OCCLUSIVE DISEASE: AORTA & ILIAC ARTERIES
ESSENTIALS OF DIAGNOSIS
Claudication: cramping pain or tiredness in the calf, thigh, or hip while walking.
Diminished femoral pulses.
Tissue loss (ulceration, gangrene) or rest pain.
Occlusive atherosclerotic lesions developing in the extremities, or peripheral arterial disease (PAD), is evidence of a systemic atherosclerotic process. The prevalence of PAD is 30% in patients who are 50 years old patients who have either diabetes mellitus or a history of tobacco use or in patients who are 70 years old without those risk factors. Pathologic changes of atherosclerosis may be diffuse, but flow-limiting stenoses occur segmentally. In the lower extremities, they classically occur in three anatomic segments: the aortoiliac segment (eFigure 12–1), femoral-popliteal segment, and the infrapopliteal or tibial segment of the arterial tree. Lesions in the distal aorta and proximal common iliac arteries classically occur in white male smokers aged 50–60 years. Disease progression may lead to complete occlusion of one or both common iliac arteries, which can precipitate occlusion of the entire abdominal aorta to the level of the renal arteries.
Magnetic resonance angiography showing atherosclerotic occlusive disease of the aortoiliac segment. The vessels proximally and distally are relatively unaffected.
Approximately two-thirds of patients with PAD are either asymptomatic or do not have classic symptoms. Intermittent claudication, which is pain that occurs from insufficient blood flow when there is increased demand from exercise, is typically described as severe and cramping and primarily occurs in the calf muscles. The pain from aortoiliac lesions may extend into the thigh and buttocks with continued exercise and erectile dysfunction may occur from bilateral common iliac disease. Rarely, patients complain only of weakness in the legs when walking, or simply extreme limb fatigue. The symptoms are relieved with rest and are reproducible when the patient walks again. Femoral pulses are absent or very weak as are the distal pulses. A bruit may be heard over the aorta, iliac, or femoral arteries or over all three arteries.
B. Doppler and Vascular Findings
The ratio of systolic blood pressure detected by Doppler examination at the ankle compared with the brachial artery (referred to as the ankle-brachial index [ABI]) is reduced to below 0.9 (normal ratio is 0.9–1.2); this difference is exaggerated by exercise. Both the dorsalis pedis and the posterior tibial arteries are measured and the higher of the two artery pressures is used for calculation. Segmental waveforms or pulse volume recordings obtained by strain gauge technology through blood pressure cuffs demonstrate blunting of the arterial inflow throughout the lower extremity.
CT angiography (CTA) and magnetic resonance angiography (MRA) can identify the anatomic location of disease. Due to overlying bowel, duplex ultrasound has a limited role in imaging the aortoiliac segment. Imaging is required only when symptoms require intervention, since a history and physical examination with vascular testing should appropriately identify the involved levels of the arterial tree.
The cornerstones of PAD treatment are risk factor reduction, medical optimization, and exercise program. A program that includes smoking cessation, lipid and blood pressure management, and weight loss is essential. Nicotine replacement therapy, bupropion, and varenicline have established benefits in smoking cessation (see Chapter 1). A strategy to motivate individuals to quit smoking uses “5Rs”; Relevance of smoking cessation to the patient, discussing the Risk of smoking, Rewards of quitting (eg, cost savings, health benefits, sense of well-being), identification of Roadblocks, and importance of Repetition of a motivational intervention at all subsequent visits. All patients with PAD should receive high-dose statin (eg, atorvastastin 80 mg daily if tolerated) to treat hypercholesterolemia and inflammation. A trial of phosphodiesterase inhibitors, such as cilostazol 100 mg orally twice a day, may be beneficial in approximately two-thirds of patients. Antiplatelet agents, such as aspirin, 81 mg daily, reduce overall cardiovascular morbidity but do not ameliorate symptoms.
B. Endovascular Techniques
When the atherosclerotic lesions are focal, they can be effectively treated with angioplasty and stenting. This approach matches the results of surgery for single stenoses but both effectiveness and durability decrease with longer or multiple stenoses.
