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The treatment algorithm for aortoiliac disease is similar to that for lower extremity occlusive disease, outlined previously. Patients with asymptomatic atherosclerosis of the aortoiliac segment do not require treatment. For patients with claudication, an attempt at medical therapy, involving an exercise program, risk factor modification, and pentoxifylline, should be instituted prior to consideration for revascularization.
Revascularization is indicated in patients with aortoiliac disease, via either percutaneous or surgical means, for the same reasons as lower extremity occlusive symptoms:
Incapacitating claudication
Ischemic rest pain
Tissue loss
Percutaneous intervention. Angioplasty and stenting of aortoiliac segment is the preferred procedure for focal, short-segment stenoses or occlusions. Bilateral lesions can generally be treated via a single common femoral artery approach. In cases of distal aortic stenosis or high-grade bilateral common iliac artery lesions, simultaneously inserted “kissing” stents are placed at the same level of the distal aorta through each common iliac artery.
Operative procedures. Symptomatic patients who are not candidates for percutaneous interventions may be offered surgical therapy for relief, provided they are good risks for surgery. Two techniques are available to improve inflow in one or both lower extremities.
Aortoiliac endarterectomy. For patients with shorter -segment occlusion/stenosis of the distal aorta and common iliac arteries, open surgical removal of the plaque and adjacent medial layers will restore patency to the system. Concomitant diffuse disease of the external iliac arteries warrants against endarterectomy and necessitates bypass. Many patients with localized disease who previously were treated with endarterectomy or bypass now undergo percutaneous procedures, obviating the need for this extensive surgery.
Bypass procedures. In patients with diffuse disease of the aorta, iliac, and femoral systems not amenable to angioplasty and stenting, a bypass procedure is the treatment of choice. In each of these procedures, unlike the infrainguinal bypasses described previously, prosthetic conduits (either polytetrafluoroethylene or Dacron) are preferred.
Aortobifemoral bypass represents the gold standard in revascularization procedures for inflow disease.
Proximal anastomosis. Ideally, this is placed as close to the renal arteries as possible to avoid proximal anastomotic failure should the disease progress proximally. The anastomosis is generally performed end -to -end; in this case, the pelvis is perfused retrograde back up the external iliac systems. In situations in which the pelvic blood flow would be compromised by an end -to -end configuration, an end -to -side aortic anastomosis is created, maintaining antegrade flow to the pelvis. There is no proven difference in long-term graft function between the two techniques.
Distal anastomoses. Because of the diffuse nature of the disease, the bifurcated graft limbs are tunneled retroperitoneally, behind the ureters, and down to the common femoral arteries. Distal anastomoses are then performed in an end -to -side fashion. On occasion, anastomoses may be made to the iliac systems; in these cases, the advantage lies in avoiding groin wounds and possible future graft infection.
Extra -anatomic bypass. The contralateral common femoral artery and the axillary artery may be used as alternate inflow sources for aortoiliac disease. These procedures avoid the
morbidities associated with aortic cross clamping and laparotomy.
Femoral-femoral bypass may be the preferred procedure for patients with unilateral iliac disease. The cross-femoral prosthetic conduit is tunneled subcutaneously or in the space of Retzius (behind the rectus muscles).
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Axillobifemoral bypass is preferred in patients with extensive, bilateral aortoiliac disease who otherwise could not tolerate aortobifemoral bypass. The conduit is tunneled subcutaneously. The procedure can be performed with low mortality rates by using local anesthesia with sedation. This procedure may also be used for treatment of aortic graft infection in combination with removal of the infected abdominal graft.
Results. The best results are achieved with aortic grafting, yielding up to 85% 10 -year primary patency rates. Femoral -femoral grafts can achieve up to 75% 5-year primary patency rates. Axillobifemoral grafts achieve more variable 5-year patencies, between 50% and 70%, depending on patient selection.
IV Acute Arterial Insufficiency of the Lower Extremity
Acute limb ischemia, unlike chronic ischemia, may lead to irreversible tissue loss within hours if rapid diagnosis and restoration of flow are not achieved.
A Pathology
These are two general causes of limb ischemia.
Embolism refers to the translocation of material within the arterial stream to a more distal site, resulting in the acute interruption of blood flow at that level. Larger (macro) emboli will lodge at a distal bifurcation, the most common site being the common femoral artery, followed by the aortoiliac system and popliteal arteries. Smaller (micro) embolic debris generally lodges in the distal tibial system or digital arteries (“blue toe syndrome”). Sources of emboli include:
Cardiac pathology. Eighty -five percent of cases originate from the heart.
