J-LSMS 2017 | Annual Archive

JOURNAL OF THE LOUISIANA STATE MEDICAL SOCIETY

One and a half hours after admission, the edema continued to worsen and prompted concern regarding possible airway compromise due to evolving pharyngeal edema. The emergency medicine physician documented posterior pharyngeal wall edema (Figure 2) and recommended elective intubation to protect the patient’s airway. However, the patient elected to refuse intubation in hopes that the swelling would resolve shortly. While in the ED, a working diagnosis of ACEi-induced angioedema was established and the patient was treated with an immediate transfusion of two units of fresh frozen plasma (FFP). During this time, the hospital pharmacy was consulted about the availability of icatibant, a bradykinin B2-receptor antagonist used in the treatment of Hereditary Angiodema which has also been used off-label in management of ACEi- induced angioedema. To rule out hereditary angioedema and acquired angioedema, C1 inhibitor function and protein levels, C4 complement, and C1q levels were ordered. Results of all were within normal limits.

Figure 2: Prior to ICU admission

Figure 2: Pharyngeal Edema

Two hours after his initial presentation to the ED, the patient was admitted to the Intensive Care Unit (ICU) due to concern for impending airway compromise secondary to worsening facial and pharyngeal swelling. Five hours after admission to the ICU, the patient was emergently intubated (Figure 4). On the day following his admission to the ICU, the patient’s angioedema continued to progress and he was given another two units of FFP. During this time, the patient began exhibiting symptoms of alcohol withdrawal, most notably tachycardia

Figure 4: Post-intubation

172 J La State Med Soc VOL 169 NOVEMBER/DECEMBER 2017

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