British Journal of Obstetrics and Gynaecology July 1992, Vol. 99, pp. 595-597
CLINICAL PRACTICE
Ruptured splenic artery aneurysm in pregnancy. A review R. J . HOLDSWORTH Surgical Registrar A. GUNN Consultant Surgeon Department of Surgery Ninewells Hospital and Medical School Dundee DD1 9SY, UK
Rupture of any arterial aneurysm is a rare event in young women. Half of all arterial aneurysm ruptures in women of child bearing age occur during pregnancy (Barret et al. 1982) and this diagnosis should always be considered in any pregnant patient who has unexplained hypotension and abdominal pain. The splenic artery is the third most common site of intraabdominal aneurysm formation after the abdominal aorta and the iliac vessels. Splenic artery aneurysms are unusual because they occur more frequently in women and they are seen at a relatively younger age than aneurysms of the great vessels. They are associated with increasing parity and have a particular tendency to rupture in pregnancy. Rupture of these aneurysms carries a high maternal and fetal mortality and only with prompt treatment can this high mortality be reduced.
Historical background A splenic artery aneurysm was first described in 1776 by Beussier (Lie et al. 1990) and rupture in pregnancy in 1869 by Corson (Ho 1977). In 1889 President Garfield died from a ruptured splenic artery aneurysm which was traumatic in origin following a bullet wound (Moore & Lewis 1961). An aneurysm was first described in a living person in 1903 by Winkler when several small dilatations of the splenic artery were found at operation (Lie et al. 1990). In 1920, the first pre-operative diagnosis was made by Hoegler who heard a murmur over a pulsatile mass investigated by fluoroscopy and, in 1930, the phenomenon of a double rupture was described by Brockman (Lie et al. 1990). In 1932, the first pre-operative diagnosis followed by a successful operation was made by Lindboe (Lie et al. 1990). The first maternal survivor following rupture in pregnancy was not described until 1940 by MacLeod and the first report of both fetal and maternal survival was in 1967 (Vassalotti & Schaller 1967).
Incidence and occurrence The overall prevalence of splenic artery aneurysms is Correspondence: Mr R. J. Holdsworth, M.D., F.R.C.S.
unknown. They are found in approximately 0.07% of routine post-mortems; however, the incidence at post-mortem in those over 60 years of age is as high as 10.4%. Overall 79% of splenic artery aneurysms occur in people over 50 years of age. A high prevalence has been reported in some angiographic series ranging from 0.78-7.1%, but these are in selected patients with known arteriopathic disease (Moore & Lewis 1961; Stanley & Fry 1974; De Vries et al. 1982; Trastek et al. 1985; Williams 1988). In contrast to aneurysms of the great vessels, which are more frequent in men, splenic artery aneurysms are 2-5 times more common in women and tend to occur at a younger age (Stanley & Fry 1974; Lie et al. 1990; Trastek et al. 1985; Williams 1988). The two principal factors that are of importance in the development of these aneurysms are grandmultiparity and portal hypertension. About 25% of women with a splenic artery aneurysm have been pregnant more than six times. In one report 87% of the aneurysms were found in women and 92% of them had had between 1 and 16 pregnancies, the mean number of pregnancies being 4.5 (Trastek et al. 1982). Aneurysms have also been described in the first pregnancy although this is unusual (Trastek et al. 1985; Williams 1988). Up to 24% of splenic artery aneurysms are found in patients with portal hypertension (De Vries et al. 1982; Pomerantz et al. 1986; Lowry et al. 1986) and the incidence is said to be 7. I % in cirrhotics (Stanley & Fry 1974). Aneurysms have been found in 8.4% of patients having routine coeliac angiography prior to liver transplantation (Ayalon et al. 1988).
