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Management of True Aneurysms of the Splenic Artery
Management of True Aneurysms of the Splenic Artery Marc de Perrot, Le´o Bu¨hler, Jeff Dele´aval, Bettina Borisch, Gilles Mentha, Philippe Morel, Geneva, Switzerland
BACKGROUND: Splenic artery aneurysms (SAA) are detected with increasing frequency but their management still remains controversial. This paper relates our experience in the outcome and management of ruptured aneurysms of the splenic artery. METHODS: Between 1977 and 1996, 8 patients presented to our institution with a ruptured SAA. Their ages ranged from 25 to 72 years (mean 55 ys). RESULTS: All patients presented with rupture as the first sign of SAA. One patient was at 32 weeks of gestation and rupture suggested placental abruption. Three patients required cardiopulmonary reanimation prior to surgical procedures. Splenopancreatectomy (n 5 4), splenectomy (n 5 2), and ligation of the splenic artery (n 5 1) were performed. Seven of the 8 patients survived. Size of aneurysms ranged from 2 cm to 3.5 cm (mean 3 cm). CONCLUSIONS: SAA may rupture at any age. Diagnosis during pregnancy rests upon a high index of suspicion. The mortality rate remains low if immediate resuscitation is performed and an aggressive surgical approach is taken. Am J Surg. 1998;175:466 – 468. © 1998 by Excerpta Medica, Inc.
T
he splenic artery is the third most common site of intraabdominal aneurysm formation after the abdominal aorta and iliac arteries.1 They are of particular interest, because, in contrast to aneurysms of large vessels, atherosclerosis is rarely the primary causative factor.1,2 Development of splenic artery aneurysms (SAA) generally result from a degeneration of the media, and they are frequently associated with multiparity or portal hypertension.1,3 Etiologic mechanisms remain uncertain, but considerable evidence exists to implicate hormonal and local hemodynamic events in the evolution of most of these aneurysms.2 Although rupture is the main complication with massive intraperitoneal hemorrhage, their management still remains controversial.1,3,4
From the Departments of Surgery (MD, LB, JD, GM, PM) and Pathology (BB), University Hospital of Geneva, Geneva, Switzerland. Requests for reprints should be addressed to Marc de Perrot, MD, Department of Surgery, University Hospital of Geneva, 1211 Geneva 14, Switzerland. Manuscript submitted August 1, 1997 and accepted in revised form January 12, 1998.
466
© 1998 by Excerpta Medica, Inc. All rights reserved.
In order to better determine the outcome and management of these aneurysms, we report 8 cases of ruptured SAA that occurred during the past 20 years at our institution. Since the clinical course of aneurysms and pseudoaneurysms of the splenic artery is different, the latter being mostly associated with chronic pancreatitis, they were excluded from our study.5,6
PATIENTS AND METHODS All patients who presented with spontaneous rupture of a true SAA at the University Hospital of Geneva between 1977 and 1996 were reviewed. We collected 8 cases. There were 5 male and 3 female patients. Their ages ranged between 25 and 72 years (mean 55 ys), 4 patients being older than 60 years. Six patients were known for systemic hypertension and 4 for atherosclerotic disease. Parity among women ranged from 0 to 3. None of these patients were known to have SAA prior to rupture, and none of them suffered from portal hypertension, nor from thrombosis of the splenic vein. These patients were analyzed with regard to the mode of presentation, preoperative investigations, treatment, and outcome. Location and size of SAA are also reported.
