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Aortic pseudoaneurysm secondary to pancreatitis
Aortic pseudoaneurysm secondary to pancreatitis Rebecca A. Giles, MD, and William C. Pevec, MD, Sacramento, Calif A patient with a pseudoaneurysm of the distal abdominal aorta, which developed as the result of complicated gallstone pancreatitis, is reported. The aorta was bypassed with an axillofemoral-femorofemoral graft; the pseudoaneurysm was resected, and the infrarenal aorta was oversewn. The patient survived a complicated postoperative course and was discharged with well-perfused lower extremities. No previous description of a pseudoaneurysm of the aorta as a complication of pancreatitis was found on review of the literature. (J Vasc Surg 2000;31:1056-9.)
Most pseudoaneurysms that result from pancreatitis arise in peripancreatic arteries. This case report describes a pseudoaneurysm of the infrarenal aorta that developed as the result of gallstone pancreatitis. Extra-anatomic bypass grafting was considered appropriate because of the possibility of infection of the pseudoaneurysm and the potential for ongoing inflammation and autodigestion. CASE REPORT A 40-year-old woman with gallstone pancreatitis was seen in early January 1998 at the referring hospital. Her condition responded initially to conservative therapy, and she was discharged without undergoing cholecycstectomy. She returned a few weeks later with right upper quadrant abdominal pain, nausea, and vomiting. On January 20, 1998, an abdominal computed tomography (CT) scan demonstrated multiple fluid collections in the retroperitoneum adjacent to the pancreas and aorta (Fig 1). On February 9, 1998, ultrasound and CT scans showed resolution of the pseudocysts but also showed a new, large multiloculated infrarenal aortic pseudoaneurysm (Fig 2). On February 10, 1998, she was transferred to this hospital for further evaluation and treatment. On arrival, she was afebrile, and her condition was hemodynamically stable. Her abdomen was diffusely tender without guarding, masses, or organomegaly. Her pulse examination, which included the carotid, radial, femoral, popliteal, and dorsalis pedis pulses, was normal bilaterally. Laboratory results included an alkaline phosphatase level From the Division of Vascular Surgery, University of California Davis Medical Center. Competition of interest: nil. Reprint requests: Dr William C. Pevec, Division of Vascular Surgery, UC Davis Medical Center, 4301 X St, 2310 Professional Building, Sacramento, CA 95817. Copyright © 2000 by the Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter. 0741-5214/2000/$12.00 + 0 24/4/102850 doi:10.1067/mva.2000.102850
1056
of 303 U/L, a gamma-glutamyl transferase level of 337 U/L, and an amylase level of 98 U/L. Coagulation studies were normal. Her leukocyte count was significantly elevated at 39,000. An aortogram was obtained to evaluate the pseudoaneurysm. The study demonstrated a large pseudoaneurysm at the L4 level, in the left lateral wall of the distal abdominal aorta. It extended posteriorly and inferiorly, compressing the lumen of the aorta and the lumen of the left common iliac artery. Femoral runoff was normal (Fig 3). The pseudoaneurysm was believed to have developed as the result of pancreatitis, and the aorta was presumed to be infected. Thus extra-anatomic bypass grafting and resection of the distal abdominal aorta were performed. The axillary and femoral arteries were of very small caliber. The left axillofemoral-femorofemoral artery bypass graft was constructed with the use of externally supported 6-mm polytetrafluoroethylene. The femoral anastomoses were placed end-to-side to the bifurcations of the common femoral arteries. The wounds were closed and covered with sterile, occlusive dressings. An existing midline scar was used to gain access to the peritoneal cavity. Dense adhesions were encountered from prior laparotomies. The bowel was friable, and a small enterotomy was repaired without gross contamination. Because of the severe adhesions, an extensive exploration was not performed. The aorta was approached through a right medial visceral rotation, including an extensive Kocher maneuver and mobilization of the right colon and small intestine. The duodenum and pancreas were without lesions, and there was no active pancreatitis. There was severe, periaortic inflammation, but there were no pseudocysts in the retroperitoneum. Heparin was administered, and the infrarenal aorta was clamped before the distal aorta was dissected at the level of the false aneurysm and iliac arteries. After the iliac arteries were clamped, the aorta was opened and several large lumbar arteries were oversewn. There was a smooth, oval-shaped hole in the left lateral aspect of the distal aorta, which measured 4 cm in length and 1 cm in width, and involved 180 degrees of the circumference of the aorta. Organized thrombus
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Giles and Pevec
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Fig 1. Computed tomographic scan shows multiple retroperitoneal fluid collections adjacent to the pancreas.
