Splenic Artery Aneurysms: Two Decades Experience at Mayo Clinic

Splenic Artery Aneurysms: Two Decades Experience at Mayo Clinic Maher A. Abbas, MD,1 William M. Stone, MD,1 Richard J. Fowl, MD,1 Peter Gloviczki, MD,2 W. Andrew Oldenburg, MD,3 Peter C. Pairolero, MD,2 John W. Hallett, MD,2 Thomas C. Bower, MD,2 Jean M. Panneton, MD,2 and Kenneth J. Cherry, MD,2 Scottsdale, Arizona, Rochester, Minnesota, and Jacksonville, Florida

Although rare, splenic artery aneurysms (SAAs) have a de®nite risk of rupture. The optimal management of these aneurysms remains elusive. A retrospective chart review of all patients treated at our institutions with the diagnosis of SAA from January 1980 until December 1998 was undertaken. Follow-up was obtained via chart review and by direct phone contact of the patient or relative. No speci®c protocol was followed for management. From analysis of the patient data we concluded that although SAAs may rupture, not all intact aneurysms need intervention. Calci®cation does not appear to protect against rupture, although beta-blockade may be protective. Growth rates of SAA are slow and growth is infrequent. Selective management of SAAs is safe. Open ligation or transcatheter embolization should be considered for symptomatic aneurysms, for aneurysms ³2 cm in size, or for any SAA in women of childbearing years.

INTRODUCTION Aneurysms of the splenic artery (SAA), previously considered rare, are being diagnosed more frequently as incidental ®ndings on radiological studies.1-6 Historically, most aneurysms presented with rupture or were incidentally discovered at autopsy. The rapid proliferation and acceptance of cross-sectional imaging will undoubtedly increase the prevalence of SAA and may identify aneurysms earlier in their natural history. While the treatment options of 1 Department of Surgery, Division of Vascular Surgery, Mayo Clinic Scottsdale, Scottsdale, AZ. 2 Department of Surgery, Department of Vascular Surgery, Mayo Clinic Rochester, Rochester, MN. 3 Department of Surgery, Division of Vascular Surgery, Mayo Clinic Jacksonville, Jacksonville, FL.

Correspondence to: W.M. Stone, MD, Department of Surgery, Mayo Clinic Scottsdale, 13400 E. Shea Boulevard, Scottsdale, AZ 85259, USA, E-mail: stone.william@ mayo.edu. Ann Vasc Surg 2002; 16: 442±449 DOI: 10.1007/s10016-001-0207-4 Ó Annals of Vascular Surgery Inc. Published online: 10 July 2002 442

ruptured or symptomatic SAA are well established, controversy remains regarding the optimal management of asymptomatic aneurysms. Furthermore, the risk-bene®t ratio of treating asymptomatic SAA can be dif®cult to assess in the absence of comprehensive natural history data. Unfortunately, most modern recommendations are derived from studies with a small cohort of subjects and limited long-term follow-up.6 In addition, most series of SAA do not distinguish between true and false aneurysms. We previously reported 100 cases of SAA seen at our institution between 1960 and 1980.1 Since that report, numerous opinions have been expressed in the literature regarding the etiology and management of SAA.3,5-9 In an attempt to resolve some of the ongoing management controversy, we reviewed our experience with SAA in patients seen at our institutions over the last two decades.

PATIENTS AND METHODS A retrospective review of all patients with documented SAA seen at the Mayo Clinic (Rochester,

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MN; Scottsdale, AZ; Jacksonville, FL) between January 1, 1980, and December 31, 1998, was undertaken. The study was reviewed and approved by our institutional review board. Included for review were those patients with SAA diagnosed by imaging studies, surgical exploration, or autopsy evaluation. Excluded from review were those patients with pseudoaneurysms of the splenic artery. The records of all patients were identi®ed utilizing the Mayo Clinic Medical Record Registry, which is a comprehensive database listing all patients by diagnoses. These records were analyzed with regard to demographics, comorbidities, clinical presentation, aneurysm characteristics, imaging studies, management including operative intervention, and outcome. Long-term follow-up was obtained via chart review and/or by direct phone contact of the patient or relative. No speci®c protocol was followed for management of these aneurysms. Surgeon preference and judgement dictated all management decisions.

