JOURNAL OF THE LOUISIANA STATE MEDICAL SOCIETY
to rule out or confirm other etiologies of angioedema. Tests used to evaluate for hereditary (HEA) or acquired angioedema include serum C4 levels, C1 inhibitor serum levels and function tests and serum C1q levels. 9,10 While abnormal values of these tests may point to other causes of angioedema, results within normal ranges can help to rule out other etiologies and help to support the diagnosis of ACEi-induced angioedema.
extubation. 21,22 Antihistamines should be administered in all cases of angioedema of unknown etiology due to their relatively benign safety profile and significant efficacy in histamine- induced angioedema and clinically similar allergic reactions.
CONCLUSION
ACEi-induced angioedema is a potentially life-threatening adverse effect of ACEi medications. African Americans are disproportionally affected relative to Caucasians, however the percentage of patients that use these medications and develop angioedema remains low. A significant number of people use ACEi’s, as such, angioedema is not an uncommon presentation to the ED. When these patients are identified early and treated appropriately, the outcome is generally favorable.
TREATMENT
The initial management of ACEi-induced angioedema is well defined and includes: 1) the immediate cessation of the offending medication and 2) assessment of the airway to evaluate for current or the possibility of future airway compromise. In the event of oropharyngeal swelling, emergent intubation and mechanical ventilation should undertaken to ensure airway patency. It is imperative to continuously monitor the patient’s airway and respiratory status for signs of compromise. ACEi-induced angioedema is typically self-limited and resolves within 24-72 hours after cessation of the offending medication. However for cases of severe or refractory ACEi- induced angioedema, additional therapies may be initiated. High concentrations of endogenous bradykinin pathway inhibitors, have shown significant efficacy in the treatment of ACEi-inducedangioedema. Fresh frozenplasma (FFP), inaddition to clotting factors and other plasma proteins, contains high levels of angiotensin converting enzyme (ACE). The ACE present in FFP inactivates bradykinin and thus is generally a very effective treatment in ACEi-induced angioedema, with typical symptom improvement beginning within two hours of infusion. Two units of FFP is the typical dose required for symptom improvement in adult patients with ACEi-induced angioedema. In addition, FFP has been shown to reduce symptom recurrence. 11,12,13 Purified concentrates of C1 inhibitor, a protein which functions to inhibit kallikrein, have also been reported as an effective therapy for ACEi-induced angioedema in several case reports. 14,15,16,17,18 In addition to transfusions of endogenous bradykinin pathway inhibitors, there are synthetic medications that are FDA- approved for the use in Hereditary Angioedema (HAE) which have also shown efficacy in ACEi-induced angioedema. Icatibant, as was discussed in this case report, is a synthetic bradykinin B2- receptor antagonist. Icatibant is administered in a single dose subcutaneously and shows best results when administered within the first several hours of an ACEi-induced angioedema attack. 19,20 Additional doses can be administered if there is worsening of symptoms after six hours, but it is recommended that no more than three injections be given within a 24 hour period. 19 Antihistamines, one of the mainstays of treatment in histamine- induced angioedema, have no biologic effect on bradykinin activity or metabolism. However, antihistamines administered in typical adult doses have been shown in a small number of studies to improve the clinical status in patient’s suffering from ACEi-induced angioedema and were associated with earlier
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