A prosthetic aorto-femoral bypass graft that bypasses the diseased segments of the aortoiliac system is a highly effective and durable treatment for this disease. Patients may be treated with a graft from the axillary artery to the femoral arteries (axillo-femoral bypass graft) or with a graft from the contralateral femoral artery (fem-fem bypass) when iliac disease is limited to one side. The axillo-femoral and femoral-to-femoral grafts are extra-anatomic bypasses because the abdominal cavity is not entered and the aorta is not cross-clamped; the operative risk is less than with aorto-bifemoral bypass, but the grafts are less durable.
The complications of the aorto-femoral bypass are those of any major abdominal reconstruction in a patient population that has a high prevalence of cardiovascular disease. Mortality is low (2–3%), but morbidity is higher and includes a 5–10% rate of myocardial infarction. While endovascular approaches are safer and the complication rate is 1% to 3%, they are less durable with extensive disease.
Patients with isolated aortoiliac disease may have a further reduction in walking distance without intervention, but symptoms rarely progress to rest pain or threatened limb loss. Life expectancy is limited by their attendant cardiac disease with a mortality rate of 25–40% at 5 years.
Symptomatic relief is generally excellent after intervention. After aorto-femoral bypass, a patency rate of 90% at 5 years is common. Endovascular patency rates and symptom relief for patients with short stenoses are also good with 20% symptom return at 3 years. Recurrence rates following endovascular treatment of extensive disease are 30–50%.
Patients with progressive reduction in walking distance in spite of risk factor modification and consistent walking programs and those with limitations that interfere with their activities of daily living should be referred for consultation to a vascular surgeon.
et al. Antithrombotic therapy in peripheral artery disease: Antithrombotic Therapy and Prevention of Thrombosis, 9th ed: American College of Chest Physicians Evidence-Based Clinical Practice Guidelines. Chest. 2012 Feb;141(2 Suppl):e669S–90S.
et al. Endovascular stents for intermittent claudication. Cochrane Database Syst Rev. 2010 Jan 20;(1):CD003228.
et al. 2016 AHA/ACC Guideline on the management of patients with lower extremity peripheral artery disease: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines. Circulation. 2017 Mar 21;135(12):e726-79.
et al. Supervised exercise, stent revascularization, or medical therapy for claudication due to aortoiliac peripheral artery disease: the CLEVER study. J Am Coll Cardiol. 2015 Mar 17;65(10):999–1009. Erratum in: J Am Coll Cardiol. 2015 May 12;65(18):2055.
et al; Incremental Decrease in End Points Through Aggressive Lipid Lowering Study Group. High-dose atorvastatin is superior to moderate-dose simvastatin in preventing peripheral arterial disease. Heart. 2015 Mar;101(5):356–62.
OCCLUSIVE DISEASE: FEMORAL & POPLITEAL ARTERIES
ESSENTIALS OF DIAGNOSIS
Cramping pain or tiredness in the calf with exercise.
Reduced popliteal and pedal pulses.
Foot pain at rest, relieved by dependency.
Foot gangrene or ischemic ulcers.
The superficial femoral artery is the peripheral artery most commonly occluded by atherosclerosis. Atherosclerosis of the femoral-popliteal segment usually occurs about a decade after the development of aortoiliac disease, has an even gender distribution, and commonly affects black and Hispanic patients. The disease frequently occurs where the superficial femoral artery passes through the abductor magnus tendon in the distal thigh (Hunter canal). The common femoral artery and the popliteal artery are less commonly diseased but lesions in these vessels are debilitating, resulting in short-distance claudication.
Symptoms of intermittent claudication caused by lesions of the common femoral artery, superficial femoral artery, and popliteal artery are confined to the calf. Occlusion or stenosis of the superficial femoral artery at the adductor canal when the patient has good collateral vessels from the profunda femoris will cause claudication at approximately 2–4 blocks (eFigure 12–2). However, with concomitant disease of the profunda femoris or the popliteal artery, much shorter distances may trigger symptoms. With short-distance claudication, dependent rubor of the foot with blanching on elevation may be present. Chronic low blood flow states will also cause atrophic changes in the lower leg and foot with loss of hair, thinning of the skin and subcutaneous tissues, and disuse atrophy of the muscles. With segmental occlusive disease of the superficial femoral artery, the common femoral pulsation is normal, but the popliteal and pedal pulses are reduced.