Complications Over 80% of splenic artery aneurysms are asymptomatic and are discovered incidentally at angiography, laparotomy or post-mortem (Trastek et al. 1985). The principal complication of a splenic artery aneurysm is rupture. This can lead to either a sudden onset of hypovolaemic shock if rupture is into the peritoneal cavity or it may lead to a more insidious anaemia associated with rupture into the gastrointestinal tract. Rupture into the stomach, small bowel, colon and pancreatic duct have all been reported and gastro-intestinal bleeding is a presentation in one third of cases (Lie et al. 1990; Bishop 1984; De Vries et al. 1982). Overall, rupture of a splenic artery aneurysm is an uncommon event and is reported in 2-9% of cases. However, between 20% and 50% of ruptures occur in pregnancy and another 20% occur in patients with portal hypertension (Stanley & Fry 1974; Barrett et al. 1982; De Vries et al. 1982; Trastek et al. 1985). Rupture is said to be unlikely in aneurysms smaller than
595
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R . J. HOLDSWORTH & A . G U N N
2.5 cm although it has been reported in lesions of 1-2 cm in size (Trastek et al. 1985; De Vries et al. 1982; Salo et al. 1986). The mortality from rupture was historically very high but this has been reduced due to advances in surgery and resuscitation. The mortality from rupture is now approximately 10% rising to 25% when there is free rupture into the peritoneum. (Trastek et al. 1985; Mehrota et al. 1983; De Vries et al. 1982; Bishop 1984).
Rupture in pregnancy Up to one half of all ruptured splenic artery aneurysms occur in pregnancy; 69% rupture in the third trimester, 12% in the first two trimesters, 13% in labour and 6% in the puerperium (Barrett et al. 1982).Although gastrointestinal bleeding is a presentation in one third of all ruptures, this is never a feature of rupture in pregnancy which is always into the peritoneal cavity (Lowry et al. 1986; Walker et al. 1988). The maternal mortality from rupture in pregnancy is 7 1% and fetal mortality is as high as 95% (Trastek et al. 1985; Mehrota et al. 1983; De Vries et al. 1982; Bishop 1984). Only nine instances of both maternal and fetal survival have been reported (Vassalotti & Schaller 1967; Mehrota et al. 1983; Lowry et al. 1986; Donovitz e al. 1986; Salo et al. 1986).
Clinical features Splenic artery aneurysms usually remain undetected unless they rupture (Lie et al. 1990). Large aneurysms may give rise to pain (Jones & Finney 1968) and in one series, chronic nonspecific abdominal pain, usually in the left hypochondrium, occurred in 13% and bruits were audible in 11% (Trastek et al. 1982). When aneurysms rupture there is a sudden onset of severe abdominal pain associated with hypotension. The pain is usually felt in the epigastrium, penetrating to the back, or radiating to the shoulder tip (Moore & Lewis 1961). The pain is often associated with nausea and vomiting. If the aneurysm has ruptured into the gastrointestinal tract both haematemesis and melaena may occur. Occasionally aneurysms can give rise to a chronic iron-deficiency anaemia (Lie et al. 1990). Tenderness in the upper abdomen is often the only clinical sign. This can vary in severity from mild tenderness with guarding, to a picture of generalized peritonitis. There can be a palpable abdominal mass but this may be confused with the spleen in patients with portal hypertension. In pregnant women the tenderness can be diffuse or maximal over the fundus of the uterus (Williams 1988). The phenomenon of a ‘double rupture’ is reported in 20% of patients. The patient presents with a sudden onset of abdominal pain and hypotension which recovers rapidly with simple fluid replacement. There is then a latent period followed by a sudden cardiovascular collapse, usually within 48 h. This picture results from a small premonitory bleed into the lesser sac which becomes contained and is followed by free rupture into the peritoneum (De Vries et al. 1982; Lie et al. 1990; Lowry et al. 1986).
Pathological features Aneurysms have been described from 1 to 30 cm in diameter
but they are usually 2-3 cm in size; 78% are located in the distal one third of the vessel and are saccular in nature (Trastek et al. 1985). The aetiology of these aneurysms remains uncertain. Although arterio-sclerosis is reported in 95% of lesions and calcification in 70%, these are believed to be secondary changes resulting from increased turbulance rather than the primary causative factors Fibromuscular arterial dysplasia is described in 4-30% of patients. Mycotic aneurysms of the splenic artery are very rare and only account for 2% of all mycotic aneurysms (Moore & Lewis 1961; Stanley & Fry 1974; De Vries et al. 1982; Trastek et al. 1985).
