Occlusive Disease of the Upper Abdominal Aorta
Rajabrata Sarkar and Ronald J. Stoney
Occlusive disease of the primary paired and unpaired branches of the upper abdominal aorta exhibits a wide variety of clinical presentations from silent but insidious renal failure to fatal intestinal infarction. This chapter will review the patho-physiology, clinical presentation, diagnosis and treatment of these conditions.
Acute Mesenteric Ischemia
Pathophysiology and Clinical Presentation
An embolus to the superior mesenteric artery is the most frequent (50%) cause of acute mesenteric ischemia. This sudden occlusion of a relatively normal superior mesenteric artery, usually originating in the heart, produces severe constant abdominal pain, vomiting and diarrhea as the bowel constricts with progressive ischemia. A leukocytosis then ensues. The triad of severe pain out of proportion to tenderness, elevated white blood cell count and both nausea and diarrhea should lead to the diagnosis embolic ischemia. Conditions associated with mesenteric emboli are longstanding atrial fibrillation, recent myocardial infarction and a history of other systemic arterial embolic events.
Acute mesenteric ischemia may also be due to thrombosis of severely diseased mesenteric vessels. This produces varied clinical presentations that often lead to delay in diagnosis and treatment. A history of abdominal angina is not uncommon. However, acute thrombosis is usually associated with a precipitating event, such as hypotension, dehydration or other systemic illness. Arterial occlusion occurs more slowly during thrombosis than with an embolus. Thus, symptoms of abdominal pain, nausea and vomiting often develop over the course of one to two days. If the thrombosis occurs after major surgery (e.g., post-CABG) or in a critically ill patient in the hospital, the symptoms and signs are frequently masked by postoperative pain, decreased level of consciousness and inability to communicate in the ventilated or obtunded patient. In such patients, the diagnosis is delayed and often only established at laparotomy performed for acute abdomen due to infarcted intestine.
Other less common causes of acute mesenteric ischemia are nonocclusive mesenteric ischemia and mesenteric venous thrombosis. Both of these presents with gradual onset of ischemic symptoms, although nonocclusive mesenteric ischemia due to decreased perfusion often occurs in the hypotensive ICU patient with myocardial dysfunction in whom symptoms are unreliable. Mesenteric venous thrombosis is associated with systemic hypercoagulable states and is often confused with other gastrointestinal disorders due to the vague and initially nonspecific symptoms.
Diagnosis of Acute Mesenteric Ischemia
The diagnosis of acute mesenteric ischemia can be suspected on clinical grounds, particularly when the etiology is an acute embolus. An abdominal catastrophe in a patient with an underlying cardiac condition warrants immediate visceral angiogra-phy. Lateral aortography is necessary to visualize the visceral branch origins in profile, as they arise from the anterior surface of the upper abdominal aorta (Fig. 19.1). When symptoms are of greater duration, particularly when there are signs of peritonitis and acidosis, intestinal infarction is the likely diagnosis. In these patients immediate operation without aortography is not uncommon. However, aortography will delineate severity and distribution of visceral branch atherosclerosis (Fig. 19.2) which allows precise revascularization to restore vital blood flow to the remaining viable intestine.
There are no other reliable imaging modalities for the visceral circulation to unmistakably diagnose mesenteric occlusion. Magnetic resonance angiography (MRA) is used for screening for chronic mesenteric ischemia but cannot be used in ventilated patients and does not provide imaging detail to precisely visualize branches of the superior mesenteric artery. When clinical evidence suggests the possibility of acute mesenteric ischemia, early aortography to definitively exclude or confirm this life-threatening condition is essential.
Aortography is also a critical aid in the diagnosis and treatment of nonocclusive diseases of the mesenteric arteries. Nonocclusive mesenteric ischemia secondary to low cardiac output is an angiographic diagnosis. Treatment of nonocclusive mesenteric ischemia requires hemodynamic support for the heart to increase mesenteric blood flow and avoidance of agents that cause peripheral vasoconstriction. Selective infusion of vasodilators into the mesenteric arteries is frequently effective at relieving ischemia. Laparotomy is indicated if the patient develops signs of peritonitis or bowel infarction.