Magnetic resonance angiography of the lower extremity demonstrating preocclusive disease of the superficial femoral artery on the right and occlusion on the left. The left profunda femoris artery is the source of a rich collateral network in this patient.
B. Doppler and Vascular Findings
ABI values less than 0.9 are diagnostic of PAD and levels below 0.4 suggest critical limb ischemia. ABI readings depend on arterial compression. Since the vessels may be calcified in diabetes mellitus, chronic kidney disease, and in older adults, ABIs can be misleading. In such patients, the toe-brachial index is usually reliable with a value less than 0.7 considered diagnostic of PAD. Pulse volume recordings with cuffs placed at the high thigh, mid-thigh, calf, and ankle will delineate the levels of obstruction with reduced pressures and blunted waveforms.
Duplex ultrasonography, CTA, or MRA all adequately show the anatomic location of the obstructive lesions and are done only if revascularization is planned.
As with aortoiliac disease, risk factor reduction, medical optimization with a high-dose statin, and exercise treatment are the cornerstone of therapy. Cilostazol may improve intermittent claudication symptoms.
Intervention is indicated if claudication is progressive, incapacitating, or interferes significantly with essential daily activities or employment. Intervention is mandatory if there is rest pain or ischemic ulcers threaten the foot.
The most effective and durable treatment for lesions of the superficial femoral artery is a femoral-popliteal bypass with autogenous saphenous vein. Synthetic material, usually polytetrafluoroethylene (PTFE), can be used, but these grafts do not have the durability of vein bypass.
Endovascular techniques such as angioplasty and stenting, are often used for lesions of the superficial femoral artery. These techniques have lower morbidity than bypass surgery but also have lower rates of durability.
Endovascular therapy is most effective when it is done in patients undergoing aggressive risk factor modification in whom lesions measure less than 10 cm long. Paclitaxel-eluting stents or paclitaxel-coated balloons offer modest improvement over bare metal stents and noncoated balloons, but the success of local drug delivery in peripheral arteries is not as robust as in the coronary arteries. The 1-year patency rate is 50% for balloon angioplasty, 70% for drug-coated balloons, and 80% for stents. However, by 3 years the patency rates are significantly worse for all three techniques and reintervention for restenosis is common. In general, treating restenosis in stents is more difficult than in arteries that have undergone angioplasty.
Removal of the atherosclerotic plaque is limited to the lesions of the common femoral and the profunda femoris arteries where bypass grafts and endovascular techniques have a more limited role.
Open surgical procedures of the lower extremities, particularly long bypasses with vein harvest, have a risk of wound infection that is higher than in other areas of the body. Wound infection or seroma can occur in as many as 10–15% of cases. Myocardial infarction rates after open surgery are 5–10%, with a 1–4% mortality rate. Complication rates of endovascular surgery are 1–5%, making these therapies attractive despite their lower durability.
The prognosis for motivated patients with isolated superficial femoral artery disease is excellent, and surgery is not recommended for mild or moderate claudication in these patients. However, when claudication significantly limits daily activity and undermines quality of life as well as overall cardiovascular health, intervention may be warranted. All interventions require close postprocedure follow-up with repeated ultrasound surveillance so that recurrent narrowing can be treated promptly to prevent complete occlusion. The reported patency rate of bypass grafts of the femoral artery, superficial femoral artery, and popliteal artery is 65–70% at 3 years, whereas the patency of angioplasty is less than 50% at 3 years.
Because of the extensive atherosclerotic disease, including associated coronary lesions, 5-year mortality among patients with lower extremity disease can be as high as 50%, particularly with involvement of the infrapopliteal vessels. However, with aggressive risk factor modification, substantial improvement in longevity has been reported.
Patients with progressive symptoms, short-distance claudication, rest pain, or any ulceration should be referred to a peripheral vascular specialist.
et al; BASIL trial Participants. Bypass versus Angioplasty in Severe Ischaemia of the Leg (BASIL) trial: analysis of amputation free and overall survival by treatment received. J Vasc Surg. 2010 May;51(5 Suppl):18S–31S.
