Lisinopril-Induced Small Bowel Angioedema: An Unusual Cause of Severe Abdominal Pain.

BACKGROUND Angiotensin-converting enzyme inhibitors (ACE-I) are one of the most frequently prescribed classes of medications with the rare adverse effect of angioedema, and isolated small bowel angioedema is a small subset of these cases. Isolated angioedema of the small bowel is a rare adverse effect of this commonly prescribed medication, and it mimics, symptomatically and radiographically, several other illnesses and is often misdiagnosed. While ACE-I are thought to be safe, the risk of angioedema is approximately 0.7%. Isolated small bowel angioedema is often not diagnosed in a timely manner, and misdiagnosis leads to significant morbidity in afflicted patients. CASE REPORT We present the case of a 63-year-old woman with angioedema of the small bowel causing abdominal pain, nausea, vomiting, and diarrhea. Computed tomography demonstrated small bowel edema and ascites. The patient had been taking lisinopril for 7 years prior to presentation and had previously been seen by multiple physicians for abdominal pain. A diagnosis of ACE-I-induced small bowel angioedema was made and lisinopril therapy was immediately stopped. Her symptoms improved with cessation of lisinopril, and follow-up imaging showed resolution of the angioedema 3 months later. CONCLUSIONS The course of ACE-I-induced angioedema is unpredictable and often overlooked as a cause of abdominal pain. It commonly presents soon after starting ACE-I therapy, but can present years after therapy initiation, as in this case. Significant morbidity, including unnecessary exploratory laparotomy, is associated with misdiagnosis of ACE-I-induced angioedema of the small bowel. Prompt recognition and cessation of the offending drug is crucial but often delayed.

Mechanical Effects of Lag Screw Retightening in a Simulated Hindfoot Arthrodesis Model.

BACKGROUND: Nonunion following hindfoot arthrodesis may be caused by failure to maintain compression at the arthrodesis site. The ability of lag screws, commonly used in arthrodesis, to maintain compression in hindfoot bones has not been well characterized. The aim of this work was to quantify the stress relaxation response of hindfoot bone with initial and repeated compression with a lag screw. METHODS: Ten sets of 25-mm-diameter bone cylinders were cut from the talus and calcaneus in fresh-thawed cadaveric feet. A load cell was compressed between cylinders with an 8.0-mm partially threaded cannulated lag screw simulating arthrodesis. For 7 sets, screws were tightened by 3 quarter-turns, rested for 3 minutes, retightened 1 quarter-turn, and rested for 30 minutes. Three sets served as controls in which screws were not retightened. RESULTS: Maximum compression after initial screw tightening and retightening averaged 275 and 337 N (P = .07), respectively. Compression 3 minutes after initial screw tightening and retightening averaged 199 and 278 N (P = .027), respectively. The compression recorded 3 minutes after screw retightening was an average of 40% higher than that recorded 3 minutes after initial tightening. The average compression 30 minutes after screw retightening was 255 N, a compression loss of 25% from the average maximum compression after retightening. Eighty percent of this compression loss happened in an average of 5.5 minutes. CONCLUSION: Hindfoot bones exhibit compression loss over time during simulated arthrodesis. Compression maintenance in bone is improved with screw retightening. Further work is needed to understand the mechanism of action and determine optimum time for recompression. CLINICAL RELEVANCE: Retightening lag screws before wound closure may improve compression at the arthrodesis site and thereby decrease the chance of nonunion. LEVEL OF EVIDENCE: N/A, laboratory experiment.