RESULTS Demographics and Associated Conditions For a summary of patient demographics, see Table I. Of 306 patients with the diagnosis of visceral artery aneurysm seen at our institutions between 1980 and 1998, 217 patients (70.9%) had SAA. Of these 217 patients, 171 were female (78.8%) and 46 were male (21.2%). Ninety-six percent of patients were Caucasian. Mean age at presentation was 61.7 years (range, 8-88 years) including a mean age for males of 67.8 years and a mean age for females of 60.1 years. Ten patients (4.6%) (5 men and 5 women) presented with ruptured SAA. This represents 2.9% of all females and 10.9% of all males. Mean age of patients at rupture was 62 years (range, 36-80 years). None of the ruptured aneurysms occurred in females of childbearing age. The mean number of pregnancies was 3.5 in all female patients, including a mean of 1.8 in patients with ruptured SAA and a mean of 3.5 in patients with nonruptured SAA. Thirty-one patients used beta-blockers at presentation and none of these patients presented with rupture nor did any rupture during follow-up. Forty-®ve women (26.3%) were on estrogen replacement therapy and none presented ruptured nor did any rupture during follow-up. Associated clinical conditions (Table II) were documented in all patients on the basis of established diagnoses assigned by the patients' primary care physician or medical specialist at Mayo.

Splenic artery aneurysms 443

Hypertension was the most common comorbid condition present in patients with SAA (50.2%), followed by obesity (27.6%), coronary artery disease (23.5%), hypercholesterolemia (21.7%), and peptic ulcer disease or gastritis (20.3%). Less common were conditions such as malignancy (15.2%), diabetes (10.1%), cirrhosis (7.8%), chronic obstructive pulmonary disease (COPD) (6%), connective tissue disorder (6%), cerebrovascular accident (5.1%), symptomatic peripheral vascular disease (4.6%), carotid disease (2.3%), and endocarditis (1.4%). Concomitant nonsplenic visceral artery aneurysms were present in 3.3% of our patients, with extrahepatic aneurysm being the most common type (2.3%) (Table III). Concomitant nonvisceral aneurysms were documented in 14.3% of patients; renal artery aneurysms occurred most frequently (7.4%). Clinical Presentation and Diagnosis For a summary of patients' clinical presentation, see Table IV. Of 217 patients with SAA, only 10 patients presented with rupture (4.6%), 4 were symptomatic and not ruptured (1.8%), and 203 were asymptomatic (93.6%). In the nonruptured symptomatic group, two patients presented with abdominal pain, one patient had chest pain, and one had ¯ank pain. The aneurysm was felt to be the source for symptoms in these patients after all other possible causes for the symptoms were excluded. Table V summarizes the methods used to make the initial diagnosis. Plain abdominal radiographs (94 patients), computerized tomography (CT) (44 patients), and angiography (32 patients) detected the aneurysm in nearly 80% of the patients. Figure 1 demonstrates typical CT ®ndings in a patient with SAA. A minority of aneurysms (8 patients, 3.7%) were discovered incidentally at the time of abdominal operations for other reasons. The diagnosis of ruptured SAA was made during exploratory celiotomy in 8 patients (3.7%). Aneurysm Characteristics For a summary of aneurysm characteristics, see Table VI. A solitary SAA was the most common ®nding and was present in 207 patients (95%). Multiple aneurysms were present in 5% of patients. Calci®cation was present in 90% of ruptured aneurysms (9 patients) and 84.5% of nonruptured ones (175 patients). The size of the aneurysm was documented in only 145 patients (66.8%). The mean diameter of SAA was 3.1 cm (range, 2.3-5 cm)

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Table I. Demographics

Factor

All patients (N = 217) [n (%)]

Nonruptured (N = 207) [n (%)]

Ruptured (N = 10) [n (%)]

Male Female Age, mean ‹ SD (years) (range) Smokers Years of tobacco, mean ‹ SD Alcohol use Beta-blockade use Estrogen replacement Previous or current steroid use Number of pregnancies, mean ‹ SD History of spontaneous miscarriages Pregnant at presentation

46 (21.2) 171 (78.8) 61.7 ‹ 13.9 (8-88) 60 (27.7) 23.8 ‹ 12.3 97 (44.7) 31 (14.3%) 45 (26) 30 (13.8%) 3.5 ‹ 2.5 20 (11.7) 0

41 (19.8) 166 (80.2) 61.6 ‹ 13.9 (8-88) 55 (26.6) 23 ‹ 12.2 90 (43.5) 31 (15) 45 (27) 29 (14) 3.5 ‹ 2.5 20 (12.1) 0