MS. Bypass versus Angioplasty in Severe Ischaemia of the Leg (BASIL) and the (hoped for) dawn of evidence-based treatment for advanced limb ischemia. J Vasc Surg. 2010 May;51(5 Suppl):69S–75S.
et al; Zilver PTX Investigators. Durable clinical effectiveness with paclitaxel-eluting stents in the femoropopliteal artery: 5-year results of the Zilver PTX randomized trial. Circulation. 2016 Apr 12;133(15):1472–83.
et al. Drug-coated balloon versus standard balloon for superficial femoral artery in-stent restenosis: the randomized Femoral Artery In-Stent Restenosis (FAIR) Trial. Circulation. 2015 Dec 8;132(23):2230–6.
et al; IN.PACT SFA Trial Investigators. Durability of treatment effect using a drug-coated balloon for femoropopliteal lesions: 24-month results of IN.PACT SFA. J Am Coll Cardiol. 2015 Dec 1;66(21):2329–38.
et al; LEVANT 2 Investigators. Trial of a paclitaxel-coated balloon for femoropopliteal artery disease. N Engl J Med. 2015 Jul 9;373(2):145–53.
et al. Results for primary bypass versus primary angioplasty/stent for intermittent claudication due to superficial femoral artery occlusive disease. J Vasc Surg. 2012 Apr;55(4):1001–7.
OCCLUSIVE DISEASE: TIBIAL & PEDAL ARTERIES
ESSENTIALS OF DIAGNOSIS
Severe pain of the forefoot that is relieved by dependency.
Pain or numbness of the foot with walking.
Ulceration or gangrene of the foot or toes.
Pallor when the foot is elevated.
Occlusive processes of the tibial arteries of the lower leg and pedal arteries in the foot occur primarily in patients with diabetes (eFigure 12–3). There often is extensive calcification of the artery wall. While claudication is a common initial symptom of ischemia, it may not be present. The first manifestation of ischemia is frequently an ulcer or gangrene rather than claudication.
Common sites of stenosis and occlusion of the visceral and peripheral arterial systems. (Reproduced, with permission, from Way LW [editor]. Current Surgical Diagnosis & Treatment, 10th ed. Originally published by Appleton & Lange. Copyright © 1994 by The McGraw-Hill Companies, Inc.)
Unless there are associated lesions in the aortoiliac or femoral/superficial femoral artery segments, claudication may not occur. The gastrocnemius and soleus muscles may be supplied from collateral vessels from the popliteal artery; therefore, when disease is isolated to the tibial vessels, there may be foot ischemia without attendant claudication, and rest pain or ulceration may be the first sign of severe vascular insufficiency. The presence of rest pain or ulcerations is termed critical limb ischemia and is associated with the highest rate of amputation. Classically, ischemic rest pain is confined to the dorsum of the foot and is relieved with dependency: the pain does not occur with standing or sitting. It is severe and burning in character, and because it is present only when recumbent, it may awaken the patient from sleep. Because of the high incidence of neuropathy in these patients, it is important to differentiate rest pain from diabetic neuropathic dysesthesia. If the pain is relieved by simply dangling the foot over the edge of the bed, which increases blood flow to the foot, then the pain is due to vascular insufficiency. Leg night cramps (not related to ischemia) occur often in patients with PAD and should not be confused with rest pain.
On examination, depending on whether associated proximal disease is present, there may or may not be femoral and popliteal pulses, but the pedal pulses will be absent. Dependent rubor may be prominent with pallor on elevation. The skin of the foot is generally cool, atrophic, and hairless.
B. Doppler and Vascular Findings
The ABI may be quite low (in the range of 0.4 or lower). ABIs, however, may be falsely elevated when the medial layer of the arterial wall of the tibial arteries calcify (Mönckeberg medial calcific sclerosis) and are not compressible. Toe-brachial indexes should be used if noncompressible ankle arteries are encountered.
Digital subtraction angiography is the gold standard method to delineate the anatomy of the tibial-popliteal segment (eFigure 12–4). MRA or CTA is less helpful for detection of lesions in this location due to the small vasculature and other technical issues related to image resolution.
