CARDIOVASCULAR JOURNAL OF AFRICA • Volume 34, No 1, January–April 2023 AFRICA 61 tests, the leukocyte count was15.950 cells/mm3, neutrophil count was 12.990 cells/mm3 (82%), CRP was 236.76 mg/dl and the ESR was 65 mm/h. Other biochemical values w ere normal. Blood, sputum and urine cultures were obtained from the patient for the focus of infection. Empirical broad-spectrum antibiotics were started. Since Salmonella enterica grew on the blood cultures of the patient, IV piperacillin/tazobactam + ciprofloxacin 4.5 g four times a day was started. He described severe abdominal pain and sudden-onset pain in the right leg during his follow up. On physical examination, the pulses of the right lower extremity were non-palpable. In repeat CTA, it was observed that the abdominal aortic aneurysm had progressed to 90 mm at its widest point. Signs of peri-aortic inflammation and blurred edges of the aortic wall suggested that the aneurysm was of mycotic origin (Fig. 4). Emergency surgery was decided due to the rapid enlargement of the mycotic abdominal aortic aneurysm and extremity ischaemia, but endovascular repair (EVAR) was performed due to the patient’s multiple co-morbidities. APR values regressed to normal values on the eighth postoperative day, and IV antibiotic treatment was completed in eight weeks. The patient was discharged with ciprofloxacin 2 × 500 mg/day/1 week and ASA. A patent EVAR graft with no signs of infection or periaortic accumulation was seen in the control CTA during the first month (Fig. 5). Blood culture samples of both patients were collected in BACT/ALERT FA Plus blood culture bottles and incubated in BACT/ALERT 3D 120 Combo system. Bacterial identification was done with MALDI TOF-MS (Biomerieux, France). Antibiotic susceptibility testing was done with VITEC 2 (Biomerieux, France) as a routine procedure in our institution. Discussion The first step of the aetiopathogenesis of mycotic aneurysms is micro-organism invasion into the aortic wall. Causes include septic embolism, bacterial invasion secondary to a traumatic injury, invasion from adjacent infected tissues or vegetation onto a pre-existing aneurysm or an atherosclerotic plaque. Other predisposing factors include intravascular drug use, immunosuppression due to medications or malignancies, and iatrogenic causes such as catheterisation of the vessels for diagnostic or therapeutic purposes.9-14 The incidence of non-typhoidal Salmonella infection has been increasing worldwide recently. These bacteria are usually food-borne pathogens that cause gastroenteritis, bacteraemia and focal infections.15 Advanced age, diabetes, changes in endogenous intestinal flora, cancer, human immunodeficiency virus infection, auto-immune disorders and immunosuppression are the main risk factors for non-typhoid Salmonella infections and bacteraemia.16 One of themost important extra-intestinal system involvement sites of infection is the endovascular system, and endovascular Salmonella infections in the abdominal aorta usually advance into mycotic abdominal aortic aneurysms.8 As the walls of the aorta degenerate, secondary to a local infection, an aneurysm forms or expands if present, leading to rupture and death if not managed acutely. In both of our patients, there was no sign of an overt or an occult source of infection. The patients did not have any echocardiographic evidence of cardiac vegetations that could cause a septic embolism. The patients had no history of trauma, intravenous drug abuse, immunosuppression or malignancy. Fig. 4. Abdominal aneurysm increasing from 51 to 63 mm one week after admission. Fig. 5. CT angiography in the first month after discharge, showing a patent EVAR graft.
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