RESULTS All patients presented with rupture as the first sign of SAA. Mode of presentation was acute, diffuse abdominal pain, excruciating into the back in 3 patients. In 1 case only, the pain was typically located in the left hypochondrium. No abdominal mass was palpated on physical examination. Symptomatology had lasted between 6 and 96 hours (mean 14 hours) prior to the occurrence of cardiovascular collapse. Preoperative investigations included abdominal ultrasonography (US) in 6 patients, computed tomography (CT) in 3 patients, and angiography in 3 patients. One patient (gravida 3, para 1) presented at 32 weeks of gestation with sudden onset of low abdominal pain and short episodes of hypotension suggesting placental abruption. She underwent a caesarean operation in emergency; the fetus was dead, and no intraabdominal bleeding was observed. Twelve hours later massive intraperitoneal hemorrhage required a new emergency laparotomy and a ruptured SAA was diagnosed. Management consisted in volemic resuscitation and emergency laparotomy. Three patients required cardiopulmonary reanimation, of whom 1 died prior to surgery. The diagnosis in this patient was eventually made at necropsy only. Surgical procedures were left splenopancreatectomy in 4 cases and resection of the SAA with splenectomy in 2 cases. In 1 case, proximal and distal ligation of the splenic artery was possible, but splenectomy was also required 0002-9610/98/$19.00 PII S0002-9610(98)00082-8
TRUE ANEURYSMS OF THE SPLENIC ARTERY/DE PERROT ET AL
TABLE Risk Factors Associated with Rupture of Splenic Artery Aneurysms Pregnancy Expanding aneurysms Symptomatic aneurysms Aneurysms of 2 cm or larger Portal hypertension with liver transplantation or portocaval shunt
Figure. Angiography of a ruptured splenic artery aneurysm.
because of failure of good persistent vascularization of the spleen through the short gastric vessels. All 4 patients who had not undergone preoperative angiography required cross-clamping of the aorta for 15 to 60 minutes at the beginning of the surgical procedures. A mean of 11 (10 to 14) blood transfusions was administered. All patients had an unique aneurysm of the splenic artery, located along the middle third of splenic artery in 2 patients, along the distal third of splenic artery in 5 patients, and at the splenic hilum in 1 patient. The size of aneurysms ranged from 2 cm to 3.5 cm (mean 3 cm). The Figure shows angiography of a ruptured SAA. Histologic examination of the splenic artery showed atherosclerosis in 4 patients. Congenital origin was suspected in 1 young patient without other risk factors. All patients who could be operated upon survived (n 5 7). Postoperative complications occurred in 3 patients and included multiple organ failure, bronchopneumonia, and postanoxic encephalopathy. The 2 former patients eventually became well, but the latter remained severely disabled.
COMMENTS Since the first report of SAA made by Beaussier at necropsy in 1770, large routine necropsy series have reported an incidence of SAA ranging from 0.01% to 0.2%.7 At the University Hospital of Geneva, out of 16,081 necropsies performed between 1977 and 1992, 5 SAA were found (incidence of 0.031%). Four of them were asymptomatic, whereas 1 had ruptured and was the cause of death. Higher incidence has been reported in selected groups of patients, such as in hypertensive patients (1%)8 and in series performed with pathologists paying special attention to the splenic artery (10.4%).9 The pathogenesis of SAA is not fully understood, but multiparity and portal hypertension seem to promote aneurysmal dilatation.1,3 Atherosclerotic changes, however, although observed in up to 99% of the splenic aneurysms
examined histologically,1 are most likely secondary events resulting from a primary degeneration of the media.4 The true incidence of rupture of SAA is difficult to ascertain, as it varies with the number of asymptomatic aneurysms incidentally detected during radiologic investigations or surgical exploration. Recently, Trastek et al1 who reported the largest clinical trial found 3 ruptures out of 100 documented SAA. Several factors have been associated with an increased risk of rupture (Table).4 Pregnancy has been associated with more than 100 cases of ruptured SAA, thus comprising approximately one fourth of all cases.10 Hemorrhage occurred during the third trimester of pregnancy in 69% of these patients and was often misdiagnosed as placental abruption or uterine rupture.11 The maternal and fetal mortality rate were as high as 75% and 95%, respectively.11 A high flow rate through the splenic artery due to compression of the aorta and iliac arteries by the pregnant uterus and relative portal congestion are important pathogenic factors.11 Similar increase in splenic blood flow occurs in patients with liver disease and portal hypertension who undergo orthotopic liver transplantation or end-toside portocaval shunt.12 When no pregnancy is planned or portal hypertension detected, indications to treat SAA are based on characteristics of the aneurysms and the patient’s age.4 A general consensus holds that growing or symptomatic aneurysms should be resected. However, controversy still remains with stable and asymptomatic SAA. In our experience and that of others,1,3,4,13 ruptures have occurred almost exclusively in aneurysms of 2 cm or larger. Hence, small, asymptomatic SAA may be observed, whereas those of 2 cm or larger must be treated. Advanced age, particularly if associated with systemic hypertension, should not preclude surgery. In our series, 6 patients had systemic hypertension and 4 were older than 60 years of age. Rupture may initially tamponade into the lesser omental sac and entail sudden onset of acute abdominal pain with short episodes of hypotension. Free intraperitoneal hemorrhage with cardiovascular collapse ensued 6 to 96 hours after the onset of symptoms in our patients. This “double rupture phenomenon” was well demonstrated in our pregnant patient who underwent a ceaserian operation for abdominal pain and episodes of hypotension suggesting placental abruption. No signs of peritoneal bleeding could be seen at that time. Twelve hours later, however, a second laparotomy was required because of massive free intraperitoneal bleeding. The “sentinel rupture” certainly provides valuable time for diagnosis and preparation of intervention in ruptured SAA and, thus, explains the low mortality rate observed in our series.