Atrial thrombus. Patients with atrial fibrillation may develop thrombus within the atria, especially in the atrial appendage. This arrhythmia is present in 50% to 80% of patients diagnosed with embolism. Atrial cardiac myxoma may also embolize distally.
Ventricular thrombus. Mural thrombus may form following a myocardial infarction or within a ventricular aneurysm.
Valves damaged from rheumatic heart disease may produce microemboli.
A patent foramen ovale may allow a paradoxical embolism to travel from the venous circulation into the arterial circulation.
Proximal arterial pathology. Arterial -arterial embolism may also occur from several sources.
Atherosclerotic plaques may serve as a nidus for thrombus or platelet aggregates that embolize distally, or they may rupture, discharging smaller debris (atheroembolization).
An aneurysm of an arterial segment, most commonly the infrarenal aorta or popliteal arteries, may harbor a mural thrombus that may embolize distally.
In situ thrombosis of an arterial segment may result in acute ischemia. This may occur in two settings.
Thrombosis of a chronically diseased vessel, most commonly the SFA or popliteal arteries, may cause acute ischemia if collateral circulation is poorly developed or compromised by the in situ thrombosis.
Hypercoagulable states may cause arterial thrombosis, even if the arterial segment is normal. This generally occurs in the more distal segments, such as the tibial vessels or pedal arches.
B
Clinical presentation of acute lower extremity ischemia is generally dramatic because the patient generally can identify the exact moment of sudden change in his or her arterial circulation. The “5 Ps” define this syndrome:
Pain is characteristic of essentially all patients with acute ischemia. It is distinguished from chronic ischemic pain because of its acute onset and unrelenting severity. Over several hours of acute ischemia, the limb may become anesthetic as neural function is lost.
Pallor associated with coolness of the extremity usually occurs at one level below the acute arterial occlusion. Additional signs may include mottling of the extremity and flat veins.
Paralysis of the limb results, as muscle function is severely compromised. This finding may occur several hours after the acute event and heralds limb loss if blood flow is not restored promptly.
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Paresthesias signify severe neural dysfunction and also herald impending limb loss. An insensate limb is generally considered nonviable.
Pulselessness. The absence of pulses, especially if the contralateral limb has intact pulses, may help to identify the level of occlusion. Patients with chronic limb ischemia will also have absent pulses but will generally have Doppler signals distally. In contrast, patients with severe acute ischemia usually will not have detectable Doppler signals distally because their collaterals may not be developed enough to support distal flow.
C Evaluation
Rapid assessment of the level of acute occlusion is generally performed via physical examination. Comparison with the contralateral extremity, involving level of pulselessness, temperature, and mottling, is generally useful, especially if the contralateral examination is normal. Documentation of motor and sensory examination results are critical; if these results are present, further workup is not performed and the patient is taken directly to the operating room for treatment.
Noninvasive examinations. Other than the documentation of the lowest level of signals measurable by Doppler, noninvasive examinations generally are not performed in the interest of time.
Arteriography. If the motor and sensory systems are intact, the patient might benefit from arteriographic information defining the level of occlusion and distal reconstitution. This is especially true in the patient with evidence of chronic arterial insufficiency (by history or examination of the contralateral limb) with an acute change because in situ thrombosis may be the cause of the acute ischemia.
D Treatment
Management of acute arterial occlusion includes rapid diagnosis and expeditious surgical correction of the occlusion.
Heparin therapy. Initial therapy for patients with acute arterial ischemia is intravenous anticoagulation with heparin, unless there is a specific contraindication to heparin (such as heparin -induced thrombocytopenia). This should be given as a bolus of 100 U/kg and continued empirically at 1,000 U/hour up to the time of surgery.
Hydration. Patients should be given adequate hydration to maintain high urine output (preferably 100 mL/hour). Alkalinization of the urine and osmotic diuresis (mannitol) are used to protect the kidney from damage due to myoglobinuria in patients with prolonged, severe ischemia.
Revascularization. Restoration of blood flow to an ischemic extremity provides definitive treatment. In severe ischemia of the lower limb, this ideally is performed within 6 hours of the onset of the acute event to avoid irreparable nerve and muscle damage.