Pathogenesis of splenic artery aneurysms An increased splanchnic blood flow is seen in both portalhypertension and pregnancy and the increased splenic artery blood flow is probably the principal factor in the development of aneurysms at this site. In portal hypertension, an increased portal inflow pressure is required to maintain portal perfusion. This is achieved by an increased splanchnic arterial flow through both the splenic and superior mesenteric arteries (Sato et al. 1987; Nishida et al. 1986). Physiological changes induced by pregnancy include an increased blood volume and cardiac output, relative portal congestion and systemic hypertension. Ohlson (1978) also demonstrated that the pregnant uterus causes significant occlusion of the aorta and the iliac vessels during the third trimester which results in an increased blood flow through arteries more proximal to the site of compression including the splanchnic vessels. It is believed that the combined effects of increased flow and altered arterial structure places a greater stress on the vessel. Individuals who have underlying arterial disease are more suspectable to these stresses leading to aneurysm formation. In pregnancy, hormonal changes can affect the structure of the arterial wall leading to disruption of the internal elastic lamina and failure of elastin formation (Trastek et al. 1985; Barrett et al. 1982). The splenic artery is probably progressively weakened by successive pregnancies leading to an increased frequency of these aneurysms as parity rises.
Management The natural history of splenic artery aneurysms is poorly understood. Moore & Lewis (1961) who monitored 14 aneurysms, found that none ruptured, but these were all arteriosclerotic aneurysms and none of the patients was pregnant. In the series described by Trastek et al. (1982) only one of the 34 aneurysms that were treated conservatively ruptured, this was a 7 cm aneurysm and the patient had declined elective surgery. Once an aneurysm is suspected, most authors recommend the use of arteriography to confirm the diagnosis. This has the advantage of both localizing the lesion and of identifying whether multiple dilatations are present within the splenic or other splanchnic arteries. Treatment in the emergency situation has usually been by splenectomy. Although splenectomy can be avoided by ligation of the aneurysm it may still be necessary for those lesions that occur close to the splenic hilum (Taylor & Woodward
SPLENIC ARTERY ANEURYSM
1987). In elective cases, the majority are still treated by surgery although some success has been reported with embolization and this is now suggested as the treatment of choice in low risk groups (Baker et al. 1987; Reidy et (11.1990). The principal indications for surgical intervention are symptomatic aneurysms; aneurysms in pregnant women or women of child-bearing age; lesions in any age group that are greater than 2 cm in size or ones that show a progressive increase in diameter (Trastek et al. 1985).
Implications for the obstetrician Rupture of a splenic artery aneurysm in pregnancy is exceedingly rare and the vast majority of obstetricians will retire never having seen one. The possibility of this diagnosis should always be considered in the shocked obstetric patient. Treatment in the acute case is difficult even for experienced general surgeons. Lesions in the splenic artery proper may be treated by ligation of the splenic artery above the body of the pancreas and access is by way of the lesser sac by division of the gastro-colic omentum. Neither of these procedures is easy. The maternal and fetal mortality is so high that every effort should be made to maintain the patient’s blood pressure. Temporary control of bleeding may be achieved by direct pressure on the lesser sac through the stomach until suitable assistance is available. The splenic artery can be identified with duplex ultrasonography. Routine screening of all patients would not be practicable in view of the low overall incidence. An attempt to screen the splenic artery could be made in certain high risks groups such as grandmultiparity and those with known vascular abnormalities such as fibromuscular arterial dysplasia. There are no guidelines on what to do in the event that a splenic artery aneurysm is identified during pregnancy. Careful consideration should be given to undertaking arteriography. It would be incorrect to withhold this investigation to avoid a very small risk to the fetus if the information obtained increased the maternal chance of survival. The timing of appropriate surgery is more difficult. If the aneurysm is small, one option would be to allow the pregnancy to continue with the patient in hospital and aim for an elective caesarean section and treatment of the aneurysm at the same time. For larger aneurysms careful surgery during the second trimester would probably be the best management.