THE AMERICAN JOURNAL OF SURGERY® VOLUME 175 JUNE 1998
467
TRUE ANEURYSMS OF THE SPLENIC ARTERY/DE PERROT ET AL
Ruptures of SAA into a viscus,14 the Wirsung duct,15 or the splenic vein creating an arteriovenous fistula3 have been described, but are mainly the result of pseudoaneurysms.16,17 Distinction between true aneurysms and pseudoaneurysms of the splenic artery is important. Pseudoaneurysms are more common in men and result from the destruction of the whole arterial wall by chronic pancreatitis, septic emboli (mycotic aneurysm), or arteritis. They are extremely fragile and often cause intermittent and repetitive bleeding rather than massive hemorrhage.5,6 Surgery or transcatheter embolization is always recommended. Preoperative investigations for ruptured SAA should be performed if the patient condition remains sufficiently stable. US or CT of the abdomen may confirm an intraperitoneal hemorrhage and localize the aneurysm. However, angiography still remains the most valuable investigative modality to precisely localize the source of bleeding and assess the collateral flow. In our series, 3 patients underwent preoperative angiography. In these patients, the hemorrhage was rapidly controlled by dividing the gastrosplenic ligament and reaching the splenic artery through the lesser sac, whereas in the remaining 4 patients cross-clamping of the aorta was required for 15 to 60 minutes. Although elective resection of SAA should aim at preserving the spleen whenever possible,18 once rupture has occurred, this is rarely possible.11 In our experience, the spleen had to be resected in all cases. The choice of operation, however, is determined by location of the aneurysm. When located at splenic hilum or in the distal third of the splenic artery, the aneurysm is resected with either the spleen or the spleen and left pancreas. Alternatively, when it is located in the middle third of the splenic artery, proximal and distal ligation of the splenic artery may be attempted. The extensive short gastric vessels will then most of the time prevent an infarction of the retained spleen. This is, however, not always the case, as illustrated by our patient requiring a subsequent splenectomy. Aneurysms located in the proximal third of the splenic artery can be removed without resecting the pancreas and/or spleen, providing that the short gastric vessels are also present and sufficient.18 Transcatheter arterial embolization has not been performed in this series. This technique is not relevant for rupture of true aneurysms of the splenic artery, since the hemorrhage may be rapidly and safely controlled by surgery. In conclusion, we report 8 cases of true SAA that ruptured over a 20-year period. All aneurysms were sized 2 cm
468
or larger. Six patients were known for systemic hypertension, 4 were older than 60 years of age, and 1 was at 32 weeks of gestation when rupture occurred. All patients presented with rupture as the first sign of SAA. Seven of the 8 patients survived after immediate resuscitation and aggressive surgical approach.