5 (50) 5 (50) 62.0 ‹ 14.7 (36-80) 5 (50) 34 ‹ 10.8 7 (70) 0 0 1 (10) 1.8 ‹ 1.3 0 0

Table II. Associated medical conditions

Condition Hypertension Obesity Coronary artery disease Hypercholesterolemia Peptic ulcer disease/gastritis Malignancy Diabetes Cirrhosis COPD Connective tissue disorder Cerebrovascular accident Symptomatic peripheral vascular disease Carotid disease Endocarditis

All patients (N = 217) [n (%)]

Nonruptured (N = 207) [n (%)]

Ruptured (N = 10) [n (%)]

109 (50.2) 59 (27.6) 51 (23.5) 47 (21.7) 44 (20.3) 33 (15.2) 22 (10.1) 17 (7.8) 13 (6) 13 (6) 11 (5.1) 10 (4.6)

105 (50.7) 56 (27.1) 47 (22.7) 47 (22.7) 42 (20.3) 33 (15.9) 22 (10.6) 17 (8.2) 11 (5.3) 12 (5.8) 8 (3.9) 10 (4.8)

4 4 4 0 2 0 0 0 2 1 3 0

5 (2.3) 3 (1.4)

5 (2.4) 3 (1.5)

0 0

in patients who presented with ruptured aneurysms. Male patients presenting with ruptured aneurysms had a SAA mean diameter of 3.2 cm, whereas females presenting with a ruptured aneurysm had a mean diameter of 2.3 cm. In contrast, mean diameter of nonruptured SAA was 2.2 cm (range, 0.8-5 cm). Males presenting with a nonruptured SAA had a mean diameter of 2.6 cm whereas females presenting with a nonruptured SAA had a mean diameter of 2.1 cm. Operative Management and Outcome For a summary of operative interventions and complications, see Table VII. Forty-nine patients

(40) (40) (40) (20)

(20) (10) (30)

underwent surgical interventions (22.6%); 10 had emergency or urgent procedures because of SAA rupture and 39 patients underwent elective operations. The size of the SAA was documented in 32 of the 39 patients (82%) operated on electively with a mean size of 2.7 cm (range, 0.9-5 cm). In the electively operated group, 4 patients underwent repair for symptoms, 3 patients for enlarging SAA (range, 3-4 cm), and 32 patients for other reasons such as risk of rupture, liver transplant, or during abdominal operations for other indications. The incidence of splenectomy and distal pancreatectomy was higher in the ruptured than in the elective group (100% vs. 28.2%, and 50% vs.

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Splenic artery aneurysms 445

Table III. Frequency of associated aneurysms

Types of aneurysm

All patients (N = 217) [n (%)]

Nonruptured (N = 207) [n (%)]

Ruptured (N = 10) [n (%)]

Visceral aneurysms Extrahepatic Celiac Superior mesenteric artery Gastric Pancreaticoduodenal Nonvisceral aneurysms Renal Abdominal aorta Carotid Cerebral Thoracic aorta Popliteal

7 (3.3) 5 (2.3) 1 (0.5) 1 (0.5) 1 (0.5) 1 (0.5) 31 (14.3) 16 (7.4) 8 (3.7) 4 (1.8) 4 (1.4) 1 (0.5) 1 (0.5)

7 (3.4) 5 (2.4) 1 (0.5) 1 (0.5) 1 (0.5) 1 (0.5) 29 (14) 15 (7.2) 8 (3.9) 4 (1.9) 3 (1.4) 0 1 (0.5)

0 0 0 0 0 0 2 (20) 1 (10) 0 0 0 1 (10) 0

Table IV. Clinical presentation

Symptom

Ruptured (N = 10) [n (%)]

Nonruptured (N = 207) [n (%)]

Abdomincal pain Hemodynamic instability Chest pain Gastrointestinal bleeding Flank pain Nausea

9 5 2 2 1 1

2 0 1 0 1 1

(90) (50) (20) (20) (10) (10)

(1.0) (0.5) (0.5) (0.5)

Table V. Method of initial diagnosis

Method

All patients (N = 217) [n (%)]

Plain radiograph Computed tomography Arteriogram Barium enema Upper gastrointestinal series Ultrasound Incidental ®nding at operation Operation for rupture Magnetic resonance

94 (43.3) 44 (20.3) 32 (14.7) 11 (5.1) 10 (4.6) 8 (3.7) 8 (3.7) 8 (3.7) 1 (0.5)

10.3%, respectively. Ligation of the aneurysm was the most common operation in the elective group (23 patients, 59%). Elective tranascatheter embolization was performed in ®ve patients (12.8%), one of whom developed celiac artery dissection and required open repair and ligation.