Surgical therapy. Following heparinization, the patient is generally taken directly to the operating room for revascularization, especially if motor and sensory changes are present.
Embolectomy is the procedure of choice in cases of macroembolism to a larger artery, such as the common femoral artery. It is performed by introducing a balloon-tipped catheter through a transverse arteriotomy at the level of the occlusion. The catheter is advanced through the embolus (and trailing thrombus). Inflation of the balloon and withdrawal of the catheter extracts the thrombus. Completion arteriography determines the adequacy of the thromboembolectomy procedure. Morbidity and mortality are generally related to the patient's underlying medical problems.
Bypass. In cases of thrombosis, or when adequate thromboembolectomy cannot be performed, surgical bypass as described previously for chronic arterial insufficiency is necessary for revascularization. If preoperative arteriography has not been performed, intraoperative arteriography is performed to determine the level of distal arterial runoff.
Thrombolytic therapy. In selected patients, such as those with prior vascular interventions, lytic therapy may be used for revascularization. Agents such as tissue plasminogen activator and urokinase have been used in this setting to dissolve the acutely formed thrombus. Advantages include the possibility of correcting the underlying cause of the thrombosis with angioplasty (avoiding surgery altogether) or with a more limited surgical procedure. Contraindications include the presence of sensory and motor changes on presentation (because lytic therapy frequently requires >24 hours of treatment), recent (<2 weeks) surgery, and known intracranial pathology.
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Postoperative care. Patients who have suffered an embolic event should have a complete cardiac evaluation (echocardiogram and Holter monitor) to search for an embolic source. These patients should receive anticoagulation therapy to reduce the incidence of recurrent embolic events. Those with in situ thrombosis who undergo bypass are generally treated without further anticoagulation unless a hypercoagulable state is suspected. Complications of the treatment of acute ischemia include:
Compartment syndrome. Reperfusion injury to the muscle may result in swelling and increased compartment pressures within the fascial spaces of the calf. If untreated, capillary perfusion is cut off, resulting in neurological injury (usually foot drop) and/or further tissue loss. Clinical presentation includes calf pain, especially with passive stretch; tenderness; and loss of sensation in the first digital web space. Performing four compartment fasciotomies is the treatment of choice.
Myoglobinuria. With severe ischemia, necrosis of muscle leads to the release of myoglobin into the bloodstream. Myoglobin is filtered by the kidneys and is nephrotoxic. Diagnosis is suggested by the presence of heme on urine dipstick in the absence of red blood cells by microscopic urinalysis.
Definitive diagnosis is made by detection of myoglobin in the urine. Treatment is generally supportive, maintaining high urine output while the urine is positive for myoglobin.
V Mesenteric Vascular Disease
Mesenteric vascular disease may present as an acute life -threatening emergency or as a chronic debilitating problem. The involved arteries include the celiac axis (CA), superior mesenteric artery (SMA) and inferior mesenteric artery (IMA) arising from the anterior surface of the abdominal aorta.
A
Acute mesenteric ischemia is a surgical emergency with an 80% mortality rate. Classically, severe abdominal pain out of proportion to physical findings suggests the diagnosis. In the early stages of acute mesenteric ischemia, these patients are often writhing in agony without evidence of peritonitis. If diagnosis or treatment is delayed, transmural infarction of bowel results in peritoneal irritation and more pronounced physical signs.
Etiology. Acute occlusion of the mesenteric arteries may result from:
Embolization. The usual site of distal embolization is the SMA, generally several centimeters distal to the origin (at the level of the middle colic artery). As with lower extremity embolism, the source of embolism is usually the heart (atrial fibrillation or myocardial infarction).
Thrombosis. Sudden occlusion of pre -existing atherosclerotic lesions of the visceral vessels may cause acute mesenteric ischemia. Because mesenteric atherosclerosis usually involves the origin of the artery, thrombosis also begins at the origin of the vessel. These patients will frequently admit to the presence of pre -existing symptoms of chronic mesenteric ischemia.
Nonocclusive mesenteric ischemia is due to states of low flow to the mesenteric arteries, as seen in cardiogenic shock. It has been recognized in patients after cardiopulmonary bypass and in patients requiring high doses of intravenous vasoconstrictors and inotropes (e.g., epinephrine).
Diagnosis and treatment. Saving these patients depends on a high index of suspicion and prompt diagnosis and treatment. All patients suspected of acute mesenteric ischemia should have their cardiac status optimized while being aggressively volume resuscitated and treated with broad-spectrum antibiotics.
