Acute Visceral Ischemia Secondary to Aortic Graft Occlusion Anthony S. Ward, MS, William P. Joyce, MCh, Basingstoke, United K i n g d o m
This report describes a case of acute visceral ischemia precipitated by aortic graft occlusion. The importance of recognizing and treating visceral artery lesions at the time of aortic reconstruction is emphasized. (Ann Vasc Surg 1990;4:502-505). KEY WORDS: Visceral ischemia; aortic graft occlusion; aortic reconstruction.
Infarction due to mesenteric arterial occlusive disease carries a mortality rate of almost 100% [1,2], and every effort should be made to recognize and correct visceral arteriopathy before infarction supervenes. Surgical attention for the most part has centered on patients with intestinal angina. However, asymptomatic patients with mesenteric occlusive disease may also be at risk. This particularly applies to patients undergoing abdominal aortic surgery for aneurysmal or occlusive disease. Failure to recognize and treat visceral arterial lesions at the time of aortic reconstruction can lead t o fatal postoperative intestinal infarction [3]. A similar train of events was narrowly avoided in the case herein reported which is of interest because of the considerable anesthetic and surgical problems posed during th e reconstruction.
CASE REPORT A 5 1-year-old nondiabetic woman underwent insertion of an aorta-common iliac bifurcation graft for bilateral limb claudication at another hospital. A preoperative arteriogram had revealed occlusive disease at the aortic bifurcation with patent distal vessels. A large gastroduodenal-pancreatic arcade was also evident, but its significance was not appreciated at that time (Fig. 1). The
From the Department of Surgery, Basingstoke District Hospital, Basingstoke, Hampshire, United Kingdom. Reprint requests: Mr. A . S . Ward, M S , FRCS, Consultant Surgeon, Basingstoke District Hospital, Aldermaston Road, Basingstoke, Hampshire, RG24 9NA, United Kingdom.
patient’s symptoms were largely relieved following surgery but she returned five years later with recurrent left lower limb claudication. A repeat arteriogram revealed marked stenosis at the previous left iliac anastomosis and similar but less severe changes on the right. No action was taken. She presented six years later at our institution with sudden onset of painful cold legs. There were no pulses in either leg and it was apparent that the graft had occluded. She subsequently developed diarrhea, abdominal pain and distention with a leukocytosis of 23,0001mm [3]. An urgent arteriogram through a high translumbar approach revealed complete aortic occlusion just below the renal vessels. A large gastroduodenal-pancreatic arcade was again evident with refilling of the distal superior mesenteric bed (Fig. 2). Subsequent lateral films confirmed the presence of a proximal superior mesenteric artery occlusion and additional stenosis of the celiac axis. The inferior mesenteric artery had been previously ligated so that the sole visceral blood supply was through the stenosed celiac axis. In addition the left renal artery was severely narrowed just beyond its origin. At operation on the following day the small bowel and colon were found to be pale and edematous with absent mesenteric pulsation. The stomach and duodenum remained well perfused. The supraceliac aorta was clamped and the aorta transected immediately below the renal vessels. A 14 mm x 7 mm Dacron graft was anastornosed end-to-end to the infrarenal aortic cuff and the supraceliac clamp replaced just distal to the new aortic anastomosis. An 8 mm Dacron side limb was then anastornosed to the common hepatic artery and tunnelled behind the pancreas to join the main aortic prosthesis. Transfer of the aortic clamp to below this side limb restored full flow to the celiac axis. This produced a dramatic effect on the small bowel with brisk hyperemia and swelling of the bowel wall (Fig. 3). A strong pulse was now palpable in the root
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VISCERAL ISCHEMIA A N D AORTIC GRAFT OCCLUSION
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Fig. 3. Massive hyperemia of small bowel. Patient's head is to right of picture. Aortic prosthesis can be seen at bottom right with side limbs to the celiac and superior mesenteric arteries (arrows).
Fig. 1. AP aortogram showing occlusive disease in distal aorta and common Iliac arteries. Large gastroduodenal-pancreatic arcade is arrowed. of the mesentery. Intestinal revascularization resulted in a 3 0 4 0 minute period of cardiovascular instability. Mean systemic arterial pressure dropped to 55 mmHg and pulmonary artery wedge pressure rose from 8 mmHg to 22 mmHg. Serum potassium and acid-base status remained unchanged. Hemodynamic equilibrium was eventually restored after approximately 30 minutes following administration of dopamine (150 ug/min) and rapid infusion of 1.5 liters of blood.