REFERENCES 1. Trastek VF, Pairolero PC, Joyce JW, et al. Splenic artery aneurysms. Surgery. 1982;91:694 – 699. 2. Stanley JC, Fry WJ. Pathogenesis and clinical significance of splenic artery aneurysms. Surgery. 1974;76:898 –909. 3. De Vries JE, Schattenkerk ME, Malt RA. Complications of splenic artery aneurysm other than intraperitoneal rupture. Surgery. 1982;91:200 –204. 4. Mattar SG, Lumsden AB. The management of splenic artery aneurysms: experience with 23 cases. Am J Surg. 1995;169:580 – 584. 5. Woods MS, Traverso LW, Kozarek RA, et al. Successful treatment of bleeding pseudoaneurysms of chronic pancreatitis. Pancreas. 1995;10:22–30. 6. El Hamel A, Parc R, Ada G, et al. Bleeding pseudocysts and pseudoaneurysms in chronic pancreatitis. Br J Surg. 1991;78:1059 – 1063. 7. Babb RR. Aneurysm of the splenic artery. Arch Surg. 1976;111: 924 –925. 8. Jones EL, Finney GG Jr. Splenic artery aneurysms, a reappraisal. Arch Surg. 1968;97:640 – 647. 9. Bedford PD, Lodge B. Aneurysm of the splenic artery. Gut. 1960;1:312–320. 10. Caillouette JC, Merchant EB. Ruptured splenic artery aneurysm in pregnancy, twelfth reported case with maternal and fetal survival. Am J Obstet Gynecol. 1993;168:1810 –1813. 11. Holdsworth RJ, Gunn A. Ruptured splenic artery aneurysm in pregnancy. A review. Br J Obstet Gynecol. 1992;99:595–597. 12. Ayalon A, Wiesner RH, Perkins JD, et al. Splenic artery aneurysms in liver transplant patients. Transplantation. 1988;45: 386 –389. 13. Salo JA, Salmenkivi K, Tenhunen A, Kivilaakso EO. Rupture of splanchnic artery aneurysms. World J Surg. 1986;10:123–127. 14. Owens JC, Coffey RJ. Aneurysm of the splenic artery, including a report of 6 additional cases. Int Abstr Surg. 1953;97:313–335. 15. Camishion RC, Pello MJ, Spence RK, et al. Hemoductal pancreatitis. Surgery. 1992;111:86 – 89. 16. Cahow CE, Gusberg RJ, Gottlieb LJ. Gastrointestinal hemorrhage from pseudoaneurysms in pancreatic pseudocysts. Am J Surg. 1983;145:534 –541. 17. Clay RP, Farnell MB, Lancaster JR, et al. Hemosuccus pancreaticus. An unusual cause of upper gastrointestinal bleeding. Ann Surg. 1985;202:75–79. 18. Trastek VF, Pairolero PC, Bernatz PE. Splenic artery aneurysms. World J Surg. 1985;9:378 –383.
THE AMERICAN JOURNAL OF SURGERY® VOLUME 175 JUNE 1998
BACKGROUND: Splenic artery aneurysms (SAA) are detected with increasing frequency but their management still remains controversial. This paper relates our experience in the outcome and management of ruptured aneurysms of the splenic artery. METHODS: Between 1977 and 1996, 8 patients presented to our institution with a ruptured SAA. Their ages ranged from 25 to 72 years (mean 55 ys). RESULTS: All patients presented with rupture as the first sign of SAA. One patient was at 32 weeks of gestation and rupture suggested placental abruption. Three patients required cardiopulmonary reanimation prior to surgical procedures. Splenopancreatectomy (n 5 4), splenectomy (n 5 2), and ligation of the splenic artery (n 5 1) were performed. Seven of the 8 patients survived. Size of aneurysms ranged from 2 cm to 3.5 cm (mean 3 cm). CONCLUSIONS: SAA may rupture at any age. Diagnosis during pregnancy rests upon a high index of suspicion. The mortality rate remains low if immediate resuscitation is performed and an aggressive surgical approach is taken. Am J Surg. 1998;175:466 – 468. © 1998 by Excerpta Medica, Inc.
T
he splenic artery is the third most common site of intraabdominal aneurysm formation after the abdominal aorta and iliac arteries.1 They are of particular interest, because, in contrast to aneurysms of large vessels, atherosclerosis is rarely the primary causative factor.1,2 Development of splenic artery aneurysms (SAA) generally result from a degeneration of the media, and they are frequently associated with multiparity or portal hypertension.1,3 Etiologic mechanisms remain uncertain, but considerable evidence exists to implicate hormonal and local hemodynamic events in the evolution of most of these aneurysms.2 Although rupture is the main complication with massive intraperitoneal hemorrhage, their management still remains controversial.1,3,4
From the Departments of Surgery (MD, LB, JD, GM, PM) and Pathology (BB), University Hospital of Geneva, Geneva, Switzerland. Requests for reprints should be addressed to Marc de Perrot, MD, Department of Surgery, University Hospital of Geneva, 1211 Geneva 14, Switzerland. Manuscript submitted August 1, 1997 and accepted in revised form January 12, 1998.