Angiography of the abdominal aorta and mesenteric arteries is performed if acute mesenteric ischemia is suspected. Subsequent treatment is based on the arteriographic findings.
If embolus is found (usually involving the SMA), prompt surgical embolectomy is performed. Subsequent anticoagulation is given, assuming a cardiac source.
If thrombosis is found (usually involving the origins of the CA and SMA), urgent aortomesenteric bypass is performed. A prosthetic bypass is usually used, except in the presence of bowel infarction (then, GSV is preferred).
The treatment of nonocclusive mesenteric ischemia involves direct arterial infusion of vasodilators (i.e., papaverine or nitroglycerine) into the SMA. Supportive care to optimize cardiac output and reverse the low -flow state is critical.
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Following embolectomy or reconstruction, the bowel is assessed for viability. Overtly necrotic bowel is resected. If marginal viability is present in the remaining bowel, it should be left in place. A second - look laparotomy should be done in 24 hours to ensure viability of the residual bowel. Patients with nonocclusive mesenteric ischemia who develop peritoneal signs should undergo laparotomy to rule out necrotic bowel.
B
Chronic mesenteric ischemia results from slowly progressive stenosis/occlusion of the visceral vessels (CA, SMA, and IMA) (Fig. 7-2). Atherosclerotic lesions generally involve the anterior abdominal aorta and the origins of these vessels.
Clinical presentation. The triad of symptoms suggesting chronic mesenteric ischemia includes:
Postprandial abdominal pain, occurring in the epigastrium, generally 0.5–2 hours after a meal
“Food fear,” resulting from the chronic association of eating with subsequent pain
Weight loss
Diagnosis. The diagnosis of chronic mesenteric ischemia is suggested by the clinical triad noted previously. Additional symptoms might include gastrointestinal dysmotility. Definitive diagnosis is often delayed for up to 1–2 years, unless a high index of suspicion is maintained.
Recently, duplex scanning of the visceral vessels has been used to screen patients with suspected chronic mesenteric ischemia. Elevated velocities within the CA and superior mesenteric vessels may be seen.
Arteriography is the most useful diagnostic study. Both anterior-posterior and lateral views of the aorta must be used to visualize the origins of the visceral vessels. When symptoms occur, two of the three vessels are usually occluded and the remaining one is highly diseased. A rich collateral blood supply between the CA and SMA (pancreatoduodenal arcade) and the SMA and IMA (Riolan's arch) may be seen.
Computed tomography (CT) of the abdomen, as well as upper and lower intestinal endoscopy, is performed to rule out other causes for the patient's symptoms prior to recommending treatment of mesenteric occlusive disease.
Treatment. Surgery is recommended if severe mesenteric occlusive disease is found in a patient with the clinical presentation noted previously. In well-selected patients, the results of surgery are excellent, with 90% of patients cured of their symptoms.
Aortomesenteric bypass , usually involving the CA and SMA, is performed with a short prosthetic graft. The bypass can be constructed in an antegrade format from the supraceliac aorta or a retrograde approach from the infrarenal aorta or iliac system.
Transaortic mesenteric endarterectomy directly removes the atherosclerotic lesions from the aorta and origins of the mesenteric vessels, restoring patency without prosthetic grafting.
C
Mesenteric venous thrombosis may present more insidiously than acute mesenteric ischemia. Typically, it causes progressive abdominal pain and distention and may be confused with intestinal obstruction.
Etiology. It is frequently associated with hypercoagulable states, including patients with a neoplasm or hematologic abnormality.
Diagnosis is suggested by CT scan that reveals concentration of contrast in the wall of the mesenteric vein without luminal flow.
Treatment
Nonoperative treatment is anticoagulation (intravenous heparin) and treatment of the underlying disorder.
Celiotomy may be necessary if peritonitis develops, but 75% of patients can be treated nonoperatively if the diagnosis is made promptly and appropriate treatment is given.
VI Renal Artery Stenosis
Renal artery stenosis (RAS). Significant stenosis of the renal arteries decreases perfusion pressure to the kidney. This reduction stimulates the juxtaglomerular apparatus to release renin , initiating the formation of
angiotensin. Angiotensin is a potent vasoconstrictor and stimulates adrenal aldosterone P.157
production, resulting in sodium retention. Systemic hypertension, renal insufficiency , and pulmonary edema may result from this cascade of events.