Magnetic resonance angiography of the arteries below the knee. Only the peroneal arteries are patent, which is the typical pattern in diabetic patients with atherosclerosis.
Good foot care may prevent ulcers, and most diabetic patients will do well with a conservative regimen. However, if ulcerations appear and there is no significant healing within 2–3 weeks, blood flow studies (ankle-brachial index/toe-brachial index) are indicated. Poor blood flow and a foot ulcer or nightly ischemic rest pain requires revascularization to avoid a major amputation (eFigure 12–5). However, poor blood flow and infrequent rest pain without ulceration is not an indication for revascularization.
Typical appearance of ulceration from arterial insufficiency. (Reproduced, with permission, from Dean RH, Yao JST, Brewster DC [editors]. Current Diagnosis & Treatment in Vascular Surgery. Originally published by Appleton & Lange. Copyright © 1995 by The McGraw-Hill Companies, Inc.)
A. Bypass and Endovascular Techniques
Bypass with vein to the distal tibial or pedal arteries is an effective mechanism to treat rest pain and heal gangrene or ischemic ulcers of the foot. Because the foot often has relative sparing of vascular disease, these bypasses have had adequate patency rates (70% at 3 years). Fortunately, in nearly all series, limb salvage rates are much higher than patency rates.
Bypass grafting remains the primary technique of revascularization. Drug-coated balloons have not been successful in the tibial vessels. Coronary drug-eluting stents are associated with the best success when used in short lesions.
Patients with rest pain and tissue loss are at high risk for amputation, particularly if revascularization cannot be done. Patients with diabetes and PAD have a 4-fold risk of critical limb ischemia compared with nondiabetic patients with PAD and have a risk of amputation up to 20-fold when compared to an age-matched population. Many patients who have below-the-knee or above-the-knee amputations due to vascular insufficiency never attain independent ambulatory status and often need assisted-living facilities. These factors combine to demand revascularization whenever possible to preserve the limb.
The complications of intervention are similar to those listed for superficial femoral artery disease with evidence that the overall cardiovascular risk of intervention increases with decreasing ABI. The patients with critical limb ischemia require aggressive risk factor modification. Wound infection rates after bypass are higher if there is an open wound in the foot.
Patients with tibial atherosclerosis have extensive atherosclerotic burden and a high prevalence of diabetes. Their prognosis without intervention is poor and complicated by the risk of amputation.
Patients with diabetes and foot ulcers should be referred for a formal vascular evaluation. Intervention may not be necessary but the severity of the disease will be quantified, which has implications for future symptom development. Any patient with a diabetic foot infection should be evaluated for an emergent operative incision and drainage. Broad-spectrum antibiotics should be given to cover gram-positive, gram-negative, and anaerobic organisms. Centers that have a multidisciplinary limb preservation center staffed with vascular surgeons, podiatrists, plastic and orthopedic surgeons, prosthetics and orthotic specialists, and diabetes specialists should be sought.
MS. Challenges of distal bypass surgery in patients with diabetes: patient selection, techniques, and outcomes. J Vasc Surg. 2010 Sep;52(3 Suppl):96S–103S.
JL. Lower limb ischaemia in patients with diabetic foot ulcers and gangrene: recognition, anatomic patterns and revascularization strategies. Diabetes Metab Res Rev. 2016 Jan;32(Suppl 1):239–45.
et al. The Society for Vascular Surgery Lower Extremity Threatened Limb Classification System: risk stratification based on wound, ischemia, and foot infection (WIfI). J Vasc Surg. 2014 Jan;59(1):220–34.e1–2.
D. A prospective randomized multicenter comparison of balloon angioplasty and infrapopliteal stenting with the sirolimus-eluting stent in patients with ischemic peripheral artery disease: 1-year results from the ACHILLES trial. J Am Coll Cardiol. 2012 Dec 4;60(22):2290–5.
ACUTE ARTERIAL OCCLUSION OF A LIMB
ESSENTIALS OF DIAGNOSIS
Sudden pain in an extremity with absent extremity pulses.
Usually some neurologic dysfunction with numbness, weakness, or complete paralysis.