When the surgeon is presented with viable but severely ischemic bowel, revascu-larization before resection may improve the condition of the bowel and reduce the need for bowel resection. Although revascularization generally will not allow portions of the bowel that are already necrotic to become viable, adjacent ischemic segments will benefit. The diagnosis of acute mesenteric ischemia made at laparotomy raises the question of embolus versus thrombosis as the cause. A soft pliable pulsatile origin of the superior mesenteric artery suggests an embolus. Passage of an embolec-tomy catheter retrograde through a transverse arteriotomy confirms a disease-free origin and antegrade passage retrieves the embolus. Inability to pass the catheter proximally is indicative of significant visceral atherosclerotic occlusive disease and aortovisceral bypass or transaortic endarterectomy should be done as an immediate and definitive reconstruction of the diseased mesenteric circulation. Technical details of both these procedures are discussed below as treatment for chronic mesenteric ischemia.
- Fig. 19.1. Aortogram demonstrating embolus in superior mesenteric artery.
Treatment of Acute Mesenteric Ischemia
As soon as aortography confirms the diagnosis of mesenteric ischemia, an intravenous heparin bolus should be administered to prevent propagation of proximal and distal thrombus into vital collateral vessels. A heparin drip should also continue during surgery. A patient found to have mesenteric embolization (Fig. 19.1) should be maintained on postoperative heparin and then long-term anticoagulation to prevent further systemic embolic events.
Fig. 19.2. Lateral aortogram of patient with acute thrombosis superimposed on chronic visceral occlusive disease. The occluded orifices of the celiac axis (small arrow) and superior mesenteric artery (large arrow) are indicated.
Fig. 19.2. Lateral aortogram of patient with acute thrombosis superimposed on chronic visceral occlusive disease. The occluded orifices of the celiac axis (small arrow) and superior mesenteric artery (large arrow) are indicated.
Management of acute mesenteric ischemia secondary to thrombosis of chronic mesenteric occlusive disease is considerably more challenging than a mesenteric embolus. If the preoperative angiogram demonstrates proximal occlusive disease of the celiac axis and superior mesenteric artery (Fig. 19.2), then transaortic visceral endarterectomy will remove the occlusive lesions and allow retrieval of the superimposed thrombus. Following visceral endarterectomy, the celiac axis and superior mesenteric artery are revascularized, and restoration of flow through collateral vessels to the minor visceral arteries make any additional revascularization unnecessary. Adherent distal thrombus may require an additional arteriotomy in either the celiac axis or the superior mesenteric artery to complete extraction of occlusive thrombus.
Transaortic endarterectomy does not require graft material. This is particularly advantageous in the face of intestinal infarction and gangrene, where contamination of the abdomen with bacteria increases the risk of infection of any prosthetic material. An alternative procedure in the patient with acute mesenteric ischemia secondary to thrombosis of a chronic occlusive lesion is reimplantation of the superior mesenteric artery into the aorta. This is done from an infracolic approach where the origin of the superior mesenteric artery is exposed at the base of the small bowel mesentery. The superior mesenteric artery is divided close to the aorta, an eversion endarterectomy is performed and the vessel is reimplanted into a soft site on the infrarenal aorta. This procedure avoids the hemodynamic stress of a supraceliac clamp in an unstable patient, but cannot address lesions of the celiac axis. Further, it is not recommended when the juxtarenal aorta has significant occlusive disease.
If the chronic atherosclerotic disease extends several centimeters into the superior mesenteric artery, then an antegrade aortovisceral bypass with prosthetic or autogenous conduits allows revascularization prior to resection of acutely ischemic bowel. The long-term patency of prosthetic aortovisceral grafts is superior to autogenous vein. 1 Consequently, aortovisceral vein grafts are recommended only in the unusual case of chronic occlusive disease too extensive for transaortic endarterec-tomy coupled with gross peritoneal contamination that would pose a risk of prosthetic graft infection.
