The visceral arteries comprise the coeliac, superior mesenteric, inferior mesenteric, and renal arteries together with all their branches. Aneurysms of these vessels are uncommon and in order of frequency rank below aneurysms of the abdominal and thoracic aorta, and those of the iliac, femoral, and popliteal arteries.

In common with other arterial aneurysms the majority are asymptomatic and since no easy non-invasive investigation can reliably detect their presence their true prevalence in the community is unknown. Any epidemiological data that exist are certainly suspect since they are obtained either from highly selected groups of patients undergoing angiography or computerized tomographic scanning or from autopsy studies in which small visceral aneurysms could easily be overlooked. No single vascular surgical unit has sufficient overall experience of visceral arterial aneurysms to allow useful analysis of the relative importance of different aetiologies or the indications for and results of various management options. Most accounts in the literature still comprise single case reports, small series, or larger analyses comprising collections of such cases from literature reviews. Any overview which attempts to give a didactic account of aetiology, presentation, and management of visceral artery aneurysms is therefore handicapped by the absence of a sound database and this fact should be borne in mind.

In common with aneurysms of the aorta, the aetiology in the majority of cases is unknown, but the proximate cause is local failure of the connective tissue of the arterial wall to maintain the integrity of the vessel. Most patients are middle aged and, inevitably, atherosclerosis has been implicated, but in contradistinction to abdominal aortic aneurysms, a high proportion of cases occur in young people in their 30s and the majority of patients are women.

The single most interesting fact about this disease is that in developed countries ruptured visceral arterial aneurysm is now one of the major causes of maternal mortality. Between 1967 and 1982 there were 14 maternal deaths from this cause (10 splenic, three renal, and one hepatic artery aneurysm) in England and Wales, with most ruptures occurring in the last weeks of pregnancy. Similar observations in the United States have given rise to speculation by a number of authors that systemic and portal hypertension, increased cardiac output, and increased blood flow in some vessels, together with the hormonal and connective tissue changes in pregnancy may all be contributory factors.

A number of other aetiologies have been implicated with differing importance in various reports, including congenital malformations, trauma, arteritis, connective tissue disorders, and infection. Trauma, either accidental or iatrogenic during percutaneous biopsy, plays a major role in the causation of aneurysms within the liver or kidney but, fortunately, the majority are small and of no clinical significance (Fig. 1) 281. Of the arteritides, Takayasu's disease is particularly important and can give rise to visceral aneurysm, with or without associated occlusive arterial disease.

In the past mycotic aneurysms were usually a consequence of bacterial endocarditis but more recently intravenous drug abuse and cardiac catheterization have contributed an increasing proportion of cases.

Splenic aneurysms (Fig. 2) 282 account for around two-thirds of all ruptured visceral artery aneurysms, with most of the remainder being ruptured renal, hepatic (Fig. 3) 283, gastric, or superior mesenteric artery aneurysms (Fig. 4) 284. Aneurysms of the inferior mesenteric artery are extremely rare, as are gastroduodenal and pancreaticoduodenal artery aneurysms.

Most visceral artery aneurysms are asymptomatic or give rise to vague abdominal discomfort perhaps related to compression or stretching of adjacent nerves by aneurysm expansion. Occasionally hepatic, gastroduodenal, or pancreaticoduodenal aneurysms may produce bile duct compression and jaundice while splenic aneurysms may be associated with pancreatitis. Mesenteric aneurysms may produce gut ischaemia by releasing emboli from mural thrombus within the aneurysm. Apart from rupture, renal artery aneurysms are those most likely to give rise to major symptoms due to either hypertension or renal failure. This impression could well be flawed, however, since patients with hypertension or renal failure are more likely to undergo angiography and some aneurysms discovered will be incidental and insignificant findings.

The most dramatic symptoms occur when an aneurysm ruptures. Initially the rupture may be partially contained either by the adjacent connective tissue or, in the case of splenic, gastric, and hepatic artery aneurysms, within the lesser sac. In such circumstances the main symptoms are abdominal pain and a variable amount of circulatory collapse, depending on the volume of blood lost. Sooner or later the connective tissues which have partially contained the bleeding will give way with free rupture into the peritoneal cavity, and profound circulatory collapse.

Unusual presentations occur when a visceral aneurysm erodes into an adjacent structure, for example the hepatic artery into the common bile duct or a gastric, gastroduodenal, or pancreaticoduodenal artery into the foregut. The resultant haemobilia, haematemesis, and melaena are likely to be attributed preoperatively to other more common causes of upper gastrointestinal haemorrhage and even at operation the correct diagnosis may not be obvious.

The mainstay of precise anatomical diagnosis remains angiography with selective catheterization of the appropriate visceral artery. Angiograms will also display collateral circulation and allow planning of any operative procedure which may be necessary. Incidental diagnoses of visceral aneurysms will be made from abdominal radiographs if the aneurysm wall is calcified or from abdominal computerized tomograms. Computerized tomography may also give useful anatomical information or may be diagnostic in cases where a visceral aneurysm is suspected or presents as an abdominal mass.

The diagnosis of a ruptured visceral aneurysm is based on the clinical signs of circulatory collapse from blood loss together with evidence of intra-abdominal bleeding. The patient's condition will usually not permit time to be spent on confirming the diagnosis preoperatively, since emergency laparotomy to control the haemorrhage is mandatory.

Management decisions are clear-cut and uncontroversial when a visceral artery aneurysm has ruptured: emergency surgery is life-saving. There is considerable uncertainty about management of an intact aneurysm, particularly when it is asymptomatic, since not enough is known of the natural history of the disease for an informed recommendation to be made. When the aneurysm is very large or causes symptoms and is in an anatomical location which allows safe surgical exclusion, resection or arterial bypass to be performed, then surgery will usually be the sensible choice. An aneurysm discovered in early pregnancy or in a woman who plans to have children is also usually best treated by operation because of the risk of rupture during pregnancy.

The greatest uncertainty is caused by a small asymptomatic visceral artery aneurysm in an anatomical location where surgery is potentially difficult or dangerous. Many such aneurysms are best managed conservatively with regular monitoring of their size and the patient's condition. Others will lend themselves to treatment by interventional radiographic techniques, the scope of which continues to expand. Provided the aneurysmal artery can be cannulated the aneurysm can usually be satisfactorily occluded by the insertion of metal coils or inflatable detachable balloons.

Mycotic aneurysms of visceral arteries have the same sinister prognosis as they do elsewhere with a tendency to rapid enlargement and rupture. For this reason elective surgery is best undertaken as early as possible in conjunction with systemic antibiotic therapy to treat the underlying infection.

King TA, McDaniel MD, Flinn WR, Yao JST, Bergan JJ. Visceral artery aneurysms. In: Moore WS, ed. Vascular surgery; a comprehensive review. New York: Grune and Stratton 1983: 351–65.

Skudder PA. Visceral artery aneurysms. In: Persson AV, Skudder PA, eds. Vascular Surgery. New York: Marcel Dekker, 1987: 145–73.