Fig 2. Computed tomographic scan reveals a large, multiloculated infrarenal aortic pseudoaneurysm. formed the wall of the false aneurysm. This thrombus and some of the surrounding inflammatory tissue were sent for Gram stain and culture. No aortic tissue was sent for histopathologic examination. The infrarenal aorta and common iliac arteries were oversewn in two layers. The pseudoaneurysm was debrided. Because there were no associated fluid collections, a drain was not used. Retrograde pulses were palpable in both common iliac arteries. With the aortic resection complete, cholecystec-
tomy was performed. Histologic examination showed chronic cholecystitis with multiple small gallstones. The patient tolerated the procedure well, with an easily palpable dorsalis pedis pulse on the left after the operation. No distal pulses were palpable on the right, but the feet were symmetrically warm. A few hours after the operation, the patient was noted to have a mottled right lower extremity. Occlusion of the femorofemoral graft was likely the result of a thrombus
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1058 Giles and Pevec
Fig 3. Aortogram shows a large aortic pseudoaneurysm at L4. Femoral runoff is normal. that developed during the operation, while there was competitive aortoiliac flow, and progressed as the effects of the heparin wore off. The patient was given a bolus of heparin and taken urgently to the operating room for thrombectomy of the left femoral to right femoral artery bypass graft. No technical defects were found, and normal perfusion of the right lower extremity was restored. The patient required large amounts of fluid in the operating room and in the immediate postoperative period. Over the next 2 days anasarca developed, and ventilation became increasingly difficult. The abdomen was opened at the bedside, and ventilation improved significantly. The edema resolved quickly, allowing primary abdominal closure on February 16, 1998. She remained afebrile, and both blood and pseudoaneurysm cultures were negative. After 4 weeks, she was transferred back to the referring hospital and was subsequently discharged in good condition. The patient returned to the referring hospital in June 1998 with anorexia, weight loss, and dehydration. The axillofemoral-femorofemoral grafts were occluded. The operating surgeon believed the thrombus to be the result of a gradient across the 6-mm axillofemoral graft and hypercoagulability as a result of dehydration. The axillofemoral graft was replaced with an 8-mm externally supported polytetrafluoroethylene graft, and a thrombectomy was performed on the femorofemoral graft. The patient was discharged on warfarin (Coumadin) therapy with a patent graft. At 17 months after the original operation, the patient
is alive and gaining weight. A recurrent pancreatic pseudocyst is being followed. The left axillofemoral graft is patent, but the femorofemoral graft is occluded. The right femoral arteries reconstitute by way of well-developed pelvic collaterals, and the patient tolerates mild right lower extremity claudication. The patient remains on Coumadin therapy.