After revascularization and restoration of pulses in distal mesenteric vessels, the intestine is allowed to perfuse for several minutes prior to its re-examination for viability. Limited ischemic infarction requires resection and reanastomosis. When diffuse ischemic changes persist after revascularization, resection and stomas are chosen so that further ischemia in residual bowel can be easily determined postoperatively by inspection of the mucosa by an endoscope passed through the stoma. The decision to return the patient for a second-look operation should be made at the time of the first operation and is particularly important if there has been extensive resection of the bowel. It is preferable to leave questionably viable bowel segments that may ultimately need to be resected at the second-look operation rather than to attempt a single definitive resection of all partially ischemic bowel which may result in the development of short bowel syndrome.
Treatment of mesenteric venous thrombosis consists of anticoagulation, resection of infarcted intestine and testing for a potential hypercoagulable condition. Management of nonocclusive mesenteric ischemia is largely nonoperative as discussed previously, except when advanced visceral infarction is the likely diagnosis.
Chronic Mesenteric Ischemia
Pathophysiology and Clinical Presentation
The patient with chronic mesenteric occlusive disease, unlike the typical older male patient with peripheral vascular occlusive disease, is often a woman in the fifth to sixth decade of life with a heavy smoking history. Two very characteristic symptoms are postprandial abdominal pain and profound weight loss. The abdominal angina of mesenteric ischemia is extremely reproducible in terms of both the onset after meals and constant nature of the pain. Progressive atherosclerosis of the celiac axis and superior mesenteric artery is the usual lesion; unusual causes include fibro-muscular dysplasia and radiation arteritis. Median arcuate ligament compression of the celiac axis alone rarely produces symptoms mimicking intestinal angina. Isolated stenoses of either vessel are compensated for by collaterals from the other mesenteric artery. Patients often have symptoms for months to years before the correct diagnosis is made with lateral aortography. It is not unusual for an exhaustive gastrointestinal evaluation, including upper and lower endoscopy, to have been performed one or more times before arriving at the correct diagnosis.
Diagnosis of Chronic Mesenteric Ischemia
The majority of these patients have undergone extensive workups for abdominal pain prior to establishment of the correct diagnosis. Cholecystectomy has often been performed to treat the postprandial pain. The best diagnostic study is contrast aor-tography, with lateral views necessary to visualize the orifices of the celiac and superior mesenteric arteries. Although duplex ultrasound and magnetic resonance angiography (MRA) are being used more widely for evaluation of the mesenteric circulation, these tests are not definitive. Aortography remains the most reliable and proven diagnostic modality for this diagnosis. This imaging modality also accurately defines extent of occlusive disease in the renal arteries and paravisceral and infrarenal aorta, which can alter the operative strategy used to treat the visceral atherosclerotic lesions.
Treatment of Chronic Mesenteric Ischemia
Treatment of chronic mesenteric occlusive disease centers on restoring blood flow to the celiac axis and superior mesenteric artery. Two basic strategies that have been shown to provide durable visceral reconstruction are antegrade aortovisceral bypass and transaortic thromboendarterectomy of the visceral vessels. For both techniques, a left-to-right medial visceral rotation provides unrestricted exposure of the supraceliac aorta (Fig. 19.3). We prefer the use of the Omni-Tract Self Retaining Retractor System (Omni-Tract Surgical-Minnesota Scientific, Minneapolis, MN) to completely free the first assistant.
For transaortic endarterectomy, following medial visceral rotation the dense neural tissue overlying the upper abdominal aorta is removed. The celiac axis and superior mesenteric artery are exposed circumferentially from the aorta to beyond palpable and angiographic evidence of disease. The aorta is clamped above the celiac axis and usually below the renal arteries and the four major visceral branches and posterior paired lumbar arteries are clamped to control back bleeding. A curvilinear incision is then made in the aorta which surrounds the orifices of the celiac axis and superior mesenteric artery (Fig. 19.4). Endarterectomy of the ventral aspect of the upper abdominal aorta and the visceral branches proceeds using an oscillating Halle dural elevator (Omni-Tract Surgical-Minnesota Scientific, Minneapolis, MN). The ventral aortic plaque is first separated from the underlying media and then the individual aortic branches are prolapsed toward the aortic lumen, while the elevator or extraction endarterectomy clamp continues the circumferential separation plane until
- Fig. 19.3. Exposure of the upper abdominal aorta following medial visceral rotation. The Omni-Tract retractor system is in place.