Fig. 2. AP aorto ram shortly after graft occlusion. Aorta is occlude just below renal arteries and large gastroduodenal-pancreatic collateral is evident refilling distal superior mesenteric tree (arrow).
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A 6 mm Dacron graft was then placed between the aortic prosthesis and the superior mesenteric artery, and a similar limb attached to the left renal artery. The limbs of the aortic prosthesis were tunnelled lateral to the old graft and anastomosed to the common femoral-profunda artery in each groin (Fig. 4). The patient made a good postoperative recovery, and an arteriogram prior to discharge revealed patency of all grafts. Five years later she remains alive and well.
DISCUSSION Small bowel ischemia following aortic surgery is rare. Most reports deal with the immediate postoperative period when the complication is invariably fatal [4]. Possible mechanisms include operative interference with the inferior mesenteric artery when this is the major supply of the small bowel, embolization of thrombus from within the aorta, or perioperative hypotension in a patient with previously compensated visceral artery occlusive disease. In the present case, acute intestinal ischemia occurred several years after aortic surgery and was precipitated by aortic graft occlusion. Presumably in this patient the small bowel and colon were supplied partly by the stenosed celiac axis through the gastroduodenal-pancreatic arcade and partly by retrograde flow from the internal iliac arteries. Loss of the latter source of supply at the time of graft occlusion could then have resulted in severe visceral ischemia. This patient came close to sustaining frank intestinal infarction. This near disaster could have been
504
VISCERAL ISCHEMIA AND AORTIC GRAFT OCCLUSION
ANNALS OF VASCULAR SURGERY
ization has been advocated in the past [61, our preference, as with symptomatic cases, is to reconstruct both the celiac and superior mesenteric arteries as a long-term insurance policy against one or other of the grafts failing. Visceral artery reconstruction by bypass grafting adds little to the overall operative procedure and can be easily performed through the same field [7]. More liberal use of these supplementary measures seems justified in an attempt to avoid the lethal consequences of postoperative visceral ischemia. The systemic response to intestinal revascularization observed in this patient is interesting. Circulatory collapse and death have been observed both experimentally and in humans following relief of intestinal ischemia, these effects being variously attributed to volume losses into the reperfused gut, hyperkalemia, acidosis, and release of gut endotoxins [8]. In our patient significant hypotension occurred on gut reperfusion associated with an elevation in pulmonary artery wedge pressure, these changes persisting for 30-40 minutes. Correction was not achieved until inotropic support had been given in addition to vigorous volume replacement. These features clearly suggest an element of myocardial depression. Agents such as oxygen-free radicals and leukotrienes are known to play a central role in ischemia-reperfusion injury at a number of sites [9,10]. The former, in particular, may be important in the small bowel which is a rich source of xanthine oxidase [11,12]. Both free radicals and leukotrienes act as a stimulus to thromboxane synthesis [13,14], an event which is associated with depression of cardiac function [15,16]. This pathway is a possible explanation for the central effects of intestinal reperfusion, though the precise mechanism remains speculative.
REFERENCES Fig. 4. Completed reconstruction showing aortofemoral bypass with side limbs to celiac, superior mesenteric and left renal arteries. Old graft remains insitu.
avoided if the graft had been revised at the stage of iliac limb stenosis, or more particularly, if the presence of significant visceral artery disease had been recognized and corrected at the initial operation. Along with a meandering mesenteric collateral and underfilling of the jejunal arteries, the presence of a large gastroduodenal-pancreaticarcade on arteriography is one of the early signs of significant visceral arterial disease [ S ] and should have prompted us to undertake lateral arteriography . Although single vessel prophylactic revascular-
1. BERGAN JJ, DEAN RH, CONN JR, et al. Revascularization in the treatment of mesenteric infarction. Ann Surg
1975:182:430-438. 2. SACHS SM, MORTON JH. SCHWARTZ SI. Acute mesenteric ischemia. Surgery 1982;92:646-653. 3. KWAAN JHM, CONNOLLY JE, COUTSOFTIDES T. Concomitant revascularization of intestines during aortoiliac reconstruction: deterrent to catastrophic bowel infarction. Canad J Surg 1980;23:534-536. 4. JOHNSON WC, NABSETH DC. Visceral infarction following aortic surgery. Ann Surg 1974;180:312-318. 5. STONEY RJ, OLCOTT C. Visceral artery syndromes and reconstructions. Surg Clin North Am 1979;59:637-647. 6. EKLOF B, HOWVELS J, IHSE I. The surgical treatment of chronic intestinal ischemia. Ann Surg 1978;187:318-324. 1. WARD AS, CORMIER JM. Surgery of the visceral arteries. In: Operative techniques in arterial surgery. Lancaster: MTP Press Limited, 1986, pp 305-327. 8. BERGAN JJ, YAO JST. Acute intestinal ischemia. In: RUTHERFORD RB (ed). Vascular Surgery. Philadelphia: WB Saunders, 1984, pp 948-963.
