Medication classes such as fluoroquinolones, ACE inhibitors and
NSAIDS are known to cause “hypersensitivity” reactions
that may manifest as angioedema (tongue, laryngeal, throat or facial edema).
We present a case of angioedema requiring an awake fiberoptic nasotracheal
intubation secondary to severe tongue edema.
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 (see 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.
A photograph of the patient following successful fiberoptic
How did the addition of levofloxacin lead to angioedema in this
patient? Angioedema can be attributed to many medications including
NSAIDS, fluoroquinolones, and ACE inhibitors. The incidence of angioedema
may be increased by a combination of drugs from these classes. In
the case described above, the patient was on chronic aspirin and
lisinopril therapy and developed angioedema when levofloxacin was
added to her regimen. Her previous episodes of angioedema did not
result in intubation.
Anaphylactoid reactions attributed to levofloxacin are thought
to occur in 0.46-1.2/100,000 patients.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 ...