Fig. 19.4. Illustration of the position of the aortotomy and technique of combined transaortic visceral and renal endarterectomy.
Fig. 19.4. Illustration of the position of the aortotomy and technique of combined transaortic visceral and renal endarterectomy.
the disease feathers and terminates. At this point, the origin plaque is removed. Backbleeding is observed from each vessel and the aortotomy is closed and blood flow restored.
Transaortic visceral endarterectomy is technically challenging and is best used for disease that is limited to the proximal several centimeters of these visceral vessels. Critical technical points in the execution of transaortic visceral endarterectomy include circumferential dissection of the vessels, establishment of the correct endarterec-tomy plane in the deep medial layer of the aortic wall and tapered termination of the endarterectomy under direct vision. Intraoperative duplex ultrasonography is used to confirm adequate flow and to exclude technical problems such as intimal flaps or residual stenosis. Should the superior mesenteric artery be thrombosed, distal propagation of thrombus and underlying plaque may occasionally extend beyond the technique of extraction endarterectomy through the aorta. In these cases following removal of the aortic and orifice lesions, the aortotomy is closed and blood flow restored, except in the clamped superior mesenteric artery. An additional longitudinal arteriotomy is made in the superior mesenteric artery at the termination of the disease and superimposed thrombus. The thromboendarterectomy is completed in an open manner with extraction of all distal thrombus. The superior mesenteric artery is then closed with a patch angioplasty technique.
Antegrade aortovisceral bypass offers a brief period of total or partial supraceliac occlusion to attach the proximal graft (Fig. 19.5). The supraceliac aorta is preferred for grafting since it is spared from significant atherosclerosis which continues in long-term follow-up. The short course of the antegrade prosthetic graft avoids kinking and buckling often seen with retrograde grafts originating from the infrarenal aorta. We prefer prosthetic conduits to autogenous vein for aortovisceral revascularization in elective circumstances and bifurcated grafts (12 by 6 mm or 14 by 7 mm) as opposed to any other configuration. The bifurcated graft avoids the necessity of a graft-to-graft anastomosis and the graft limbs are sewn end-to-end to the celiac axis and superior mesenteric artery beyond the occlusive disease. If possible, we revascularize both the celiac axis and the superior mesenteric artery as our long-term results demonstrate2 that recurrent visceral ischemia occurs more commonly when visceral revascularization was limited to a single visceral branch.
For all visceral reconstructions, an angiogram is obtained prior to discharge from the hospital to document the anatomy of the revascularization. A contrast angio-gram is best but magnetic resonance angiography may be indicated when impaired renal function contraindicates nephrotoxic contrast. This serves as a baseline for long-term follow-up should the patient develop recurrent visceral ischemic symptoms.
Renal Artery Occlusive Disease
Pathophysiology and Clinical Presentation
Occlusive disease of the renal arteries is most commonly due to pararenal aortic atherosclerotic plaque extending into the renal artery orifice. These lesions are often bilateral, and usually do not involve more than the proximal third of the vessel. Renal artery stenosis is particularly prevalent in older male patients with known risk
- Fig. 19.5. A bifurcated antegrade aortovisceral bypass graft to the celiac axis and superior mesenteric artery. The retropancreatic position of the limb to the superior mesenteric artery is shown by the cut-away illustration of the pancreas.
factors for atherosclerosis. Most patients will have evidence of atherosclerotic occlusive disease in other vascular beds. Less common causes of renal artery occlusive disease include fibromuscular dysplasia in younger female patients and congenital or developmental stenoses in children and adolescents. These nonatherosclerotic lesions typically involve the middle and distal thirds of the main renal artery and can extend into primary and secondary renal artery branches.
