A 59–year–old male presented with abdominal pain for 5 days. His past medical history was significant for hypertension, dyslipidemia and a stable 5 cm abdominal aortic aneurysm (AAA) detected 4 years ago. The pain was located in left lower quadrant associated with fever. His vital signs were T 103.0 °F, BP 102/59 mmHg, HR 98 beats/min, RR 18 breaths/min, and SpO2 98% on room air. His abdomen revealed a pulsatile mass without tenderness or bruit. No guarding was observed. Laboratory studies disclosed WBC 10200 /mL with 83% neutrophils, HGB 9.4 g/dL, PLT 455 K/mL, and his chemistry panel was unremarkable. His blood cultures yielded Escherichia coli (E. coli). A CT scan of the abdomen showed multiple diverticuli with associated bowel wall thickening. There is no evidence of progressive aortic dilatation. His fever and abdominal pain persisted after the initiation of antibiotics. 2 weeks later, he developed worsening abdominal pain. A repeat abdominal CT revealed ruptured AAA with periaortic hematoma and emergent AAA repair was performed. He received a prolonged course of antibiotics post operatively.
Infected AAA is a rare but life–threatening condition. It is caused by a primary infection or a secondary infection of an already established aneurysm. Atherosclerotic aorta is especially susceptible to infection. Prevalence of primary microbial aortitis is reported to be 0.06% to 0.65%. Many pathogens can cause infected aortitis, with Salmonella species and Staphylococcus aureus being the predominant organisms. Early diagnosis and surgical intervention is essential for survival. However, diagnosis is often delayed due to non specific presentations. For example, in a series of infected aortitis due to Salmonella, the incidence of fever, abdominal pain, and a palpable pulsatile mass was 79%, 42%, and 42%, respectively. A CT of the abdomen can help confirm the diagnosis, which typically shows thickening of aortic wall, or progressive aortic dilatation. In our case, the initial CT of the abdomen only showed a stable AAA without obvious signs of infection, and the second CT revealed dilatation of the aorta as well as ruptured AAA. In retrospect, persistent fever and abdominal pain of our patient was suggestive of infected AAA. When a patient has a preexisting arteriosclerotic aneurysm and E. coli bacteremia, it should be kept in mind that an infected aortic aneurysm is highly possible.
Infected AAA due to E. coli is a rare condition with high morbidity and mortality. Early diagnosis and surgical intervention is paramount. Nevertheless, endovascular infection due to E. coli can pose a significant diagnostic challenge owing to its rarity and non–specific presentations. When a patient has a preexisting arteriosclerotic disease or aneurysm and develops persistent E. coli bacteremia, infected aortic aneurysm should be included as a differential diagnosis.