Operative mortality was 20% and 5.1% in the ruptured and elective group, respectively. One patient who died in the elective group had a gastroesophageal anastomotic leak after concomitant gastric resection of carcinoma; another suffered a postoperative myocardial infarction. Mean follow-up was 89 months (range, 1-382) in the ruptured group and 70 months in the elective group (range, 1-232 months). In the ruptured group, 10% of patients developed gastroparesis, 10% suffered recurrent intestinal obstruction, and 10% required repair of ventral hernia. No recurrence of aneurysm was noted in any patient undergoing intervention. Nonoperative Management and Outcome Nonoperative management was chosen in 168 patients (77.4%) with a mean follow-up of 75 months (range 1-371 months). Size was available in 109 of 168 patients at presentation (64.8%). The mean size of SAA in the nonoperative group was 2.1 cm (range, 0.8-5 cm). In the group of patients with documented size, 76 patients (69.7%) had aneurysms £2 cm and 24 patients (22%) had aneurysms between 2.1 and 3 cm. Only 9 patients (8.3%) had aneurysms >3 cm. Of the 79 patients with size data documented in follow-up, 8 patients (10.1%) had interval growth of their SAA (excluding an additional 3 patients operated on electively for enlarging SAA). Mean aneurysm growth was 0.45 cm during the follow-up period or 0.06 cm/year. The most rapid growth rate noted was 1 cm over 63 months. The slowest growth rate noted was 0.2 cm over 194 months. No ruptures or

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Table VI. Aneursysm characteristics

Fig. 1. Incidental 17-mm calci®ed SAA seen on CT scan of abdomen (arrow).

other complications related to the aneurysm occurred in any patient during the follow-up period. Two patients had interval development of additional visceral aneurysms, including one with a second splenic and one with an extrahepatic and pancreaticoduodenal aneurysms.

DISCUSSION Incidence Splenic artery aneurysm is the most frequently encountered type of visceral aneurysm and the third most common abdominal aneurysm following aortic and iliac artery aneurysms.1,2,7,9-11 The true incidence of SAA is unknown, but has been reported to be between 0.02% and 10.4% in the general population.1,6,12-14 SAA has been reported to be present in 8.8 to 50% of cirrhotic patient.3,9,14-18 Women have a predilection for the development of SAA.11 In our study, 78.8% of SAA occurred in women. However, in our series no rupture occurred in women of childbearing age. This may be related to the patient demographics of our referral practice. Typically, most SAA are asymptomatic and are incidental ®ndings on plain radiographs and other imaging studies.3,5-7,11 In our series, 203 patients (93.6%) were asymptomatic. Etiology The precise etiology of SAA remains unclear, although several conditions have been associated with SAA, including atherosclerosis, arterial ®brodysplasia, arteritis, collagen vascular disease, a-1antitrypsin de®ciency, in¯ammatory and infectious

Feature

Ruptured aneurysms (N = 10)

Nonruptured aneurysms (N = 207)

Single aneurysm Multiple aneurysms Presence of calci®cation Mean diameter (cm) Median diameter (cm) Range of diameter (cm)

10 (100) 0% 9 (90%) 3.1 2.5 2.3-5

188 (90.7%) 25 (12.1%) 175 (84.5%) 2.3 2 0.8-5

Table VII. Operative interventions and complications Intervention or complication

Ruptured aneurysms (N = 10)

Nonruptured aneurysms (N = 39)

Splenectomy Ligation Distal pancreatectomy Embolization Mortality Ileus Wound infection Wound dehiscence Acute myocardial infarction Multiorgan failure Pancreatic leak with ®stula Small bowel perforation Abdominal abscess Anastomotic leak Pulmonary embolism Dissection of celiac artery Pneumonia Urinary tract infection

10 (100) 0 5 (50) 0 2 (20) 2 (20) 2 (20) 2 (20) 1 (10) 1 (10) 1 (10) 1 (10) 1 (10) 0 1 (10) 0 0 0

