Angioedema Requiring an Awake Fiberoptic Nasotracheal Intubation Following Levofloxacin Administration in a Patient on Chronic Lisinopril and Aspirin Therapy

Figure 1: A photograph of the patient following successful fiberoptic nasotracheal intubation.

A 70-year-old woman with a history of hypertension, diabetes mellitus, previous angioedema and hypercholesterolemia, presented to the emergency department with complaints of tongue swelling awakening her from sleep. Her usual medications included lisinopril and aspirin. The patient had been discharged from the hospital four days earlier following treatment for a urinary tract infection. Following discharge, she was to take a five-day course of levofloxacin that had also been administered during her two-day hospital stay. She was transported to the hospital by ambulance and had received epinephrine subcutaneously and diphenhydramine intravenously. In the emergency department she was given additional doses of epinephrine subcutaneously and methylprednisolone intravenously. She was brought immediately to the operating room due to increasing tongue edema. In the operating room a surgical team was present for a possible emergency tracheostomy. The patient was given glycopyrrolate 0.3 mg and midazolam 1mg IV as premedication. Additional sedation was achieved with ketamine 30 mg. The patient remained sitting upright for the intubation. Oxymetazoline nasal spray was administered to the nares. A 7.5 mm endotracheal tube was lubricated with viscous lidocaine. The tube was placed in the left naris, advanced to the oropharynx, and then a fiberoptic bronchoscope was inserted through the endotracheal tube. The vocal cords were easily visualized and glottic edema was absent. The fiberoptic bronchoscope was then easily passed into the trachea and the endotracheal tube was advanced over the bronchoscope into the trachea. Proper endotracheal tube placement was confirmed via the presence of end tidal carbon dioxide and a second direct visualization of the carina (Figure 1). General anesthesia was induced with sevoflurane and propofol after securing the nasotracheal tube. The patient was transferred to the intensive care unit. The patient was extubated on hospital day 2 and was continued on intravenous steroids

1. Fluoroquinolones are known to cause anaphylactoid reactions via direct histamine release from mast cells, but may also lead to IgE-mediated histamine release. According to one study, it is possible to measure quinolone specific IgE levels.
2. Angioedema can occur even after years of ACE inhibitor therapy.
3. ACE inhibitors are the most common cause of angioedema reportedly via increased kinin levels leading to increased vascular permeability.
4. Urticaria is usually absent as was the case in this patient which suggests a kinin-mediated as opposed to an IgE-mediated pathway. In addition, aspirin causes release of proinflammatory leukotrienes. A serum tryptase within four hours of the event and measurement of complement levels (c1, c4 and c1 inhibitor) may help to determine IgE- versus kinin-mediated etiologies, respectively.

1. Smythe MA, Capallety DM. Anaphylactoid reaction to levofloxacin. Pharmacotherapy. 2000;20:1520-23.
2. Mariangela M, Severino M, Testi S, et al. Detection of specific IgE to quinolones. J Allergy Clin Immunol. 2004;113:155-60.
3. Reed LK, Meng J, Joshi GP. Tongue swelling in the recovery room: a case report and discussion of postoperative angioedema. J Clin Anesth. 2006;18:226-9.
4. Rai MR, Amen F, Idrees F. Angiotensin-converting enzyme inhibitor related angioedema and the anesthetist. Anaesthesia. 2004;59:283-9.

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