A Causes
The two most common causes of RAS are atherosclerosis and fibromuscular dysplasia. Atherosclerosis occurs in older adults and involves the orifices of the renal arteries. Fibromuscular dysplasia generally affects younger women and results in multiple stenoses of the mid and distal renal arteries.
B Clinical presentation
Renovascular hypertension is a relatively rare cause of hypertension (less than 5% of all patients with hypertension). The diagnosis should be suspected in patients with the following characteristics:
Sudden onset of severe hypertension in patients less than 35 or more than 55 years of age
Sudden worsening of hypertension in a patient with previously well-controlled disease
Inability to control blood pressure despite multiple -drug therapy
The presence of abdominal or flank bruits associated with any of the preceding characteristics
C Diagnosis
Laboratory tests may be helpful to confirm the presence of hypertension caused by RAS, although no test is completely reliable.
Captopril renal scan noninvasively screens for reduced blood flow to each kidney. The administration of the angiotensin -converting enzyme inhibitor increases the sensitivity of this test to detect RAS based on the suppression of glomerular filtration in the presence of significant stenoses.
Duplex scanning of the renal arteries is another noninvasive screening test for RAS. An increase in renal artery blood flow velocity compared with aortic velocity suggests significant stenosis.
The renal/systemic renin index documents the contribution of each kidney to plasma renin and also documents suppression of the contralateral kidney in unilateral disease.
The formula is:
An index over 0.48 indicates hypersecretion by that kidney.
An index approaching 0 indicates suppression in that kidney.
Selective renal arteriography remains the definitive examination to demonstrate stenotic lesions of the renal arteries and is essential in planning therapy.
Computed tomographic angiography (CTA) and magnetic resonance angiography (MRA) are two widely used, noninvasive imaging modalities that have come into favor. Excellent resolution has been obtained with these modalities; however, they are very institution dependent when comparing one with the other.
D
Treatment of RAS depends on the etiology and location of the lesion, the status of the involved kidney, and the clinical status of the patient. Options include percutaneous dilation, endarterectomy, bypass, and nephrectomy.
PTA is a very effective treatment for patients with lesions in the midportion of the renal artery. The lesions
frequently occur in this location in patients with fibromuscular dysplasia. Early and late results in wellselected patients are excellent. Stent placement (in combination with angioplasty) is being used successfully in patients with stenosis of the renal artery orifice. When applicable, this is now the preferred mode of treatment.
Renal artery endarterectomy can be used for unilateral or bilateral localized atherosclerosis of the renal artery orifices.
Aortorenal artery bypass distal to the lesion is the most commonly performed procedure.
The saphenous vein in adults and the hypogastric artery in children are the preferred conduits.
The aorta above or below the renal artery is usually used as the origin of the graft. Other sources of inflow are the hepatic, splenic, and iliac arteries.
A small percentage of patients have multiple lesions, involving both the main renal artery and the hilar branches. In these patients, the kidney can be removed, cooled, and repaired ex vivo. The kidney is then replaced in its anatomic location or is transplanted to the pelvis.
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Nephrectomy is an alternative in patients with a unilateral vascular lesion and a normal contralateral kidney. The indication would be refractory hypertension with elevated renin from the involved kidney and suppression of the normal kidney. Nephrectomy is usually chosen for small, nonfunctioning kidneys.
Medical treatment. Antihypertensive drugs can be used to control mild to moderate hypertension from RAS (when the diastolic blood pressure is in the 90–100 range).
The risks of medical management are higher when blood pressure is erratic or difficult to control.
Medical management is a more reasonable approach than surgery in patients with generalized atherosclerosis.
Medical management is less desirable than surgery in children and in patients with fibromuscular dysplasia.
Results of treatment depend on the disease process, the accuracy of preoperative testing, and the ability to completely repair the arterial lesions.
Fibromuscular dysplasia with localized arterial lesions do very well, with improvement or cure of hypertension in 90% of patients.
Repair of isolated atherosclerotic lesions also yields good results if the distal renal artery is normal.
Nonlocalized lesions in patients with widespread atherosclerosis yield the poorest results.
VII Extracranial Cerebrovascular Disease
A Overview
Cerebrovascular accident (stroke) is an injury to the central nervous system that results in death of brain tissue. It can be a silent event or can result in temporary or permanent loss of function.
Epidemiology
Of approximately 600,000 new strokes per year in the United States, approximately 150,000 result in