Regardless of the etiology of renal artery occlusive disease, these patients are at risk to develop renovascular hypertension. This is the renin-mediated response to blood flow and pressure decrease distal to the lesion causing the juxtaglomerular apparatus of the affected kidney to release renin. Renovascular hypertension can be difficult to diagnose in older patients with generalized atherosclerosis because essential hypertension (with no defined cause of the elevated blood pressure) is quite common in this patient population. Clinical features that suggest renovascular hypertension include hypertension unresponsive to antihypertensive medications, young age or rapid onset of hypertension, lack of family history of hypertension and the presence of an abdominal bruit. Angiotensin converting enzyme (ACE) inhibitors, which inhibit the renin-angiotensin pathway, can often control renovascular hypertension but may lead to progressive renal failure particularly in patients with bilateral severe renal artery occlusive disease. Patients with severe bilateral renal artery stenosis may present with recurrent episodes of pulmonary edema, as the bilateral disease limits their ability to clear the excess plasma volume associated with their hypertension.3 An asymptomatic but progressive decline in renal function (azotemia) in an adult patient without a history of renal parenchymal disease should alert one to the possibility of worsening bilateral renal artery occlusive disease and imaging of the renal arteries should be performed.
Diagnosis of Renal Artery Occlusive Disease
Any patient suspected of having renovascular hypertension should undergo renal artery imaging, as this is the only reliable means of establishing the presence of renal artery occlusive disease. Noninvasive studies can be helpful in suggesting the diagnosis, but confirmatory angiography is required prior to an intervention. Captopril nuclear medicine renal scans are useful in localizing renovascular hypertension to one kidney and may be helpful in more than one-half of patients in whom bilateral atherosclerotic or fibromuscular lesions are present. Duplex ultrasonography of the renal arteries requires considerable technical experience and expertise and cannot satisfactorily exclude the diagnosis. MRA of the abdominal aortic branch vessels has excellent resolution and can evaluate renal artery anatomy without radiation or contrast material. However, MRA remains imprecise in evaluating segmental stenosis or subtle patterns of disease. Therefore any patient suspected of having renovascular hypertension with an equivocal MRA should have a confirmatory contrast angiogram. This is particularly true in children, young adults and middle-aged patients, where developmental stenoses and fibromuscular disease often have a focal segmental distribution.
When a unilateral renal artery lesion has been identified, renal vein renin determination may be used to confirm the physiological significance of the lesion. While this may be helpful with an equivocal stenosis, many factors can cause erroneous results. These include the use of antihypertensive medications, patient salt intake, technical problems with catheter sampling and patient posture, as well as unreliability in the presence of bilateral disease. Therefore we rarely employ renal vein renin levels in determining the need for revascularization of renal artery occlusive disease. The presence of collateral vessels on a contrast angiogram, or of spin dephasing on MRA due to turbulent flow, suggest a hemodynamically significant lesion that is contributing to renovascular hypertension. A reduction in renal length of greater than 10% on the side of the lesion suggests ischemic nephropathy of long-standing duration and should prompt revascularization. This 10% loss of length calculates to a 1/3 volume loss of the ischemic kidney.4
Treatment of Renal Artery Occlusive Disease
Surgical revascularization has become the primary treatment modality for renal artery occlusive disease and has proven to provide safe and durable relief from renovascular hypertension and progressive ischemic nephropathy. Two newer interventions have altered the management of renovascular hypertension. The first, improved antihypertensive management, centers around the use of ACE inhibitors, which can effectively control the blood pressure in most patients with renovascular hypertension. The second is the evolving success of balloon angioplasty and stenting in the revascularization of atherosclerotic renal artery lesions. We believe both of these treatments complement rather than replace surgical management and extend the spectrum of disease that can be effectively managed. Although antihypertensive medications may effectively reduce blood pressure in renovascular hypertension, they do not prevent progression of the lesion and resulting ischemic nephropathy. Hunt and Strong compared medical and surgical management of renovascular hypertension and found that medical management had poorer overall survival, greater late incidence of renal failure and progression of lesions to occlusion.5 Medical management of renovascular hypertension in patients with documented bilateral renal artery lesions, particularly when ACE inhibitors are required for pressure control, is associated with considerable risk of silent progression to renal failure. Thus, patients with renovascular hypertension most of whom have a reasonable life expectancy should be considered for renal revascularization to remove the disease and its hypertensive effects rather than blood pressure control alone.