Loss of light touch sensation requires revascularization within 3 hours for limb viability.
Acute occlusion may be due to an embolus or to thrombosis of a diseased atherosclerotic segment. Emboli large enough to occlude proximal arteries in the lower extremities are almost always from the heart. Over 50% of the emboli from the heart go to the lower extremities, 20% to the cerebrovascular circulation, and the remainder to the upper extremities and mesenteric and renal circulation. Atrial fibrillation is the most common cause of cardiac thrombus formation; other causes are valvular disease or thrombus formation on the ventricular surface of a large anterior myocardial infarct.
Emboli from arterial sources such as arterial ulcerations or calcified excrescences are usually small and go to the distal arterial tree (toes).
The typical patient with primary thrombosis has had a history of claudication and now has an acute occlusion. If the stenosis has developed over time, collateral blood vessels will develop, and the resulting occlusion may cause only minimal increase in symptoms.
The sudden onset of extremity pain, with loss or reduction in pulses, is diagnostic of acute arterial occlusion. This often will be accompanied by neurologic dysfunction, such as numbness or paralysis in extreme cases. With popliteal occlusion, symptoms may affect only the foot. With proximal occlusions, the whole leg may be affected. Signs of severe arterial ischemia include pallor, coolness of the extremity, and mottling. Impaired neurologic function progressing to anesthesia accompanied with paralysis suggests a poor prognosis.
B. Doppler and Laboratory Findings
There will be little or no flow found with Doppler examination of the distal vessels. Imaging, if done, may show an abrupt cutoff of contrast with embolic occlusion. Blood work may show myoglobin and metabolic acidosis.
Whenever possible, imaging should be done in the operating room because obtaining angiography, MRA, or CTA may delay revascularization and jeopardize the viability of the extremity (eFigure 12–6). However, in cases with only modest symptoms and where light touch of the extremity is maintained, imaging may be helpful in planning the revascularization procedure.
A: Femoral arteriogram showing occlusion of the superficial femoral and proximal popliteal arteries. B: Femoral arteriogram showing patency of the femoral and popliteal arteries after endarterectomy. (Reproduced, with permission, from Way LW [editor]. Current Surgical Diagnosis & Treatment, 10th ed. Originally published by Appleton & Lange. Copyright © 1994 by The McGraw-Hill Companies, Inc.)
Immediate revascularization is required in all cases of symptomatic acute arterial thrombosis. Evidence of neurologic injury, including loss of light touch sensation, indicates that collateral flow is inadequate to maintain limb viability and revascularization should be accomplished within 3 hours. Longer delays carry a significant risk of irreversible tissue damage. This risk approaches 100% at 6 hours.
As soon as the diagnosis is made, unfractionated heparin should be administered (5000–10,000 units) intravenously, followed by a heparin infusion to maintain the activated partial thromboplastin time (aPTT) in the therapeutic range (60–85 seconds) (12–18 units/kg/h). This helps prevent clot propagation and may also help relieve associated vessel spasm. Anticoagulation may improve symptoms, but revascularization will still be required.
B. Endovascular Techniques
Catheter-directed chemical thrombolysis into the clot with tissue plasminogen activator (TPA) may be done but often requires 24 hours or longer to fully lyse the thrombus. This approach can be taken only in patients with an intact neurologic examination who do not have absolute contraindications such as bleeding diathesis, gastrointestinal bleeding, intracranial trauma, or neurosurgery within the past 3 months. A sheath is used to advance a TPA-infusing catheter through the clot. Heparin is administered systemically to prevent thrombus formation around the sheath. Frequent vascular and access site examinations are required during the thrombolytic procedure to assess for improved vascular perfusion and to guard against the development of a hematoma.
General anesthesia is usually indicated; local anesthesia may be used in extremely high-risk patients if the exploration is to be limited to the common femoral artery. In extreme cases, it may be necessary to perform thrombo-embolectomy from the femoral, popliteal and even the pedal vessels to revascularize the limb. The combined use of devices that pulverize and aspirate clot and intraoperative thrombolysis with TPA improves outcomes.
