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A 54-year-old woman presents for a hysterectomy and oophorectomy for ovarian mass. She is induced with propofol, fentanyl, and vecuronium. Sevoflurane in air/oxygen is delivered for maintenance. She receives 2 g of cefotetan shortly after intubation. Within the next 20 minutes, she develops hypotension refractory to phenylephrine and ephedrine. End-tidal CO 2 is 22 mm Hg. Epinephrine in doses of 100 μg are repeatedly given, and she requires an epinephrine infusion to maintain a mean arterial pressure greater than 60 mm Hg. The case is canceled, and she is transferred to the intensive care unit. One week later she is rescheduled for the surgery.
Patients under anesthesia are exposed to a large number of medications given intravenously: anesthetics, antibiotics, volume expanders, blood products, analgesics, antiseptics, dyes, and contrast material. Thus anesthesiologists are likely to experience a patient developing anaphylaxis during their career. Anaphylaxis is a rapid-onset systemic life-threatening allergic reaction. However, it can present with only a single sign (bronchospasm or hypotension) and thus can be misdiagnosed, because many disorders may present similarly. In mild cases with recovery without specific treatment, lack of recognition of anaphylaxis can lead to fatal consequences on reexposure. Reactions have classically been described as anaphylactic (immunoglobulin E [IgE] mediated) or anaphylactoid (not IgE mediated). The European Academy for Allergy and Clinical Immunology has proposed to define the clinical reaction as anaphylaxis and subclassify it as allergic or nonallergic after laboratory diagnosis reveals the exact mechanism. However, the American Academy of Allergy, Asthma and Immunology still defines the reactions as anaphylactic and anaphylactoid in its most current practice parameters of 2015. Regardless of how it is classified, for the anesthesiologist it does not matter, as anaphylaxis treatment remains the same no matter what the etiology. The majority of reactions during anesthesia are mediated by IgE to an antigen, which results in mast cell (tissues) and basophil (blood) degranulation. Up to 50% of patients with type I hypersensitivity to a neuromuscular blocking drug (NMBD) deny having had prior contact with the medication. IgE specific to an NMBD can be detected by skin test even if it was the first encounter for a patient.
Although this theory has not been proven, it is thought that prior exposure to a compound with similar quaternary ammonium groups sensitized the patient to form specific IgE molecules. Food, cosmetics, disinfectants, and other medications often contain such ammonium groups. Thus when exposed to a NMBD for the first time, these preformed IgE molecules cross-react to the ammonium group of the NMBD.
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