Ruptured abdominal aortic aneurysm with aortocaval fistula

A 90-year-old man with clinical history of infrarenal aortic aneurysm and several episodes of myocardial ischemia came with dyspnea, abdominal discomfort and postprandial vomiting. Patient claimed tachycardia. Arterial pulses in the lower extremities were present. There was no lower extremities edema. Biochemistry revealed hypotension, hypoxemia, leucocytosis and haemodynamically instability.

MDCT after IVC administration depicted a huge 74 mm transverse diameter aortic aneurysm originating below the renal arteries and extending to the proximal tract of both common iliac arteries. Aneurysm included a 39 mm thickness parietal thrombosis. A 12 mm length and 9 mm wide fistulous tract from the aortic lumen to the inferior cava vein (ICV) lumen was displayed at the level of the third lumbar vertebra.  ICV appeared slightly dilated at the liver level. Narrowing of the space between the ICV and the aortic aneurysm was also appreciated. Early detection of contrast in the ICV was observed, and both ICV and adjacent aorta were isodense. Additional findings included retroperitoneal haematoma in the left psoas muscle. Delayed enhancement of the renal cortex or femoral veins was not displayed. Patient was taken to the intensive care unit (ICU) and died 2 hours later.

Aortocaval fistula (ACF) is a life-threatening rare complication of abdominal aortic aneurysm. It’s observed in 3-4% after abdominal aneurysm rupture[1]. Physiopathology includes periaortic inflammation, adhesions to adjacent vessels and pressure necrosis of the cava vein wall. Most of the fistulizing aneurysm are atherosclerotic. Other causes include syphilis, Marfan’s syndrome, Ehlers-Danlos disease and Takayasu’s arteritis.

The classic triad for ACF consists on severe low back abdominal pain, pulsatile abdominal mass and machinery-like abdominal bruit (Braham’s sign). This triad is complete in only 50% of the patients. Increased venous return leads to venous hypertension and passive venous congestion signs. ICV compression by aortic aneurysm produces marked venous hypertension that provokes lower limb oedema, cyanosis, haematuria, venous dilatation and scrotal oedema. Renal insufficiency is due to reduced renal arterial perfusion and increased venous pressure in renal veins. Decreased peripheral resistance is another sign³.

MDCT is the initial imaging method to evaluate aortic aneurysm[2]. Findings include the early detection of the contrast medium in the dilated cava vein, which appears simultaneously isodense with the adjacent aorta; loss of normal anatomic space between the aorta and the ICV, and visualisation of abnormal communication between the two vessels. Additional findings: delayed opacification of renal cortex, delayed opacification of femoral veins and distention of ICV and renal veins. MRI can also identify ACF without contrast injection but its availability is limited in most emergency departments. Aortography is the gold standard diagnosis technique.

Surgical technique is standardized and is called endoaneurysorrhaphy[3]. The surgical outcome is influenced by the extension and duration of preoperative haemodynamic alterations, blood loss, myocardial infarction, coagulopathy and renal failure. The most common causes of death include myocardial infarction, pulmonary embolism and pneumonia. Mortality rate is about 30%. Diagnosis of ACF is difficult because the classic triad may be absent in up to 50% of the cases. Nonetheless, quick diagnosis is of prime importance because prompt treatment is critical and contributes to decreased mortality.

Aortocaval fistula (ACF) is a life-threatening rare complication of abdominal aortic aneurysm. As clinical signs and symptoms may not be always present, clinical suspicion and imaging are essential for the diagnosis. MDCT is the initial imaging method. Aortography is the gold standard imaging technique. Findings include early detection of contrast in the ICV and abnormal communication between ICV and aortic lumen. Surgical technique is endoaneurysorrhaphy. Prognosis depends on prompt diagnosis. Mortality rate is around 30%