466
© 1998 by Excerpta Medica, Inc. All rights reserved.
In order to better determine the outcome and management of these aneurysms, we report 8 cases of ruptured SAA that occurred during the past 20 years at our institution. Since the clinical course of aneurysms and pseudoaneurysms of the splenic artery is different, the latter being mostly associated with chronic pancreatitis, they were excluded from our study.5,6
PATIENTS AND METHODS All patients who presented with spontaneous rupture of a true SAA at the University Hospital of Geneva between 1977 and 1996 were reviewed. We collected 8 cases. There were 5 male and 3 female patients. Their ages ranged between 25 and 72 years (mean 55 ys), 4 patients being older than 60 years. Six patients were known for systemic hypertension and 4 for atherosclerotic disease. Parity among women ranged from 0 to 3. None of these patients were known to have SAA prior to rupture, and none of them suffered from portal hypertension, nor from thrombosis of the splenic vein. These patients were analyzed with regard to the mode of presentation, preoperative investigations, treatment, and outcome. Location and size of SAA are also reported.
RESULTS All patients presented with rupture as the first sign of SAA. Mode of presentation was acute, diffuse abdominal pain, excruciating into the back in 3 patients. In 1 case only, the pain was typically located in the left hypochondrium. No abdominal mass was palpated on physical examination. Symptomatology had lasted between 6 and 96 hours (mean 14 hours) prior to the occurrence of cardiovascular collapse. Preoperative investigations included abdominal ultrasonography (US) in 6 patients, computed tomography (CT) in 3 patients, and angiography in 3 patients. One patient (gravida 3, para 1) presented at 32 weeks of gestation with sudden onset of low abdominal pain and short episodes of hypotension suggesting placental abruption. She underwent a caesarean operation in emergency; the fetus was dead, and no intraabdominal bleeding was observed. Twelve hours later massive intraperitoneal hemorrhage required a new emergency laparotomy and a ruptured SAA was diagnosed. Management consisted in volemic resuscitation and emergency laparotomy. Three patients required cardiopulmonary reanimation, of whom 1 died prior to surgery. The diagnosis in this patient was eventually made at necropsy only. Surgical procedures were left splenopancreatectomy in 4 cases and resection of the SAA with splenectomy in 2 cases. In 1 case, proximal and distal ligation of the splenic artery was possible, but splenectomy was also required 0002-9610/98/$19.00 PII S0002-9610(98)00082-8
TRUE ANEURYSMS OF THE SPLENIC ARTERY/DE PERROT ET AL
TABLE Risk Factors Associated with Rupture of Splenic Artery Aneurysms Pregnancy Expanding aneurysms Symptomatic aneurysms Aneurysms of 2 cm or larger Portal hypertension with liver transplantation or portocaval shunt
Figure. Angiography of a ruptured splenic artery aneurysm.
because of failure of good persistent vascularization of the spleen through the short gastric vessels. All 4 patients who had not undergone preoperative angiography required cross-clamping of the aorta for 15 to 60 minutes at the beginning of the surgical procedures. A mean of 11 (10 to 14) blood transfusions was administered. All patients had an unique aneurysm of the splenic artery, located along the middle third of splenic artery in 2 patients, along the distal third of splenic artery in 5 patients, and at the splenic hilum in 1 patient. The size of aneurysms ranged from 2 cm to 3.5 cm (mean 3 cm). The Figure shows angiography of a ruptured SAA. Histologic examination of the splenic artery showed atherosclerosis in 4 patients. Congenital origin was suspected in 1 young patient without other risk factors. All patients who could be operated upon survived (n 5 7). Postoperative complications occurred in 3 patients and included multiple organ failure, bronchopneumonia, and postanoxic encephalopathy. The 2 former patients eventually became well, but the latter remained severely disabled.