Concomitant renal artery stenting has extended the use of balloon angioplasty in the treatment of orificial atherosclerotic lesions. Many authors have noted satisfactory technical success and relief of hypertension. It is difficult to identify comparable patient populations undergoing renal artery angioplasty and surgical revascularization, because patients with significantly less complicated renal artery lesions, most of whom would not warrant surgical revascularization, are often treated with angioplasty.6 The durability of renal artery revascularization is well documented.7 in most series for at least 5 years or more,7 and comparable durability with angioplasty and stenting is unknown at this time. The use of metallic stents results in an inflammatory reaction in the renal artery and subsequent neointimal hyperplasia, causing a significant incidence of restenosis at the short (1-2 year) follow-up period. We consider using angioplasty and stenting for patients with limited life expectancy, or high operative risk.
Techniques of renal revascularization include transaortic renal endarterectomy, aortorenal bypass, various extra-anatomic bypass techniques and renal artery reimplantation. Aortorenal bypass with a saphenous vein graft originating from the infrarenal aorta was the first widely used method of renal revascularization. This technique cannot be used when significant infrarenal occlusive or aneurysmal disease is present, but is particularly useful in the presence of occlusive disease extending out to the renal hilum. The majority of atherosclerotic lesions are limited to the orifices and proximal several centimeters of the renal artery and are thus amenable to transaortic endarterectomy. This was first used at our institution in 1952 and has been our continued preference for proximal atherosclerosis of the renal arteries. This can be performed in conjunction with endarterectomy of the visceral branches (as described above), or with endarterectomy or replacement of the infrarenal aorta for either occlusive or aneurysmal disease.
The surgical approach to transaortic renal endarterectomy depends on the need for an associated mesenteric endarterectomy or infrarenal graft placement. For combined aortovisceral and renal endarterectomy left-to-right medial visceral rotation, as described previously, provides excellent surgical exposure. The endarterectomy is extended from above the celiac axis to below the renal arteries (Fig. 19.4). If renal endarterectomy is performed alone or combined with reconstruction of the infrarenal aorta (without mesenteric endarterectomy) then an infracolic approach to the aorta is preferred. The inferior border of the pancreas is mobilized and gently retracted. The pararenal aorta and renal arteries are completely mobilized circumferentially and if indicated, the infrarenal aorta is exposed for reconstruction. The aorta is clamped either above the superior mesenteric artery or above the renal arteries. The proximal site depends on whether the clamp will impair access to the renal orifices.
The aorta is transected just inferior to the renal arteries when infrarenal aortic grafting is planned.8 Transaortic endarterectomy through the transected aorta is facilitated by an oscillating endarterectomy device and extraction endarterectomy clamps. After establishing the proper medial plane a continuous separation of the circumferential aortic plaque is first achieved and the proximal end point is transected below the inferior border of the proximal clamp or orifice of the superior mesenteric artery. Now, the endarterectomy specimen is attached only by the projecting renal artery lesions. These lesions are removed by prolapsing the mobilized renal artery into the aortic lumen for direct visual inspection of the end points. If this is not possible, the extraction clamp is designed for more distal nonvisualized endpoints. Following renal artery back bleeding and flushing, the aortic graft is attached to the endarterectomized infrarenal aorta and declamping to the proximal graft ensures return of renal and mesenteric blood flow.
If reconstruction of the infrarenal aorta is not planned, the aorta is opened through an anterior midline aortotomy carried to the left above the orifice of the left renal artery. The transaortic endarterectomy proceeds as described through the transected aorta, except the visibility and exposure of the interior of the pararenal aorta is greater and the procedure is technically less demanding.
