JOURNAL OF THE LOUISIANA STATE MEDICAL SOCIETY
due to the number of patients currently prescribed ACEi’s as an anti-hypertensive (i.e., approximately 30-40 million people), this “uncommon” adverse effect is encountered in the emergency room with astounding frequency and accounts for 17% of all ED visit complaints of angioedema. 3,6 This is not a benign disease. A staggering 50% of ACEi-induced angioedema cases who present to the ED are potentially life-threatening and may be deadly secondary to larynx or oropharynx swelling. 6 But, the overall fatality-rate associated with ACEi-induced angioedema is relatively low. 4
and hypertension. These symptoms were well-controlled with clonidine patches and diazepam injections.
Approximately 36 hours after his initial presentation to the ED, the patient’s facial swelling began to subside. On hospital day three, his airway was deemed stable and the patient was extubated. The patient was discharged to home on day six of his hospital stay and was instructed to follow up in clinic as an outpatient for management of his hypertension and heart failure. The patient was instructed not to take any angiotensin converting enzyme inhibitor or angiotensin II receptor blocker class medications in the future and was told to return to the ED if any of his symptoms returned.
CLINICAL PRESENTATION
Angioedema is generally a benign, self-limiting condition characterized by swelling. Localized swelling occurs as plasma leaks from capillaries in deeper layers of subcutaneous and submucosal tissue. 7 This swelling occurs when vascular integrity decreases, in response to release or activation of vasoactive agents, and fluid is lost from local blood vessels. 4 Angioedema can be classified as histamine or bradykinin- mediated. ACEi-induced angioedema is a type of bradykinin- mediated drug-induced angioedema which classically develops over a period of one to two days and resolves spontaneously by day five. 2 This is problematic because the delayed presentation makes identifying the trigger difficult. The majority of ACEI- angioedema cases, roughly 50%, occur within one week of initiating treatment. 8 However, there are reports of onset ranging from one day and ten years of starting ACEi therapy. 4 The non-pitting, non-dependent edema associated with ACEi-induced angioedema is characteristically asymmetric, and generally involves the loose connective tissue of the face, lips, mouth, and larynx. 2 However, involvement of the extremities, genitalia, and bowel are not uncommon. 5 Unlike most hypersensitivity reactions associated with swelling, ACEi- induced angioedema is not associated with signs of anaphylaxis such as bronchospasm and urticaria, as these conditions are typically associated with mast cell degranulation and histamine release. 7
DIAGNOSIS
The diagnosis of angioedema is clinical, based primarily on the patient’s history and physical exam findings. Some of the classic clinical features that distinguish angioedema from other swelling etiologies include association with ACE inhibitor ingestion, rapidity of onset, characteristic anatomic locations of involvement, absence of common associated hypersensitivity symptoms, and an acute, self-limiting course. In patients presenting with abdominal pain, abdominal imaging using either ultrasound or computed tomography (CT) will help support diagnosis as these imaging modalities can reveal signs of abdominal fluid accumulation, including dilated bowel loops, thickened mucosal folds, mesenteric edema and ascites. While there are no laboratory evaluations that definitively detect ACEi- induced angioedema, there are laboratory tests that can help
Figure 4: Patient on the day of discharge
DISCUSSION
Epidemiology
Angioedema is a statistically uncommon adverse effect of ACEi’s; the literature suggests an incidence rate of 0.1-0.7% in all comers. 1,2,3,4 African Americans have a relative risk of 4.5 compared to Caucasians, with some literature speculating that the presentation may even be more severe in this population due to, as of yet, unknown genetic components. 3,5 However,
J La State Med Soc VOL 169 NOVEMBER/DECEMBER 2017 173
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