11 (28.2) 23 (59) 4 (10.3) 5 (12.8) 2 (5.1)a 1 (2.6) 1 (2.6) 0 1 (2.6) 1 (2.6) 0 0 1 (2.6) 1 (2.6)a 1 (2.6) 1 (2.6)b 2 (5.2) 1 (2.6)

a

Death from gastroesophageal anastomotic leak for gastric cancer resection. b Arterial dissection from embolization treated by open repair and ligation.

disorders, hemodynamic and endocrine changes of pregnancy, pancreatitis, and portal hypertension with splenomagaly.1,3,8,9,15,19-24 Rarely, SAA has been associated with disorders such as Cushing's syndrome and systemic lupus erythematosus.4,25 SAA is more common in women with a history of multiple pregnancies.1,2,11 The mean number of pregnancies in our study group was 3.5. Degenerative changes in the splenic artery, including disruption of the internal elastic lamina, fragmentation of elastic ®bers, and ®brodysplasia of media, have been observed in human and animal studies.11,23 Recent reports suggest the presence of estrogen and progesterone receptors in the wall

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of the artery.11 The signi®cant hormonal shifts of pregnancy may contribute to loss of arterial wall integrity.11 Furthermore, relaxin, a gestational hormone secreted late in pregnancy to stimulate elasticity of the pubic symphysis, may have comparable action on the arterial wall.11 Patients with portal hypertension also seem to have a predilection for SAA. The hyperdynamic circulation seen with portal hypertension has been postulated as an important factor in the development of SAA. Increased portal and splenic venous ¯ow has been demonstrated in cirrhotic patients with SAA by duplex sonography and angiography.14,16,20 In our study, 17 patients (7.8%) had a history of portal hypertension. Risk for Rupture Aneurysmal rupture has been reported in 3 to 10% of all splenic aneurysms.1,2,5,23 In our series the incidence of rupture was 2.9% in women and 10.9% in men, with an overall incidence of 4.6%. Previous reports suggest the risk of rupture may be linked to size, pregnancy, as well as cirrhosis and liver transplantation.11,18,22,23 While most SAA are smaller than 2 cm, unruptured aneurysms up to 30 cm have been previously reported.1 The smallest ruptured aneurysm in our study was 2.3 cm. In our earlier experience (1960-1980), the smallest ruptured aneurysm was 2 cm.1 SAA rupture in pregnant women carries a high mortality. Although maternal and fetal survival has been previously reported, nearly 70% of the mothers die and fetal mortality is a devastating 9095%.11,23,26,27 Rupture is most common in the third trimester but can occur during the ®rst two trimesters, labor, or postpartum.22,23,26 Multiparity has been reported to carry a higher risk of rupture; a ®nding not supported by our study.1 The risk of rupture has been well documented in cirrhotic patients undergoing liver transplantation. Often it occurs within days of transplant but occasionally may be delayed and carries a mortality of 40-80%.6,8,24,28 The risk of rupture of SAA may be greater in patients with a-1-antitrypsin de®ciency.24 In a survey of 126 transplantation centers, Gaglio and colleagues reported 21 cases of ruptured SAA in patients either awaiting or having received a liver transplant.24 Forty-seven percent of the ruptured patients had a-1-antitrypsin de®ciency.24 The excessive proteolytic activity in this setting is thought to increase the risk of rupture.24 In our study, none of the 31 patients on betablockers were found to have ruptured SAA at presentation or during follow-up. However, it is