Extra-anatomic bypass of renal artery occlusive disease has usually been reserved for patients whose medical condition would not allow an aortic-based procedure. However improved perioperative care of patients with significant comorbidity allow safe conduct of aortic repair in most circumstances. Thus, there are infrequent indications for this technique today, but the durability of these extra-anatomic reconstructions has been documented by Reilly and colleagues.9 Vein grafts are used for extra-anatomic bypass to the right kidney, and these typically originate from the common hepatic artery. The splenic artery can usually be divided distally and anastomosed end-to-end to the transected left renal artery. If the splenic artery is both calcified and tortuous, it is unsuitable for a direct renal graft but a vein graft can be used to bypass from the proximal splenic artery to the left renal artery. Rarely, the iliac vessels are used as an origin for prosthetic bypass to either renal artery because there is a high incidence of occlusive disease in the aorta that would be proximal to the graft.
Reimplantation of the renal artery into the aorta is useful for repairing developmental renal artery stenosis seen in children.10 The anastomosis employs interrupted sutures to allow for growth of the new renal artery at its aortic orifice. The saphen-ous vein, which becomes aneurysmal in pediatric patients, is avoided for renal reconstruction. Renal artery lesions which extend into branch vessels can be safely repaired with the ex vivo technique in which the entire kidney is removed from the patient and perfused to allow carefUl and meticulous repair of small renal artery branches using branched internal iliac artery autografts.7 Regardless of the surgical technique used, excellent long-term results have been achieved with renal revascularization and this remains the standard against which new treatment modalities should be compared.
Acknowledgment
This work was supported by a grant from the Pacific Vascular Research Foundation to Dr. Sarkar.
Selected Readings
1. Cunningham CG, Reilly LM, Rapp JH et al. Chronic visceral ischemia: Three decades of progress. Ann Surg 1991; 214:276.
This report compares outcomes in chronic visceral ischemia treated with either transaortic visceral endarterectomy or antegrade aortovisceral bypass. Complications, outcomes and durability of each of these procedures are similar in this report.
2. Schneider DB, Schneider PA, Reilly LM et al. Reoperation for recurrent chronic visceral ischemia. J Vasc Surg 1998; 27:286.
This report focuses on the subset of patients with recurrent visceral ischemia after previous visceral revascularization. The need for an aggressive surgical approach to this difficult problem, the techniques used in the face of a prior failed reconstruction and the durability and need for subsequent procedures are well described.
3. Messina LM, Zelenock GB, Yao KA et al. Renal revascularization for recurrent pulmonary edema in patients with poorly controlled hypertension and renal insufficiency: a distinct subgroup of patients with arteriosclerotic renal artery occlusive disease. J Vasc Surg 1992; 15:73.
This paper focuses on patients with bilateral renal artery occlusive disease who have recurrent episodes of pulmonary edema secondary to volume overload. These episodes are mistaken as cardiac failure and consequently delay surgery, but it is surgical revas-cularization that resolves the pulmonary edema.
4. Newman VS, Dean RH. Ischemic nephropathy as an indication for renal artery reconstruction in renovascular hypertension. Corr Opin Gen Surg 1994; 272-6. This review discusses renal revascularization when done for preservation of renal function rather than for treatment of renovascular hypertension. Written by the group that has defined the clinical and radiological criteria for this indication, this paper focuses on appropriately selecting patients for surgical intervention.
5. Hunt JC, Strong CG. Renovascular hypertension. Mechanisms, natural history and treatment. Am J Cardiol 1973; 32:56.
An excellent long-term comparison of medical and surgical management of renovascular hypertension. Its current applicability is limited by the era of the study, since which time both medical and surgical management have markedly improved.
6. Rodriguez-Lopez JA, Werner A, Ray LI et al. Renal artery stenosis treated with stent deployment: Indications, technique, and outcome for 108 patients. J Vasc Surg 1999; 29:617.
A recent report ofa large series of patients treated with balloon angioplasty and stenting for renal artery occlusive disease. This experience demonstrates the safety of this procedure.
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