are critical to the diagnosis and management of anaphylaxis.