COMMENTS Since the first report of SAA made by Beaussier at necropsy in 1770, large routine necropsy series have reported an incidence of SAA ranging from 0.01% to 0.2%.7 At the University Hospital of Geneva, out of 16,081 necropsies performed between 1977 and 1992, 5 SAA were found (incidence of 0.031%). Four of them were asymptomatic, whereas 1 had ruptured and was the cause of death. Higher incidence has been reported in selected groups of patients, such as in hypertensive patients (1%)8 and in series performed with pathologists paying special attention to the splenic artery (10.4%).9 The pathogenesis of SAA is not fully understood, but multiparity and portal hypertension seem to promote aneurysmal dilatation.1,3 Atherosclerotic changes, however, although observed in up to 99% of the splenic aneurysms
examined histologically,1 are most likely secondary events resulting from a primary degeneration of the media.4 The true incidence of rupture of SAA is difficult to ascertain, as it varies with the number of asymptomatic aneurysms incidentally detected during radiologic investigations or surgical exploration. Recently, Trastek et al1 who reported the largest clinical trial found 3 ruptures out of 100 documented SAA. Several factors have been associated with an increased risk of rupture (Table).4 Pregnancy has been associated with more than 100 cases of ruptured SAA, thus comprising approximately one fourth of all cases.10 Hemorrhage occurred during the third trimester of pregnancy in 69% of these patients and was often misdiagnosed as placental abruption or uterine rupture.11 The maternal and fetal mortality rate were as high as 75% and 95%, respectively.11 A high flow rate through the splenic artery due to compression of the aorta and iliac arteries by the pregnant uterus and relative portal congestion are important pathogenic factors.11 Similar increase in splenic blood flow occurs in patients with liver disease and portal hypertension who undergo orthotopic liver transplantation or end-toside portocaval shunt.12 When no pregnancy is planned or portal hypertension detected, indications to treat SAA are based on characteristics of the aneurysms and the patient’s age.4 A general consensus holds that growing or symptomatic aneurysms should be resected. However, controversy still remains with stable and asymptomatic SAA. In our experience and that of others,1,3,4,13 ruptures have occurred almost exclusively in aneurysms of 2 cm or larger. Hence, small, asymptomatic SAA may be observed, whereas those of 2 cm or larger must be treated. Advanced age, particularly if associated with systemic hypertension, should not preclude surgery. In our series, 6 patients had systemic hypertension and 4 were older than 60 years of age. Rupture may initially tamponade into the lesser omental sac and entail sudden onset of acute abdominal pain with short episodes of hypotension. Free intraperitoneal hemorrhage with cardiovascular collapse ensued 6 to 96 hours after the onset of symptoms in our patients. This “double rupture phenomenon” was well demonstrated in our pregnant patient who underwent a ceaserian operation for abdominal pain and episodes of hypotension suggesting placental abruption. No signs of peritoneal bleeding could be seen at that time. Twelve hours later, however, a second laparotomy was required because of massive free intraperitoneal bleeding. The “sentinel rupture” certainly provides valuable time for diagnosis and preparation of intervention in ruptured SAA and, thus, explains the low mortality rate observed in our series.
THE AMERICAN JOURNAL OF SURGERY® VOLUME 175 JUNE 1998
467
TRUE ANEURYSMS OF THE SPLENIC ARTERY/DE PERROT ET AL
Ruptures of SAA into a viscus,14 the Wirsung duct,15 or the splenic vein creating an arteriovenous fistula3 have been described, but are mainly the result of pseudoaneurysms.16,17 Distinction between true aneurysms and pseudoaneurysms of the splenic artery is important. Pseudoaneurysms are more common in men and result from the destruction of the whole arterial wall by chronic pancreatitis, septic emboli (mycotic aneurysm), or arteritis. They are extremely fragile and often cause intermittent and repetitive bleeding rather than massive hemorrhage.5,6 Surgery or transcatheter embolization is always recommended. Preoperative investigations for ruptured SAA should be performed if the patient condition remains sufficiently stable. US or CT of the abdomen may confirm an intraperitoneal hemorrhage and localize the aneurysm. However, angiography still remains the most valuable investigative modality to precisely localize the source of bleeding and assess the collateral flow. In our series, 3 patients underwent preoperative angiography. In these patients, the hemorrhage was rapidly controlled by dividing the gastrosplenic ligament and reaching the splenic artery through the lesser sac, whereas in the remaining 4 patients cross-clamping of the aorta was required for 15 to 60 minutes. Although elective resection of SAA should aim at preserving the spleen whenever possible,18 once rupture has occurred, this is rarely possible.11 In our experience, the spleen had to be resected in all cases. The choice of operation, however, is determined by location of the aneurysm. When located at splenic hilum or in the distal third of the splenic artery, the aneurysm is resected with either the spleen or the spleen and left pancreas. Alternatively, when it is located in the middle third of the splenic artery, proximal and distal ligation of the splenic artery may be attempted. The extensive short gastric vessels will then most of the time prevent an infarction of the retained spleen. This is, however, not always the case, as illustrated by our patient requiring a subsequent splenectomy. Aneurysms located in the proximal third of the splenic artery can be removed without resecting the pancreas and/or spleen, providing that the short gastric vessels are also present and sufficient.18 Transcatheter arterial embolization has not been performed in this series. This technique is not relevant for rupture of true aneurysms of the splenic artery, since the hemorrhage may be rapidly and safely controlled by surgery. In conclusion, we report 8 cases of true SAA that ruptured over a 20-year period. All aneurysms were sized 2 cm
468
or larger. Six patients were known for systemic hypertension, 4 were older than 60 years of age, and 1 was at 32 weeks of gestation when rupture occurred. All patients presented with rupture as the first sign of SAA. Seven of the 8 patients survived after immediate resuscitation and aggressive surgical approach.