References Ayalon A,, Wiesner R. H., Perkins J. D., Tominaga S., Hayes D. H. & Krom R. A. F. (1988) Splenic artery aneurysms in liver transplant patients. Transplanration 45, 386-389. Baker K. S., Tisnado J. Cho S. & Beachley M. C. (1987) Splanchnic artery aneurysms and pseudo-aneurysms: transcatheter embolisation. Radiology 163, 135-139. Barrett J. M., Van Hooydonk J. E. & Boehm F. H. (1982) Pregnancy
597
related rupture of arterial aneurysms. Obstet Gynecol Surv 37, 557-566. Bishop N. L. (1984) Splenic artery aneurysm rupture into the colon diagnosed by angiography.Br R Radiol 57, 1149-1 150. De Vries J. E., SchattenkerkM. E. &Malt R. A. (1982) Complications of splenic artery aneurysm other than intraperitoneal rupture. Surgery 91, 200-204. Donovitz G. S., Gagliardi C., Mabie W. C., Chester D. B. & Pernoll M. L. (1986) Splenic artery aneurysm rupture in pregnancy. A case report with both maternal and fetal survival. J Tenn bled ASSOC79,611-612. Ho W. C. (1977) Rupture of splenic artery aneurysms in pregnancy. Can Med Assoc J 117, 125-126. Jones E. L. & Finney G. G. (1968) Splenic artery aneurysms. A reappraisal. Arch Surg 97, 6 4 M 4 7 . Lie M., Ertresvag K. & Skjennard A. (1990) Rupture of a splenic artery aneurysm into the pancreatic duct. Acta Chir Scand 156, 411413. Lowry S. M., O’Dea T. P., Gallagher D. I. & Mozenter R. (1986) Splenic artery aneurysm rupture: the seventh instance of maternal and fetal survival. Obstet Gynecol67, 291-292. Mehrota D., Di Benedetto R.,Thenot E., Moreland J. & Mehta P. (1983) Spontaneous rupture of splenic artery aneurysm: sixth instance of both maternal and fetal survival. Obstet Gynecol 62, 665466. Moore S. W. &Lewis R. J. (1961) Splenic artery aneurysm. Ann Surg 153, 1033-1046. Nishida O., Moriyasu F., Nakamura T., eta/.(1986) Hernodynamics of splenic artery aneurysm. Gastroenterology 90, 1042-1 046. Ohlson L. (1978) Effects of the pregnant uterus on the abdominalaorta and its branches. Acta Radiol Diagn 19, 369-376. Pomerantz R. A., Eckhauser F. E., Strode1W. E., Knol J. A. & Turcotte J. G. (1986) Splenic aneurysm rupture in cirrhotic patients. Arch Surg 121, 1095-1096. Reidy J. F., Rowe P. H. & Ellis P. G. (1990) Splenic artery aneurysm embolisation-the preferred technique to surgery. Clin Radiol 41, 281-282. Salo J. A., Salmenkivi K., Tenhunen A. & Kivilaakso E. 0. (1986) Rupture of splanchnic artery aneurysms. World J Surg 10, 123-127. Sato S., Ohnishi K., Sugita S. & Okuda K. (1987) Splenic artery and superior mesenteric blood flow; nonsurgical doppler US measurement in healthy subjects and patients with chronic liver disease. Radiology 164, 347-352. Stanley J. C. &Fry W. J. (1974) Pathogenesis and clinical significance of splenic artery aneurysms. Surgery 76,898-909. Taylor J. L. & Woodward D. A. K. (1987) Splenic conservation and the managementof splenic artery aneurysm.Ann R CollSurg Engl 69, 179-180. Trastek V. F., Pairolero P. C., Joyce J. W., Hollier L. H. & Bernatz P. E. (1982) Splenic artery aneurysms. Surgery 91,694-699. Trastek V. F., Pairolero P. C. & Bematz P. E. (1985) Splenic artery aneurysms. World J Surg 9,378-383. Vassalotti S. B. & Schaller J. A. (1967) Spontaneousrupture of splenic artery aneurysm in pregnancy. Obstet Gynecol30,264-268. Williams J. J. (1988) Splenic artery aneurysm rupture: an uncommon obstetrical catastrophy.J Fam Pract 26, 73-75. Walker T. G., Geller S. C. & Waltman A. C. (1988) Splenic artery pseudoaneurysmscausing lower gastrointestinal hemorrhage.AJR 150,433434.