VOLUME4 S o 5 - 1990
VISCERAL ISCHEMIA A N D AORTIC GRAFT OCCLUSION
9. BULKLEY BG. Pathophysiology of free radical-mediated reperfusion injury. In: Symposium: nutrient bed protection during arterial reconstruction. J Vnsc Surg 1987;5:512-517. 10. KLAUSNER JM, PATERSON IS, KOBZIK L, et al. Leukotrienes but not complement mediate limb ischemia-induced lung injury. Ann Surg 1989;209:462-470. 1 1 . BATTELLI MG, DELLA CORTE E, et al. Xanthine oxidase type D (dehydrogenase) in the intestine and other organs of the rat. Biochem J 1972;126:747-749. 12. GRANGER D N , HOLLWARTH ME, PARKS DA. Ischemia-reperfusion injury: role of oxygen-derived free radicals. Actn Physiol Scnnd 1986;548:47-63. 13. TATE RM, MORRIS HG, SCHROEDER WR. et al. Oxy-
505
gen metabolites stimulate thromboxane production and vasoconstriction in isolated saline-perfused rabbit lungs. J Clin Invest 1984;74:608-613. 14. MULLANE KM, SALMON JA, KRAEMER R. Leukocyte-derived metabolites of arachidonic acid in ischemiainduced myocardial injury. Fed Proc 1987;46:2422-2433. 15. MATHIESON MA, DUNHAM BM, HUVAL WV, et al. Ischemia of the limb stimulates thromboxane production and myocardial depression. Surg Gynecol Obsrer 1983;157500504. 16. HUVAL WV, LELCUK S, ALLEN PD, et al. Determinants of cardiovascular stability during abdominal aortic aneurysmectomy (AAA). Ann Surg 1984;199:216-222.
...
This report describes a case of acute visceral ischemia precipitated by aortic graft occlusion. The importance of recognizing and treating visceral artery lesions at the time of aortic reconstruction is emphasized. (Ann Vasc Surg 1990;4:502-505). KEY WORDS: Visceral ischemia; aortic graft occlusion; aortic reconstruction.
Infarction due to mesenteric arterial occlusive disease carries a mortality rate of almost 100% [1,2], and every effort should be made to recognize and correct visceral arteriopathy before infarction supervenes. Surgical attention for the most part has centered on patients with intestinal angina. However, asymptomatic patients with mesenteric occlusive disease may also be at risk. This particularly applies to patients undergoing abdominal aortic surgery for aneurysmal or occlusive disease. Failure to recognize and treat visceral arterial lesions at the time of aortic reconstruction can lead t o fatal postoperative intestinal infarction [3]. A similar train of events was narrowly avoided in the case herein reported which is of interest because of the considerable anesthetic and surgical problems posed during th e reconstruction.
CASE REPORT A 5 1-year-old nondiabetic woman underwent insertion of an aorta-common iliac bifurcation graft for bilateral limb claudication at another hospital. A preoperative arteriogram had revealed occlusive disease at the aortic bifurcation with patent distal vessels. A large gastroduodenal-pancreatic arcade was also evident, but its significance was not appreciated at that time (Fig. 1). The
From the Department of Surgery, Basingstoke District Hospital, Basingstoke, Hampshire, United Kingdom. Reprint requests: Mr. A . S . Ward, M S , FRCS, Consultant Surgeon, Basingstoke District Hospital, Aldermaston Road, Basingstoke, Hampshire, RG24 9NA, United Kingdom.