Splenic artery aneurysms 447

unclear whether our observation re¯ects a protective effect of beta-blockers or is a product of our small sample size of ruptured aneurysms in our study. As has previously been reported, calci®cation does not appear to protect against rupture, as 90% of ruptured SAA in our study were calci®ed.1 Mortality from rupture has been reported to be between 10 and 76%.1,2,6,8,10,22 However, contemporary reports suggest a mortality rate of 36%.3 In our review, 20% of patients with ruptured SAA died. Indications for Treatment Indications for intervention for treatment of SAA remains controversial. Within our institution, we noted a trend towards observation of most small aneurysms after reviewing our initial experience between 1960 and 1980. While 81% of all SAA seen at the Mayo Clinic during our previous review underwent intervention, only 22.6% seen between 1980 and 1998 underwent an operation. Clearly most surgeons would agree that SAA in patients with symptoms possibly related to it, as well as SAA discovered during pregnancy or in patients of childbearing age should be considered for repair.5,6,23 Likewise, SAA in a liver transplant recipient should be treated at the time of transplantation because of the risk of rupture, regardless of size.5,8,9,18,24,29,30 This recommendation is based upon the ®ndings of other reports and not based upon our current data. No consensus regarding the size criteria for intervention in asymptomatic SAA exists in the literature. Previously, we recommended repair in all SAA >2 cm.1 However, others have used 1.5, 2.5, or 3 cm as size criteria for intervention.5,6,8,18,23 Asymptomatic SAA >2 cm in size are at increased risk of rupture, a ®nding supported by our current data. Our recommendation remains to surgically treat or consider embolization of any asymptomatic SAA >2 cm in a patient who is a reasonable operative risk and has a life expectancy of 2 years. Treatment Options Appropriate therapy for SAA depends primarily on the location of the aneurysm, age of the patient, operative risks, and clinical status. Open surgical treatment options for SAA include ligation, resection, and splenectomy. Laparoscopic ligation may provide a viable alternative to the traditional open surgical approaches. Several laparoscopic techniques have been described including splenic artery

448 Abbas et al.

ligation,31,32 resection of the aneurysm,20,33,34 and obliteration of the aneurysm with a vascular stapling device.19 However, the laparoscopic approach may be dif®cult in patients with previous abdominal operations or in obese patients, or when the SAA is embeded in the pancreatic parenchyma or deep in the splenic hilum. Embolization has recently gained popularity and is an alternative to open and laparoscopic repair.2,3,5,6 An 85% success rate with embolization has been reported.2 Our experience is similar to this report, with an 80% success rate. Embolization can be performed successfully, but is dependent on the location of the aneurysm and remains an option for high-risk surgical candidates. This technique, however, is associated with the risk of luminal occlusion of the main trunk of the artery, leading to splenic infarction or dissection, as seen in one of our patients. Although SAA may rupture, not all need intervention. Most SAA remain relatively small and rarely enlarge, become symptomatic, or rupture. Calci®cation does not appear to protect against rupture, although beta-blockade may carry some protective effect. Growth of SAA appears to be slow and infrequent. A selective approach to the management of these aneurysms appears to be justi®ed and safe. On the basis of our ®ndings as well as those of others,6,8,11,22-24,26-28 we recommend that ligation or embolization be considered for symptomatic aneurysms, aneurysms ³2 cm, aneurysms in cirrhotic patients undergoing liver transplant, SAA in patients with a-1-antitrypsin de®ciency, or SAA in pregnant women or those of childbearing age. REFERENCES 1. Trastek VF, Pairolero PC, Joyce JW, Hollier LH, Bernatz PE. Splenic artery aneurysms. Surgery 1982;91:694-699. 2. McDermott VG, Shlansky-Goldberg R, Cope C. Endovascular management of splenic artery aneurysms and pseudoaneurysms. Cardiovasc Intervent Radiol 1994;17:179-184. 3. Carr SC, Pearce WH, Vogelzang RL, McCarthy WJ, Nemcek AA, Yao JST. Current management of visceral artery aneurysms. Surgery 1996;120:627-634. 4. Tazawa K, Yasuda M, Ohtani Y et al. Splenic artery aneurysm associated with systemic lupus erythematosus: report of a case. Surg Today 1999;29:76-79. 5. Dave SP, Reis ED, Hossain A, Taub PJ, Kerstein MD, Hollier LH. Splenic artery aneurysm in the 1990s. Ann Vasc Surg 2000;14:223-229. 6. Carr SC, Mahvi DM, Hoch JR, Archer CW, Turnipseed D. Visceral artery aneurysm rupture. J Vasc Surg 2001;33:806811. 7. Taylor JL, Woodward DA. Splenic conservation and the management of splenic artery aneurysm. Ann R Coll Surg Eng 1987;69:179-180.