CLINICAL PRACTICE
Ruptured splenic artery aneurysm in pregnancy. A review R. J . HOLDSWORTH Surgical Registrar A. GUNN Consultant Surgeon Department of Surgery Ninewells Hospital and Medical School Dundee DD1 9SY, UK
Rupture of any arterial aneurysm is a rare event in young women. Half of all arterial aneurysm ruptures in women of child bearing age occur during pregnancy (Barret et al. 1982) and this diagnosis should always be considered in any pregnant patient who has unexplained hypotension and abdominal pain. The splenic artery is the third most common site of intraabdominal aneurysm formation after the abdominal aorta and the iliac vessels. Splenic artery aneurysms are unusual because they occur more frequently in women and they are seen at a relatively younger age than aneurysms of the great vessels. They are associated with increasing parity and have a particular tendency to rupture in pregnancy. Rupture of these aneurysms carries a high maternal and fetal mortality and only with prompt treatment can this high mortality be reduced.
Historical background A splenic artery aneurysm was first described in 1776 by Beussier (Lie et al. 1990) and rupture in pregnancy in 1869 by Corson (Ho 1977). In 1889 President Garfield died from a ruptured splenic artery aneurysm which was traumatic in origin following a bullet wound (Moore & Lewis 1961). An aneurysm was first described in a living person in 1903 by Winkler when several small dilatations of the splenic artery were found at operation (Lie et al. 1990). In 1920, the first pre-operative diagnosis was made by Hoegler who heard a murmur over a pulsatile mass investigated by fluoroscopy and, in 1930, the phenomenon of a double rupture was described by Brockman (Lie et al. 1990). In 1932, the first pre-operative diagnosis followed by a successful operation was made by Lindboe (Lie et al. 1990). The first maternal survivor following rupture in pregnancy was not described until 1940 by MacLeod and the first report of both fetal and maternal survival was in 1967 (Vassalotti & Schaller 1967).
Incidence and occurrence The overall prevalence of splenic artery aneurysms is Correspondence: Mr R. J. Holdsworth, M.D., F.R.C.S.
unknown. They are found in approximately 0.07% of routine post-mortems; however, the incidence at post-mortem in those over 60 years of age is as high as 10.4%. Overall 79% of splenic artery aneurysms occur in people over 50 years of age. A high prevalence has been reported in some angiographic series ranging from 0.78-7.1%, but these are in selected patients with known arteriopathic disease (Moore & Lewis 1961; Stanley & Fry 1974; De Vries et al. 1982; Trastek et al. 1985; Williams 1988). In contrast to aneurysms of the great vessels, which are more frequent in men, splenic artery aneurysms are 2-5 times more common in women and tend to occur at a younger age (Stanley & Fry 1974; Lie et al. 1990; Trastek et al. 1985; Williams 1988). The two principal factors that are of importance in the development of these aneurysms are grandmultiparity and portal hypertension. About 25% of women with a splenic artery aneurysm have been pregnant more than six times. In one report 87% of the aneurysms were found in women and 92% of them had had between 1 and 16 pregnancies, the mean number of pregnancies being 4.5 (Trastek et al. 1982). Aneurysms have also been described in the first pregnancy although this is unusual (Trastek et al. 1985; Williams 1988). Up to 24% of splenic artery aneurysms are found in patients with portal hypertension (De Vries et al. 1982; Pomerantz et al. 1986; Lowry et al. 1986) and the incidence is said to be 7. I % in cirrhotics (Stanley & Fry 1974). Aneurysms have been found in 8.4% of patients having routine coeliac angiography prior to liver transplantation (Ayalon et al. 1988).
