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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 or left upper quadrant of the abdomen is an ominous portent of imminent or contained rupture (2, 10, 11).
The question of critical size of SAA in liver transplant candidates or recipients should be left open until there is more information. The incidence of rupture of documented SAA in nontransplant patients is 3% to 10% (2), but extra risk factors in liver recipients could include the higher rupture rate following any intraabdominal operation (12), abrupt changes in celiac trunk blood flow caused by OLT (6, 7), the addition of postoperative corticosteroids, inadvertent trauma to the aneurysm intraoperatively, opening of the retroperitoneal space, and the coagulopathy that often is a feature of perioperative recovery.
Only one previously reported patient has survived a post-transplant SAA rupture (4), and in our series, the mortality rate following rupture was 80%. Improvement will require identification of the pathology during pretransplantation workup. MRI is the most discriminating procedure, and we recommend it routinely. Doppler ultrasound of the splenic artery is less discriminating, and angiography is too dangerous in many patients with end-stage liver disease. With MRI, other essential information about liver size, portal vein patency, and the structure and flow patterns of the visceral arterial supply are obtained at the same time (13).
Operative management should include ligation of the splenic artery distal and proximal to the aneurysm and resection if feasible (5). Proximal splenic artery ligation alone is apt to be ineffective because of rich collateral arterial supply. A delayed operation may be indicated if multiple or large distal SAAs are found that can not be ligated without splenectomy at the time of orthotopic liver transplantation. Although there may be a role for splenic artery embolization before or after transplantation, we have not had personal experience. Splenic infarction and the formation of a splenic abscess is a potential complication of either splenic artery ligation without splenectomy or of embolization.
1This work was supported by research grants from the Veterans Administration and by project grant No. DK 29961 from the National Institutes of Health, Bethesda, Maryland.
*Abbreviation: SAA, splenic artery aneurysm.