patient’s symptoms were largely relieved following surgery but she returned five years later with recurrent left lower limb claudication. A repeat arteriogram revealed marked stenosis at the previous left iliac anastomosis and similar but less severe changes on the right. No action was taken. She presented six years later at our institution with sudden onset of painful cold legs. There were no pulses in either leg and it was apparent that the graft had occluded. She subsequently developed diarrhea, abdominal pain and distention with a leukocytosis of 23,0001mm [3]. An urgent arteriogram through a high translumbar approach revealed complete aortic occlusion just below the renal vessels. A large gastroduodenal-pancreatic arcade was again evident with refilling of the distal superior mesenteric bed (Fig. 2). Subsequent lateral films confirmed the presence of a proximal superior mesenteric artery occlusion and additional stenosis of the celiac axis. The inferior mesenteric artery had been previously ligated so that the sole visceral blood supply was through the stenosed celiac axis. In addition the left renal artery was severely narrowed just beyond its origin. At operation on the following day the small bowel and colon were found to be pale and edematous with absent mesenteric pulsation. The stomach and duodenum remained well perfused. The supraceliac aorta was clamped and the aorta transected immediately below the renal vessels. A 14 mm x 7 mm Dacron graft was anastornosed end-to-end to the infrarenal aortic cuff and the supraceliac clamp replaced just distal to the new aortic anastomosis. An 8 mm Dacron side limb was then anastornosed to the common hepatic artery and tunnelled behind the pancreas to join the main aortic prosthesis. Transfer of the aortic clamp to below this side limb restored full flow to the celiac axis. This produced a dramatic effect on the small bowel with brisk hyperemia and swelling of the bowel wall (Fig. 3). A strong pulse was now palpable in the root
502
VOLUME4 NO 5 - 1990
VISCERAL ISCHEMIA A N D AORTIC GRAFT OCCLUSION
503
Fig. 3. Massive hyperemia of small bowel. Patient's head is to right of picture. Aortic prosthesis can be seen at bottom right with side limbs to the celiac and superior mesenteric arteries (arrows).
Fig. 1. AP aortogram showing occlusive disease in distal aorta and common Iliac arteries. Large gastroduodenal-pancreatic arcade is arrowed. of the mesentery. Intestinal revascularization resulted in a 3 0 4 0 minute period of cardiovascular instability. Mean systemic arterial pressure dropped to 55 mmHg and pulmonary artery wedge pressure rose from 8 mmHg to 22 mmHg. Serum potassium and acid-base status remained unchanged. Hemodynamic equilibrium was eventually restored after approximately 30 minutes following administration of dopamine (150 ug/min) and rapid infusion of 1.5 liters of blood.
Fig. 2. AP aorto ram shortly after graft occlusion. Aorta is occlude just below renal arteries and large gastroduodenal-pancreatic collateral is evident refilling distal superior mesenteric tree (arrow).
t9
A 6 mm Dacron graft was then placed between the aortic prosthesis and the superior mesenteric artery, and a similar limb attached to the left renal artery. The limbs of the aortic prosthesis were tunnelled lateral to the old graft and anastomosed to the common femoral-profunda artery in each groin (Fig. 4). The patient made a good postoperative recovery, and an arteriogram prior to discharge revealed patency of all grafts. Five years later she remains alive and well.
DISCUSSION Small bowel ischemia following aortic surgery is rare. Most reports deal with the immediate postoperative period when the complication is invariably fatal [4]. Possible mechanisms include operative interference with the inferior mesenteric artery when this is the major supply of the small bowel, embolization of thrombus from within the aorta, or perioperative hypotension in a patient with previously compensated visceral artery occlusive disease. In the present case, acute intestinal ischemia occurred several years after aortic surgery and was precipitated by aortic graft occlusion. Presumably in this patient the small bowel and colon were supplied partly by the stenosed celiac axis through the gastroduodenal-pancreatic arcade and partly by retrograde flow from the internal iliac arteries. Loss of the latter source of supply at the time of graft occlusion could then have resulted in severe visceral ischemia. This patient came close to sustaining frank intestinal infarction. This near disaster could have been
504
VISCERAL ISCHEMIA AND AORTIC GRAFT OCCLUSION
ANNALS OF VASCULAR SURGERY
ization has been advocated in the past [61, our preference, as with symptomatic cases, is to reconstruct both the celiac and superior mesenteric arteries as a long-term insurance policy against one or other of the grafts failing. Visceral artery reconstruction by bypass grafting adds little to the overall operative procedure and can be easily performed through the same field [7]. More liberal use of these supplementary measures seems justified in an attempt to avoid the lethal consequences of postoperative visceral ischemia. The systemic response to intestinal revascularization observed in this patient is interesting. Circulatory collapse and death have been observed both experimentally and in humans following relief of intestinal ischemia, these effects being variously attributed to volume losses into the reperfused gut, hyperkalemia, acidosis, and release of gut endotoxins [8]. In our patient significant hypotension occurred on gut reperfusion associated with an elevation in pulmonary artery wedge pressure, these changes persisting for 30-40 minutes. Correction was not achieved until inotropic support had been given in addition to vigorous volume replacement. These features clearly suggest an element of myocardial depression. Agents such as oxygen-free radicals and leukotrienes are known to play a central role in ischemia-reperfusion injury at a number of sites [9,10]. The former, in particular, may be important in the small bowel which is a rich source of xanthine oxidase [11,12]. Both free radicals and leukotrienes act as a stimulus to thromboxane synthesis [13,14], an event which is associated with depression of cardiac function [15,16]. This pathway is a possible explanation for the central effects of intestinal reperfusion, though the precise mechanism remains speculative.