DISCUSSION Formation of arterial pseudoaneurysms is not an uncommon complication of pancreatitis, occurring in 7% to 31% of all cases.1 The proposed mechanism of vascular injury involves the release of proteolytic pancreatic enzymes, particularly trypsin and elastase, into the perivascular space with subsequent enzymatic digestion of the arterial wall.2-4 This autodigestion may then weaken the vessel wall sufficiently to allow aneurysmal changes to occur.5 Acute hemorrhage from peripancreatic pseudoaneurysms is the most rapidly fatal complication of chronic pancreatitis, with mortality rates ranging from 12% to 50% despite aggressive surgical management.6-8 Any vessel in continuity with a collection of pancreatic fluid may be affected, but an extensive review of the literature suggests aortic involvement occurs rarely if at all. Peripancreatic arteries are most frequently involved, including the splenic artery (the most common site) and the left gastric, hepatic, gas-
JOURNAL OF VASCULAR SURGERY Volume 31, Number 5
troduodenal, and pancreaticoduodenal arteries.9-11 The largest retrospective study of arterial complications of pancreatitis to date confirms these findings and reports the rare but documented involvement of more distal arteries (eg, superior mesenteric, jejunal, ileocecal). However, none of the 104 cases reviewed involved the aorta.12 Extrapancreatic fluid collections have also been shown to dissect the wall of the abdominal aorta during acute pancreatitis, but none of the cases reported has been associated with aneurysm formation.13 A thorough search of the literature fails to explain the reason that the aorta seems less susceptible to autodigestion by pancreatic enzymes than other peripancreatic vessels. Repair of pseudoaneurysms that arise in peripancreatic arteries is commonly achieved by transcatheter embolization, which, given the location and extent of the aneurysm in this patient, was not an option.14 In this case, extra-anatomic bypass grafting was considered appropriate because of the possibility of infection at the pseudocyst/pseudoaneurysm and the potential for ongoing inflammation and autodigestion of an in situ graft.15 Although in situ repair was not undertaken, the patient is a relatively young woman who may well tolerate an in situ revision in the future, once the abdominal inflammatory process has resolved.
Giles and Pevec
4.
5.
6.
7.
8. 9.
10.
11. 12.
13. 14.
REFERENCES 1. Marshall GT, Howell DA, Hansen BL, Amberson SM, Abourjaily GS, Bredenberg CE. Multidisciplinary approach to pseudoaneurysms complicating pancreatic pseudocysts. Arch Surg 1996;131 278-82. 2. Geokas, MC. The role of elastase in acute pancreatitis. Arch Pathol 1968;86:135-41. 3. Halpern VJ, Nackman GB, Gandhi RH, Irizarry E, Scholes
15.
1059
JV, Ramey WG, et al. The elastase infusion model of experimental aortic aneurysms: synchrony of induction of endogenous proteinases with matrix destruction and inflammatory cell response. J Vasc Surg 1994;20:51-60. Stanley JC, Frey CF, Miller TA, Lindenauer SM, Child CG. Major arterial hemorrhage: a complication of pancreatic pseudocysts and chronic pancreatitis. Arch Surg 1976;111:435-40. Bresler L, Boissel P, Grosdidier J. Major hemorrhage from pseudocysts and pseudoaneurysms caused by chronic pancreatitis: surgical therapy. World J Surg 1991;15: 649-53. Waltman AC, Luers PR, Athanasoulis CA, Warshaw AL. Massive arterial hemorrhage in patients with pancreatitis. Arch Surg 1986;121:439-43. Hamel AE, Parc R, Adda G, Bouteloup PY, Huguet C, Malafosse M. Bleeding pseudocysts and pseudoaneurysms in chronic pancreatitis. Br J Surg 1991;78:1059-63. Gadacz TR, Trunkey D, Kieffe, RF. Visceral vessel erosion associated with pancreatitis. Arch Surg 1978;113:1438-40. Abbott GT, McDermott VG, Smith TP. Successful endovascular treatment of a celiac artery pseudoaneurysm complicating pancreatitis. J Vasc Interv Radiol 1996;7:103-6. Burke JW, Erickson SJ, Kellum CD, Tegtmeyer CJ, Williamson BRJ, Hansen MF. Pseudoaneurysms complicating pancreatitis: detection by CT. Radiology 1996;161:447-50. White AF, Baum S, Buranasiri S. Aneurysms secondary to pancreatitis. Am J Roentgenol 1976;127:393-6. Boudghene F, L’Hermine C, Bigot JM. Arterial complications of pancreatitis: diagnostic and therapeutic aspects in 104 cases. J Vasc Interv Radiol 1993;4:551-8. Goff WB, Lawrence DP, Burkhard TK. Aortic dissection in acute pancreatitis. J Am Osteopath Assoc 1992;92:921-3. Savastano S, Feltrin GP, Antonio T, Miotto D, ChiesuraCorona M, Castellan L. Arterial complications of pancreatitis: diagnostic and therapeutic role of radiology. Pancreas 1993;8:687-92. Blaisdell, FW, Pevec, WC. Extra-anatomic bypass grafting. In: Dean RH, Yao JT, Brewster DC, editors. Current diagnosis and treatment in vascular surgery. 1st ed. Norwalk (CT): Appleton and Lange; 1995. p. 325-31.