Complications Over 80% of splenic artery aneurysms are asymptomatic and are discovered incidentally at angiography, laparotomy or post-mortem (Trastek et al. 1985). The principal complication of a splenic artery aneurysm is rupture. This can lead to either a sudden onset of hypovolaemic shock if rupture is into the peritoneal cavity or it may lead to a more insidious anaemia associated with rupture into the gastrointestinal tract. Rupture into the stomach, small bowel, colon and pancreatic duct have all been reported and gastro-intestinal bleeding is a presentation in one third of cases (Lie et al. 1990; Bishop 1984; De Vries et al. 1982). Overall, rupture of a splenic artery aneurysm is an uncommon event and is reported in 2-9% of cases. However, between 20% and 50% of ruptures occur in pregnancy and another 20% occur in patients with portal hypertension (Stanley & Fry 1974; Barrett et al. 1982; De Vries et al. 1982; Trastek et al. 1985). Rupture is said to be unlikely in aneurysms smaller than
595
596
R . J. HOLDSWORTH & A . G U N N
2.5 cm although it has been reported in lesions of 1-2 cm in size (Trastek et al. 1985; De Vries et al. 1982; Salo et al. 1986). The mortality from rupture was historically very high but this has been reduced due to advances in surgery and resuscitation. The mortality from rupture is now approximately 10% rising to 25% when there is free rupture into the peritoneum. (Trastek et al. 1985; Mehrota et al. 1983; De Vries et al. 1982; Bishop 1984).
Rupture in pregnancy Up to one half of all ruptured splenic artery aneurysms occur in pregnancy; 69% rupture in the third trimester, 12% in the first two trimesters, 13% in labour and 6% in the puerperium (Barrett et al. 1982).Although gastrointestinal bleeding is a presentation in one third of all ruptures, this is never a feature of rupture in pregnancy which is always into the peritoneal cavity (Lowry et al. 1986; Walker et al. 1988). The maternal mortality from rupture in pregnancy is 7 1% and fetal mortality is as high as 95% (Trastek et al. 1985; Mehrota et al. 1983; De Vries et al. 1982; Bishop 1984). Only nine instances of both maternal and fetal survival have been reported (Vassalotti & Schaller 1967; Mehrota et al. 1983; Lowry et al. 1986; Donovitz e al. 1986; Salo et al. 1986).
Clinical features Splenic artery aneurysms usually remain undetected unless they rupture (Lie et al. 1990). Large aneurysms may give rise to pain (Jones & Finney 1968) and in one series, chronic nonspecific abdominal pain, usually in the left hypochondrium, occurred in 13% and bruits were audible in 11% (Trastek et al. 1982). When aneurysms rupture there is a sudden onset of severe abdominal pain associated with hypotension. The pain is usually felt in the epigastrium, penetrating to the back, or radiating to the shoulder tip (Moore & Lewis 1961). The pain is often associated with nausea and vomiting. If the aneurysm has ruptured into the gastrointestinal tract both haematemesis and melaena may occur. Occasionally aneurysms can give rise to a chronic iron-deficiency anaemia (Lie et al. 1990). Tenderness in the upper abdomen is often the only clinical sign. This can vary in severity from mild tenderness with guarding, to a picture of generalized peritonitis. There can be a palpable abdominal mass but this may be confused with the spleen in patients with portal hypertension. In pregnant women the tenderness can be diffuse or maximal over the fundus of the uterus (Williams 1988). The phenomenon of a ‘double rupture’ is reported in 20% of patients. The patient presents with a sudden onset of abdominal pain and hypotension which recovers rapidly with simple fluid replacement. There is then a latent period followed by a sudden cardiovascular collapse, usually within 48 h. This picture results from a small premonitory bleed into the lesser sac which becomes contained and is followed by free rupture into the peritoneum (De Vries et al. 1982; Lie et al. 1990; Lowry et al. 1986).
Pathological features Aneurysms have been described from 1 to 30 cm in diameter
but they are usually 2-3 cm in size; 78% are located in the distal one third of the vessel and are saccular in nature (Trastek et al. 1985). The aetiology of these aneurysms remains uncertain. Although arterio-sclerosis is reported in 95% of lesions and calcification in 70%, these are believed to be secondary changes resulting from increased turbulance rather than the primary causative factors Fibromuscular arterial dysplasia is described in 4-30% of patients. Mycotic aneurysms of the splenic artery are very rare and only account for 2% of all mycotic aneurysms (Moore & Lewis 1961; Stanley & Fry 1974; De Vries et al. 1982; Trastek et al. 1985).