REFERENCES Fig. 4. Completed reconstruction showing aortofemoral bypass with side limbs to celiac, superior mesenteric and left renal arteries. Old graft remains insitu.
avoided if the graft had been revised at the stage of iliac limb stenosis, or more particularly, if the presence of significant visceral artery disease had been recognized and corrected at the initial operation. Along with a meandering mesenteric collateral and underfilling of the jejunal arteries, the presence of a large gastroduodenal-pancreaticarcade on arteriography is one of the early signs of significant visceral arterial disease [ S ] and should have prompted us to undertake lateral arteriography . Although single vessel prophylactic revascular-
1. BERGAN JJ, DEAN RH, CONN JR, et al. Revascularization in the treatment of mesenteric infarction. Ann Surg
1975:182:430-438. 2. SACHS SM, MORTON JH. SCHWARTZ SI. Acute mesenteric ischemia. Surgery 1982;92:646-653. 3. KWAAN JHM, CONNOLLY JE, COUTSOFTIDES T. Concomitant revascularization of intestines during aortoiliac reconstruction: deterrent to catastrophic bowel infarction. Canad J Surg 1980;23:534-536. 4. JOHNSON WC, NABSETH DC. Visceral infarction following aortic surgery. Ann Surg 1974;180:312-318. 5. STONEY RJ, OLCOTT C. Visceral artery syndromes and reconstructions. Surg Clin North Am 1979;59:637-647. 6. EKLOF B, HOWVELS J, IHSE I. The surgical treatment of chronic intestinal ischemia. Ann Surg 1978;187:318-324. 1. WARD AS, CORMIER JM. Surgery of the visceral arteries. In: Operative techniques in arterial surgery. Lancaster: MTP Press Limited, 1986, pp 305-327. 8. BERGAN JJ, YAO JST. Acute intestinal ischemia. In: RUTHERFORD RB (ed). Vascular Surgery. Philadelphia: WB Saunders, 1984, pp 948-963.
VOLUME4 S o 5 - 1990
VISCERAL ISCHEMIA A N D AORTIC GRAFT OCCLUSION
9. BULKLEY BG. Pathophysiology of free radical-mediated reperfusion injury. In: Symposium: nutrient bed protection during arterial reconstruction. J Vnsc Surg 1987;5:512-517. 10. KLAUSNER JM, PATERSON IS, KOBZIK L, et al. Leukotrienes but not complement mediate limb ischemia-induced lung injury. Ann Surg 1989;209:462-470. 1 1 . BATTELLI MG, DELLA CORTE E, et al. Xanthine oxidase type D (dehydrogenase) in the intestine and other organs of the rat. Biochem J 1972;126:747-749. 12. GRANGER D N , HOLLWARTH ME, PARKS DA. Ischemia-reperfusion injury: role of oxygen-derived free radicals. Actn Physiol Scnnd 1986;548:47-63. 13. TATE RM, MORRIS HG, SCHROEDER WR. et al. Oxy-
505
gen metabolites stimulate thromboxane production and vasoconstriction in isolated saline-perfused rabbit lungs. J Clin Invest 1984;74:608-613. 14. MULLANE KM, SALMON JA, KRAEMER R. Leukocyte-derived metabolites of arachidonic acid in ischemiainduced myocardial injury. Fed Proc 1987;46:2422-2433. 15. MATHIESON MA, DUNHAM BM, HUVAL WV, et al. Ischemia of the limb stimulates thromboxane production and myocardial depression. Surg Gynecol Obsrer 1983;157500504. 16. HUVAL WV, LELCUK S, ALLEN PD, et al. Determinants of cardiovascular stability during abdominal aortic aneurysmectomy (AAA). Ann Surg 1984;199:216-222.
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