Submitted Mar 22, 1999; accepted Aug 26, 1999.
Most pseudoaneurysms that result from pancreatitis arise in peripancreatic arteries. This case report describes a pseudoaneurysm of the infrarenal aorta that developed as the result of gallstone pancreatitis. Extra-anatomic bypass grafting was considered appropriate because of the possibility of infection of the pseudoaneurysm and the potential for ongoing inflammation and autodigestion. CASE REPORT A 40-year-old woman with gallstone pancreatitis was seen in early January 1998 at the referring hospital. Her condition responded initially to conservative therapy, and she was discharged without undergoing cholecycstectomy. She returned a few weeks later with right upper quadrant abdominal pain, nausea, and vomiting. On January 20, 1998, an abdominal computed tomography (CT) scan demonstrated multiple fluid collections in the retroperitoneum adjacent to the pancreas and aorta (Fig 1). On February 9, 1998, ultrasound and CT scans showed resolution of the pseudocysts but also showed a new, large multiloculated infrarenal aortic pseudoaneurysm (Fig 2). On February 10, 1998, she was transferred to this hospital for further evaluation and treatment. On arrival, she was afebrile, and her condition was hemodynamically stable. Her abdomen was diffusely tender without guarding, masses, or organomegaly. Her pulse examination, which included the carotid, radial, femoral, popliteal, and dorsalis pedis pulses, was normal bilaterally. Laboratory results included an alkaline phosphatase level From the Division of Vascular Surgery, University of California Davis Medical Center. Competition of interest: nil. Reprint requests: Dr William C. Pevec, Division of Vascular Surgery, UC Davis Medical Center, 4301 X St, 2310 Professional Building, Sacramento, CA 95817. Copyright © 2000 by the Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter. 0741-5214/2000/$12.00 + 0 24/4/102850 doi:10.1067/mva.2000.102850
1056
of 303 U/L, a gamma-glutamyl transferase level of 337 U/L, and an amylase level of 98 U/L. Coagulation studies were normal. Her leukocyte count was significantly elevated at 39,000. An aortogram was obtained to evaluate the pseudoaneurysm. The study demonstrated a large pseudoaneurysm at the L4 level, in the left lateral wall of the distal abdominal aorta. It extended posteriorly and inferiorly, compressing the lumen of the aorta and the lumen of the left common iliac artery. Femoral runoff was normal (Fig 3). The pseudoaneurysm was believed to have developed as the result of pancreatitis, and the aorta was presumed to be infected. Thus extra-anatomic bypass grafting and resection of the distal abdominal aorta were performed. The axillary and femoral arteries were of very small caliber. The left axillofemoral-femorofemoral artery bypass graft was constructed with the use of externally supported 6-mm polytetrafluoroethylene. The femoral anastomoses were placed end-to-side to the bifurcations of the common femoral arteries. The wounds were closed and covered with sterile, occlusive dressings. An existing midline scar was used to gain access to the peritoneal cavity. Dense adhesions were encountered from prior laparotomies. The bowel was friable, and a small enterotomy was repaired without gross contamination. Because of the severe adhesions, an extensive exploration was not performed. The aorta was approached through a right medial visceral rotation, including an extensive Kocher maneuver and mobilization of the right colon and small intestine. The duodenum and pancreas were without lesions, and there was no active pancreatitis. There was severe, periaortic inflammation, but there were no pseudocysts in the retroperitoneum. Heparin was administered, and the infrarenal aorta was clamped before the distal aorta was dissected at the level of the false aneurysm and iliac arteries. After the iliac arteries were clamped, the aorta was opened and several large lumbar arteries were oversewn. There was a smooth, oval-shaped hole in the left lateral aspect of the distal aorta, which measured 4 cm in length and 1 cm in width, and involved 180 degrees of the circumference of the aorta. Organized thrombus
JOURNAL OF VASCULAR SURGERY Volume 31, Number 5
Giles and Pevec
1057
Fig 1. Computed tomographic scan shows multiple retroperitoneal fluid collections adjacent to the pancreas.