Pathogenesis of splenic artery aneurysms An increased splanchnic blood flow is seen in both portalhypertension and pregnancy and the increased splenic artery blood flow is probably the principal factor in the development of aneurysms at this site. In portal hypertension, an increased portal inflow pressure is required to maintain portal perfusion. This is achieved by an increased splanchnic arterial flow through both the splenic and superior mesenteric arteries (Sato et al. 1987; Nishida et al. 1986). Physiological changes induced by pregnancy include an increased blood volume and cardiac output, relative portal congestion and systemic hypertension. Ohlson (1978) also demonstrated that the pregnant uterus causes significant occlusion of the aorta and the iliac vessels during the third trimester which results in an increased blood flow through arteries more proximal to the site of compression including the splanchnic vessels. It is believed that the combined effects of increased flow and altered arterial structure places a greater stress on the vessel. Individuals who have underlying arterial disease are more suspectable to these stresses leading to aneurysm formation. In pregnancy, hormonal changes can affect the structure of the arterial wall leading to disruption of the internal elastic lamina and failure of elastin formation (Trastek et al. 1985; Barrett et al. 1982). The splenic artery is probably progressively weakened by successive pregnancies leading to an increased frequency of these aneurysms as parity rises.
Management The natural history of splenic artery aneurysms is poorly understood. Moore & Lewis (1961) who monitored 14 aneurysms, found that none ruptured, but these were all arteriosclerotic aneurysms and none of the patients was pregnant. In the series described by Trastek et al. (1982) only one of the 34 aneurysms that were treated conservatively ruptured, this was a 7 cm aneurysm and the patient had declined elective surgery. Once an aneurysm is suspected, most authors recommend the use of arteriography to confirm the diagnosis. This has the advantage of both localizing the lesion and of identifying whether multiple dilatations are present within the splenic or other splanchnic arteries. Treatment in the emergency situation has usually been by splenectomy. Although splenectomy can be avoided by ligation of the aneurysm it may still be necessary for those lesions that occur close to the splenic hilum (Taylor & Woodward
SPLENIC ARTERY ANEURYSM
1987). In elective cases, the majority are still treated by surgery although some success has been reported with embolization and this is now suggested as the treatment of choice in low risk groups (Baker et al. 1987; Reidy et (11.1990). The principal indications for surgical intervention are symptomatic aneurysms; aneurysms in pregnant women or women of child-bearing age; lesions in any age group that are greater than 2 cm in size or ones that show a progressive increase in diameter (Trastek et al. 1985).
Implications for the obstetrician Rupture of a splenic artery aneurysm in pregnancy is exceedingly rare and the vast majority of obstetricians will retire never having seen one. The possibility of this diagnosis should always be considered in the shocked obstetric patient. Treatment in the acute case is difficult even for experienced general surgeons. Lesions in the splenic artery proper may be treated by ligation of the splenic artery above the body of the pancreas and access is by way of the lesser sac by division of the gastro-colic omentum. Neither of these procedures is easy. The maternal and fetal mortality is so high that every effort should be made to maintain the patient’s blood pressure. Temporary control of bleeding may be achieved by direct pressure on the lesser sac through the stomach until suitable assistance is available. The splenic artery can be identified with duplex ultrasonography. Routine screening of all patients would not be practicable in view of the low overall incidence. An attempt to screen the splenic artery could be made in certain high risks groups such as grandmultiparity and those with known vascular abnormalities such as fibromuscular arterial dysplasia. There are no guidelines on what to do in the event that a splenic artery aneurysm is identified during pregnancy. Careful consideration should be given to undertaking arteriography. It would be incorrect to withhold this investigation to avoid a very small risk to the fetus if the information obtained increased the maternal chance of survival. The timing of appropriate surgery is more difficult. If the aneurysm is small, one option would be to allow the pregnancy to continue with the patient in hospital and aim for an elective caesarean section and treatment of the aneurysm at the same time. For larger aneurysms careful surgery during the second trimester would probably be the best management.
References Ayalon A,, Wiesner R. H., Perkins J. D., Tominaga S., Hayes D. H. & Krom R. A. F. (1988) Splenic artery aneurysms in liver transplant patients. Transplanration 45, 386-389. Baker K. S., Tisnado J. Cho S. & Beachley M. C. (1987) Splanchnic artery aneurysms and pseudo-aneurysms: transcatheter embolisation. Radiology 163, 135-139. Barrett J. M., Van Hooydonk J. E. & Boehm F. H. (1982) Pregnancy
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