Splenic artery aneurysms occurring in liver transplant recipients.

Splenic artery aneurysms (SAA)* are found in 0.1% of the cases in large autopsy series (1) and in 0.8% of un selected abdominal aortograms (2). The incidence of SAA is higher in patients with portal hypertension, in whom it is reported to occur in 8.8% to 50% of cases (3, 4). Rupture of SAA carries a high mortality rate. Rupture of SAA in liver transplant recipients has been reported (4,5). To assess the importance of this complication in the liver transplant population, we reviewed the medical records of all liver recipients whose 1311 transplants were performed at the Presbyterian University Hospital from January 1, 1988 until July 1, 1990. Of 5 patients with ruptured SAA, 4 died. An additional patient was recognized to have a SAA following his second orthotopic liver transplantation and this was removed electively by splenectomy and distal pancreatectomy. Summaries of these 6 cases are in Table 1. SAAs are the most common visceral arterial aneurysms and account for 60% of all aneurysms found within the splanchnic arterial bed (2). The pathogenesis of SAA is multifactorial, and Stanley et al. (2) have recognized 4 conditions that place patients at high risk: (1) arterial dysplasia, (2) portal hypertension, (3) focal arterial inflammatory processes, and (4) multiparity in women. Anatomically, about 70% of the SAAs in patients with cirrhosis and portal hypertension are located in the distal third of the artery, and half of the aneurysms are multiple (2, 3). In our series, 4 of the 5 liver transplant patients had aneurysms greater than 2 cm in diameter, and one had multiple aneurysms. Multiple factors could contribute to the higher incidence and larger size of SAAs in patients with chronic liver disease and portal hypertension. These include: increased splenic and overall splanchnic blood flow secondary to arteriovenous shunts and collateral formation; dilatation and elongation of the splenic artery (6, 7); increased cardiac output and splanchnic vasodilatation from hyperglucagonemia (8); and vascular changes caused by other hormone changes, such as those which "feminize" male cirrhotic patients (9). Whatever the explanation, the impact of SAA in liver transplantation needs emphasis. In a recent study at the Mayo Clinic (4),60 patients with portal hypertension who were being considered for OLT were submitted to routine preoperative celiac angiography, and 5 (8.3%) were found to have SAA 8 to 25 mm in diameter. A sixth patient in this series developed a SAA 3 months postoperatively. The size at which an asymptomatic SAA should arouse alarm has been reported to be 15 mm (4, 5). There have been no reported ruptures of smaller SAAs in liver transplant recipients. Whatever the size, most SAAs are asymptomatic, as in 4 of our 5 patients. Pain in the mid upper