Fig 2. Computed tomographic scan reveals a large, multiloculated infrarenal aortic pseudoaneurysm. formed the wall of the false aneurysm. This thrombus and some of the surrounding inflammatory tissue were sent for Gram stain and culture. No aortic tissue was sent for histopathologic examination. The infrarenal aorta and common iliac arteries were oversewn in two layers. The pseudoaneurysm was debrided. Because there were no associated fluid collections, a drain was not used. Retrograde pulses were palpable in both common iliac arteries. With the aortic resection complete, cholecystec-
tomy was performed. Histologic examination showed chronic cholecystitis with multiple small gallstones. The patient tolerated the procedure well, with an easily palpable dorsalis pedis pulse on the left after the operation. No distal pulses were palpable on the right, but the feet were symmetrically warm. A few hours after the operation, the patient was noted to have a mottled right lower extremity. Occlusion of the femorofemoral graft was likely the result of a thrombus
JOURNAL OF VASCULAR SURGERY May 2000
1058 Giles and Pevec
Fig 3. Aortogram shows a large aortic pseudoaneurysm at L4. Femoral runoff is normal. that developed during the operation, while there was competitive aortoiliac flow, and progressed as the effects of the heparin wore off. The patient was given a bolus of heparin and taken urgently to the operating room for thrombectomy of the left femoral to right femoral artery bypass graft. No technical defects were found, and normal perfusion of the right lower extremity was restored. The patient required large amounts of fluid in the operating room and in the immediate postoperative period. Over the next 2 days anasarca developed, and ventilation became increasingly difficult. The abdomen was opened at the bedside, and ventilation improved significantly. The edema resolved quickly, allowing primary abdominal closure on February 16, 1998. She remained afebrile, and both blood and pseudoaneurysm cultures were negative. After 4 weeks, she was transferred back to the referring hospital and was subsequently discharged in good condition. The patient returned to the referring hospital in June 1998 with anorexia, weight loss, and dehydration. The axillofemoral-femorofemoral grafts were occluded. The operating surgeon believed the thrombus to be the result of a gradient across the 6-mm axillofemoral graft and hypercoagulability as a result of dehydration. The axillofemoral graft was replaced with an 8-mm externally supported polytetrafluoroethylene graft, and a thrombectomy was performed on the femorofemoral graft. The patient was discharged on warfarin (Coumadin) therapy with a patent graft. At 17 months after the original operation, the patient
is alive and gaining weight. A recurrent pancreatic pseudocyst is being followed. The left axillofemoral graft is patent, but the femorofemoral graft is occluded. The right femoral arteries reconstitute by way of well-developed pelvic collaterals, and the patient tolerates mild right lower extremity claudication. The patient remains on Coumadin therapy.
DISCUSSION Formation of arterial pseudoaneurysms is not an uncommon complication of pancreatitis, occurring in 7% to 31% of all cases.1 The proposed mechanism of vascular injury involves the release of proteolytic pancreatic enzymes, particularly trypsin and elastase, into the perivascular space with subsequent enzymatic digestion of the arterial wall.2-4 This autodigestion may then weaken the vessel wall sufficiently to allow aneurysmal changes to occur.5 Acute hemorrhage from peripancreatic pseudoaneurysms is the most rapidly fatal complication of chronic pancreatitis, with mortality rates ranging from 12% to 50% despite aggressive surgical management.6-8 Any vessel in continuity with a collection of pancreatic fluid may be affected, but an extensive review of the literature suggests aortic involvement occurs rarely if at all. Peripancreatic arteries are most frequently involved, including the splenic artery (the most common site) and the left gastric, hepatic, gas-
JOURNAL OF VASCULAR SURGERY Volume 31, Number 5
troduodenal, and pancreaticoduodenal arteries.9-11 The largest retrospective study of arterial complications of pancreatitis to date confirms these findings and reports the rare but documented involvement of more distal arteries (eg, superior mesenteric, jejunal, ileocecal). However, none of the 104 cases reviewed involved the aorta.12 Extrapancreatic fluid collections have also been shown to dissect the wall of the abdominal aorta during acute pancreatitis, but none of the cases reported has been associated with aneurysm formation.13 A thorough search of the literature fails to explain the reason that the aorta seems less susceptible to autodigestion by pancreatic enzymes than other peripancreatic vessels. Repair of pseudoaneurysms that arise in peripancreatic arteries is commonly achieved by transcatheter embolization, which, given the location and extent of the aneurysm in this patient, was not an option.14 In this case, extra-anatomic bypass grafting was considered appropriate because of the possibility of infection at the pseudocyst/pseudoaneurysm and the potential for ongoing inflammation and autodigestion of an in situ graft.15 Although in situ repair was not undertaken, the patient is a relatively young woman who may well tolerate an in situ revision in the future, once the abdominal inflammatory process has resolved.