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8. Lee PC, Rhee RY, Gordon RY, Fung JJ, Webster MW. Management of splenic artery aneurysms: the signi®cance of portal and essential hypertension. J Am Coll Surg 1999;189: 483-490. 9. Robertson AJ, Rela M, Karani J, Heaton ND. Splenic artery aneurysm and orthotopic liver transplantation. Transpl Int 1999;12:68-70. 10. Mullen JT, Hawkins ML. Splenic artery aneurysm. Am Surg 1975;41:370-372. 11. Hallett JW. Splenic artery aneurysms. Semin Vasc Surg 1995;8:321-326. 12. Owens JC, Coffey RJ. Aneurysm of the splenic artery, including report of 6 additional cases. Int Abst Surg 1953; 97:312-320. 13. Bedford PD, Lodge B. Aneurysm of the splenic artery. Gut 1960;1:312-320. 14. Ohta M, Hashizume M, Ueno K, Tanoue K, Sugimachi K, Hasuo. Hemodynamic study of splenic artery aneurysm in portal hypertension. Hepatogastroenterology 1994;41:181184. 15. Puttini M, Aseni P, Brambilla G, Belli L. Splenic artery aneurysms in portal hypertension. J Cardiovasc Surg 1982;23:490-493. 16. Ohta M, Hashizume M, Tanoue K, Kitano S, Sugimachi K, Yasumori K. Splenic hyperkinetic state and splenic artery aneurysm in portal hypertension. Hepatogastroenterology 1992;39:529-532. 17. Manenti F, Williams R. Injection of the splenic vasculature in portal hypertension. Gut 1966;7:175. 18. Ayalon A, Wiesner RH, Perkins JD, Tominaga S, Hayes DH, Krom RA. Splenic artery aneurysms in liver transplant patients. Transplantation 1988;45:386-389. 19. Matsumoto K, Ohgami M, Shirasugi N, Nohga K, Kitajima M. A ®rst case report of the successful laparoscopic repair of splenic artery aneurysm. Surgery 1997;121:462464. 20. Nishida O, Moriyasu F, Nakamura T, et al. Hemodynamics of splenic artery aneurysm. Gastroenterology 1986;90:10421046. 21. Saw EC, Ku W, Ramachandra S. Laparoscopic resection of a splenic artery aneurysm. J Laparoendosc Surg 1993;3:167171. 22. Herbeck M, Horbach T, Putzenlechner C, Klein P, Lang W. Ruptured splenic artery aneurysm during pregnancy: a rare case with both maternal and fetal survival. Am J Obstet Gynecol 1999;181:763-764. 23. Angelakis EJ, Bair WE, Barone JE, Lincer RM. Splenic artery aneurysm rupture during pregnancy. Obstet Gynecol Surg 1993;48:145-148. 24. Gaglio PJ, Regenstein F, Slakey D, et al. Alpha- 1 antitrypsin de®ency and splenic artery aneurysm rupture: an association? Am J Gastroenterol 2000;95:1531-1534. 25. Yoshitomi Y, Yoshimi H, Yutani C. A case of splenic artery aneurysm with Cushing's syndrome. Int J Cardiol 1996;54:263-265. 26. Cailouette JC, Merchant EB. Ruptured splenic artery aneurysm in pregnancy. Am J Obstet Gynecol 1993;168:18101813. 27. Dunlop W, Iwanicki S, Akierman A, Pasieka J, Higgin JR. Spontaneous rupture of splenic artery aneurysm: maternal and fetal survival. Can J Surg 1990;33:407-408. 28. Bronsther O, Merhav H, Thiel DV, Starzl TE. Splenic artery aneurysms occuring in liver transplant recipients. Transplantation 1991;52:723-724.

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29. Brems JJ, Hiatt JR, Klein AS, Colonna JO, Busuttil RW. Splenic artery aneurysm rupture following orthotopic liver transplantation. Transplantation 1988;45:1136-1137. 30. Hashizume M, Ohta M, Ueno K, Okadome K, Sugimachi K. Laparoscopic ligation of splenic artery aneurysm. Surgery 1993;113:352-354. 31. Jovine E, Mazziotti JE, Grazi GL, et al. Rupture of splenic artery aneurysm after liver transplantation. Clin Transplant 1996;10:451-454.

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32. Leung KL, Kwong KH, Tam YH, Lau WY, Li AKC. Laparoscopic resection of splenic artery aneurysm. Surg Endosc 1998;12:53. 33. Adham M, Blanc P, Douek P, Henri L, Ducerf C, Baulieux J. Laparoscopic resection of a proximal splenic artery aneurysm. Surg Endosc 2000;14:372-374. 34. Trias M, Targarona EM, Espert JJ, Balague C. Laparoscopic surgery for splenic disorders. Surg Endosc 1998;12: 66-72.