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Therapies used for hereditary angioedema (HAE) have been associated with adverse events to include thrombosis, emboli, hepatocellular carcinoma (HCC), exacerbation of attacks, and anaphylaxis. It is difficult to determine incidence of these adverse events from the literature. For this reason we surveyed multiple HAE physicians to determine the risk associated with therapies used in HAE. This study was designed to determine by survey the risk of thrombosis associated with C1-inhibitor (C1-INH), worsening attacks with fresh frozen plasma (FFP), and carcinoma secondary to androgens (mainly danazol). An Internet-based survey was sent to physicians internationally who treat patients with HAE. The survey queried physicians about their observations while treating HAE. Of the 66 physicians who participated in the survey, 37 had patients (856 patients) who were on C1-INH but only 4 (total of 5 patients) had patients on C1-INH who experienced an thromboembolic episode. Of the 17 patients on C1 esterase inhibitor and an indwelling catheter, 3 experienced an embolic, thrombosis, or thromboembolic event. The likelihood of an abnormal event when a patient is on a C1-INH is 5/856 (0.6%), compared with 3/17 (18%) with a central catheter. The incidence of HCC is rare. The incidence of adverse effects to FFP is greater than the literature suggests. Patients with HAE should avoid indwelling catheters, use FFP only when other therapies are unavailable, and use androgens with caution. Most importantly, adverse events to drugs should be reported so that the true incidence of adverse events can be determined.

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These data provide useful information to guide the surgeon in avoiding middle vault collapse postoperatively and when evaluating those patients with presurgical middle vault concerns. With less ability to support the upper lateral cartilages, short nasal bones can predispose an individual to middle vault collapse postoperatively.

Background Various theories exist to explain the etiology of iatrogenic symmastia. Subglandular over-dissection of the medial breast pocket over the sternum, disruption of midline sternal fascia, oversized implant base diameter, and over-dissection of the medial pectoralis muscle attachments to the sternum are popular explanations. Objectives The authors hypothesized that the most common risk factor for iatrogenic symmastia is subpectoral breast augmentation. Methods A retrospective chart review was conducted including all symmastia patients who underwent surgery from January 2008 to April 2018 by a single surgeon (C.L.M.). ASAPS members were also surveyed regarding the etiology and incidence of symmastia in their practice. Results Twenty-three patients with symmastia were included in the retrospective chart review. All had previous subpectoral breast augmentation. In the ASAPS survey, 91 plastic surgeons reported seeing an average of 2.2 consults for acquired symmastia over the preceding year; 1.9 of the 2.2 (84.9%) acquired symmastia consults previously underwent subpectoral breast augmentation. Most surgeons attributed these patients’ symmastia to over-dissection of the medial pectoralis muscle attachments to the sternum. Conclusions Symmastia is most often caused by pectoralis major sternal dehiscence during subpectoral breast augmentation. In the senior author’s experience, all patients with iatrogenic symmastia previously had a submuscular breast augmentation. The ASAPS survey supports multiple causes for symmastia with retromuscular breast augmentation occurring in the majority of patients. Repair of symmastia should include securing Scarpa’s fascia to the sternum, reattaching the pectoralis major to the sternum, avoiding another subpectoral implant, and using postoperative modalities to protect the repair. Level of Evidence: 4