Giles and Pevec
4.
5.
6.
7.
8. 9.
10.
11. 12.
13. 14.
REFERENCES 1. Marshall GT, Howell DA, Hansen BL, Amberson SM, Abourjaily GS, Bredenberg CE. Multidisciplinary approach to pseudoaneurysms complicating pancreatic pseudocysts. Arch Surg 1996;131 278-82. 2. Geokas, MC. The role of elastase in acute pancreatitis. Arch Pathol 1968;86:135-41. 3. Halpern VJ, Nackman GB, Gandhi RH, Irizarry E, Scholes
15.
1059
JV, Ramey WG, et al. The elastase infusion model of experimental aortic aneurysms: synchrony of induction of endogenous proteinases with matrix destruction and inflammatory cell response. J Vasc Surg 1994;20:51-60. Stanley JC, Frey CF, Miller TA, Lindenauer SM, Child CG. Major arterial hemorrhage: a complication of pancreatic pseudocysts and chronic pancreatitis. Arch Surg 1976;111:435-40. Bresler L, Boissel P, Grosdidier J. Major hemorrhage from pseudocysts and pseudoaneurysms caused by chronic pancreatitis: surgical therapy. World J Surg 1991;15: 649-53. Waltman AC, Luers PR, Athanasoulis CA, Warshaw AL. Massive arterial hemorrhage in patients with pancreatitis. Arch Surg 1986;121:439-43. Hamel AE, Parc R, Adda G, Bouteloup PY, Huguet C, Malafosse M. Bleeding pseudocysts and pseudoaneurysms in chronic pancreatitis. Br J Surg 1991;78:1059-63. Gadacz TR, Trunkey D, Kieffe, RF. Visceral vessel erosion associated with pancreatitis. Arch Surg 1978;113:1438-40. Abbott GT, McDermott VG, Smith TP. Successful endovascular treatment of a celiac artery pseudoaneurysm complicating pancreatitis. J Vasc Interv Radiol 1996;7:103-6. Burke JW, Erickson SJ, Kellum CD, Tegtmeyer CJ, Williamson BRJ, Hansen MF. Pseudoaneurysms complicating pancreatitis: detection by CT. Radiology 1996;161:447-50. White AF, Baum S, Buranasiri S. Aneurysms secondary to pancreatitis. Am J Roentgenol 1976;127:393-6. Boudghene F, L’Hermine C, Bigot JM. Arterial complications of pancreatitis: diagnostic and therapeutic aspects in 104 cases. J Vasc Interv Radiol 1993;4:551-8. Goff WB, Lawrence DP, Burkhard TK. Aortic dissection in acute pancreatitis. J Am Osteopath Assoc 1992;92:921-3. Savastano S, Feltrin GP, Antonio T, Miotto D, ChiesuraCorona M, Castellan L. Arterial complications of pancreatitis: diagnostic and therapeutic role of radiology. Pancreas 1993;8:687-92. Blaisdell, FW, Pevec, WC. Extra-anatomic bypass grafting. In: Dean RH, Yao JT, Brewster DC, editors. Current diagnosis and treatment in vascular surgery. 1st ed. Norwalk (CT): Appleton and Lange; 1995. p. 325-31.
Submitted Mar 22, 1999; accepted Aug 26, 1999.