Aortitis is the all-encompassing term ascribed to the inflammatory process in the aortic wall that can be either infective or noninfective in origin, commonly autoimmune or inflammatory large-vessel vasculitis.1 Infectious aortitis, also known as bacterial, microbial, or cryptogenic aortitis, as well as mycotic or infected aneurysm, is a rare entity in the current antibiotic era but potentially a life-threatening disorder.2 The potential complications of infectious aortitis include emphysematous aortitis (EA), pseudoaneurysm, aortic rupture, septic emboli, and fistula formation (eg, aorto-enteric fistula).2,3
EA is a rare but serious inflammatory condition of the aorta with a nonspecific clinical presentation associated with high morbidity and mortality.2-6 The condition is characterized by a localized collection of gas and purulent exudate at the aortic wall.1,3 A few cases of EA have previously been reported; however, no known cases have been reported in the literature due to Klebsiella pneumoniae (K pneumoniae).
The pathophysiology of EA is the presence of underlying damage to the arterial wall caused by a hematogenously inoculated gas-producing organism.2,3 Most reported cases of EA are due to endovascular graft complications. Under normal circumstances, the aortic intima is highly resistant to infectious pathogens; however, certain risk factors, such as diabetes mellitus (DM), atherosclerotic disease, preexisting aneurysm, cystic medial necrosis, vascular malformation, presence of medical devices, surgery, or impaired immunity can alter the integrity of the aortic intimal layer and predispose the aortic intima to infection.1,4-7 Bacteria are the most common causative organisms that can infect the aorta, especially Staphylococcus, Enterococcus, Streptococcus, Salmonella, and spirochete Treponema pallidum (syphilis).1,2,4,8 The site of the primary infection remains unclear in some patients.2,3,5,6 Infection of the aorta can arise by several mechanisms: direct extension of a local infection to an existing intimal injury or atherosclerotic plaque (the most common mechanism), septic embolism from endocarditis, direct bacterial inoculation from traumatic contamination, contiguous infection extending to the aorta wall, or a distant source of bacteremia.2,3
Clinical manifestations of EA depend on the site and the extent of infection. The diagnosis should be considered in patients with atherosclerosis, fever, abdominal pain, and leukocytosis.2,4-8 The differential diagnosis for EA includes (1) noninfective causes of aortitis, including rheumatoid arthritis and systemic lupus erythematosus; (2) tuberculous aortitis; (3) syphilitic aortitis; and (4) idiopathic isolated aortitis. Establishing an early diagnosis of infectious aortitis is extremely important because this condition is associated with a high rate of morbidity and mortality secondary to aortic rupture.2-7
Imaging is critical for a reliable and quick diagnosis of acute aortic pathology. Noninvasive cross-sectional imaging modalities, such as contrast-enhanced computed tomography (CT), magnetic resonance imaging, nuclear medicine, or positron emission tomography, are used for both the initial diagnosis and follow-up of aortitis.1 CT is the primary imaging method in most medical centers because it is widely available with short acquisition time in critically ill patients.3 CT allows rapid detection of abnormalities in wall thickness, diameter, and density, and enhancement of periaortic structures, enabling reliable exclusion of other aortic pathologies that may resemble acute aortitis. Also, CT aids in planning the optimal therapeutic approach.1,3,5-8
This case illustrates EA associated with infection by K pneumoniae in a patient with poorly controlled type 2 DM (T2DM). In this single case, our patient presented to the Bay Pines Veterans Affairs Healthcare System (BPVAHS) in Florida with recent superficial soft tissue injury, severe hyperglycemia, worsening abdominal pain, and leukocytosis without fever or chills. The correct diagnosis of EA was confirmed by characteristic CT findings.
Case Presentation
A 72-year-old male with a history of T2DM, hypertension, atherosclerotic vascular disease, obstructive lung disease, and smoking 1.5 packs per day for 40 years presented with diabetic ketoacidosis, a urinary tract infection, and abdominal pain of 1-week duration that started to worsen the morning he arrived at the BPVAHS emergency department. He reported no nausea, vomiting, diarrhea, constipation, chest pain, shortness of breath, fever, chills, fatigue, or dysuria. He had a nonhealing laceration on his left medial foot that occurred 18 days before admission and was treated at an outside hospital.
The patient’s surgical history included a left common femoral endarterectomy and a left femoral popliteal above-knee reverse saphenous vein bypass 4 years ago for severe critical limb ischemia due to occlusion of his left superficial femoral artery with distal embolization to the first and fifth toes. About 6 months later, he developed disabling claudication in his left lower extremity due to distal popliteal artery occlusion and had another bypass surgery to the below-knee popliteal artery with a reverse saphenous vein graft harvested from the right thigh.