REFERENCES 1. Trastek VF, Pairolero PC, Joyce JW, et al. Splenic artery aneurysms. Surgery. 1982;91:694 – 699. 2. Stanley JC, Fry WJ. Pathogenesis and clinical significance of splenic artery aneurysms. Surgery. 1974;76:898 –909. 3. De Vries JE, Schattenkerk ME, Malt RA. Complications of splenic artery aneurysm other than intraperitoneal rupture. Surgery. 1982;91:200 –204. 4. Mattar SG, Lumsden AB. The management of splenic artery aneurysms: experience with 23 cases. Am J Surg. 1995;169:580 – 584. 5. Woods MS, Traverso LW, Kozarek RA, et al. Successful treatment of bleeding pseudoaneurysms of chronic pancreatitis. Pancreas. 1995;10:22–30. 6. El Hamel A, Parc R, Ada G, et al. Bleeding pseudocysts and pseudoaneurysms in chronic pancreatitis. Br J Surg. 1991;78:1059 – 1063. 7. Babb RR. Aneurysm of the splenic artery. Arch Surg. 1976;111: 924 –925. 8. Jones EL, Finney GG Jr. Splenic artery aneurysms, a reappraisal. Arch Surg. 1968;97:640 – 647. 9. Bedford PD, Lodge B. Aneurysm of the splenic artery. Gut. 1960;1:312–320. 10. Caillouette JC, Merchant EB. Ruptured splenic artery aneurysm in pregnancy, twelfth reported case with maternal and fetal survival. Am J Obstet Gynecol. 1993;168:1810 –1813. 11. Holdsworth RJ, Gunn A. Ruptured splenic artery aneurysm in pregnancy. A review. Br J Obstet Gynecol. 1992;99:595–597. 12. Ayalon A, Wiesner RH, Perkins JD, et al. Splenic artery aneurysms in liver transplant patients. Transplantation. 1988;45: 386 –389. 13. Salo JA, Salmenkivi K, Tenhunen A, Kivilaakso EO. Rupture of splanchnic artery aneurysms. World J Surg. 1986;10:123–127. 14. Owens JC, Coffey RJ. Aneurysm of the splenic artery, including a report of 6 additional cases. Int Abstr Surg. 1953;97:313–335. 15. Camishion RC, Pello MJ, Spence RK, et al. Hemoductal pancreatitis. Surgery. 1992;111:86 – 89. 16. Cahow CE, Gusberg RJ, Gottlieb LJ. Gastrointestinal hemorrhage from pseudoaneurysms in pancreatic pseudocysts. Am J Surg. 1983;145:534 –541. 17. Clay RP, Farnell MB, Lancaster JR, et al. Hemosuccus pancreaticus. An unusual cause of upper gastrointestinal bleeding. Ann Surg. 1985;202:75–79. 18. Trastek VF, Pairolero PC, Bernatz PE. Splenic artery aneurysms. World J Surg. 1985;9:378 –383.
THE AMERICAN JOURNAL OF SURGERY® VOLUME 175 JUNE 1998