Complications of revascularization of an acutely ischemic limb can include severe metabolic acidosis, hyperkalemia, and cardiac arrest. In cases where several hours have elapsed but recovery of viable tissue may still be possible, significant levels of lactic acid, potassium, and other harmful agents may be released into the circulation during revascularization. Pretreatment of the patient with sodium bicarbonate (150 mEq NaHCO3 in 1 liter of dextrose 5% in water) prior to reestablishing arterial flow is required. Surgery in the presence of thrombolytic agents and heparin carries a high risk of postoperative wound hematoma.
There is a 10–25% risk of amputation with an acute arterial embolic occlusion, and a 25% or higher in-hospital mortality rate. Prognosis for acute thrombotic occlusion of an atherosclerotic segment is generally better because the collateral flow can maintain extremity viability. The longer-term survival reflects the overall condition of the patient. In high-risk patients, an acute arterial occlusion is associated with a dismal prognosis.
OCCLUSIVE CEREBROVASCULAR DISEASE
ESSENTIALS OF DIAGNOSIS
Sudden onset of weakness and numbness of an extremity or the face, aphasia, dysarthria, or unilateral blindness (amaurosis fugax).
Bruit heard loudest in the mid neck.
Unlike the other vascular territories, symptoms of ischemic cerebrovascular disease are predominantly due to emboli. The ischemia is reversible (transient ischemic attacks [TIAs]) when collateral flow reestablishes perfusion but is a sign that the risk of additional emboli and permanent deficits is high (eFigure 12–7). One-quarter of all ischemic strokes may be due to emboli from an arterial source; approximately 90% of these emboli originate from the proximal internal carotid artery, an area uniquely prone to the development of atherosclerosis. Lesions in the proximal great vessels of the aortic arch and the common carotid are less common. Intracranial atherosclerotic lesions are uncommon in the west but are the most frequent location of cerebrovascular disease in Asian populations.
Diagram showing common sites of stenosis and occlusion of the extracranial cerebral vasculature. (Reproduced, with permission, from Way LW [editor]. Current Surgical Diagnosis & Treatment, 10th ed. Originally published by Appleton & Lange. Copyright © 1994 by The McGraw-Hill Companies, Inc.)
Generally, the symptoms of a TIA last only a few seconds to minutes (but may continue up to 24 hours) while symptoms of a stroke persist beyond 24 hours. The most common lesions involve the anterior circulation in the cortex with both motor and sensory involvement. Emboli to the retinal artery cause unilateral blindness; when this blindness is transient, it is termed “amaurosis fugax.” Posterior circulation symptoms referable to the brainstem, cerebellum, and visual regions of the brain may be due to atherosclerosis of the vertebral basilar systems and are much less common.
Signs of cerebrovascular disease may include carotid artery bruits. However, there is poor correlation between the degree of stenosis and the presence of the bruit. Furthermore, the presence of a bruit does not correlate with stroke risk. Nonfocal symptoms, such as dizziness and unsteadiness, seldom are related to cerebrovascular atherosclerosis.
Duplex ultrasonography is the imaging modality of choice with high specificity and sensitivity for detecting and grading the degree of stenosis at the carotid bifurcation (eFigures 12–8 and 12–9) (see Chapter 24).
Calcified plaque. Real-time scan of the common carotid artery and internal carotid artery demonstrates echogenic foci (arrows) with acoustical shadowing. (Reproduced, with permission, from Krebs CA, Giyanani VL, Eisenberg RL. Ultrasound Atlas of Disease Processes. Originally published by Appleton & Lange. Copyright © 1993 by The McGraw-Hill Companies, Inc.)
Stenosis. Color Doppler of the common carotid artery-internal carotid artery junction shows calcified plaque obscuring a portion of the vessel (arrow). (Reproduced, with permission, from Krebs CA, Giyanani VL, Eisenberg RL. Ultrasound Atlas of Disease Processes. Originally published by Appleton & Lange. Copyright © 1993 by The McGraw-Hill Companies, Inc.)
Excellent depiction of the full anatomy of the cerebrovascular circulation from arch to cranium can be obtained with either MRA or CTA (eFigure 12–10). Each of the modalities may have false-positive or false-negative findings. Since the decision to intervene in cases of carotid stenosis depends on an accurate assessment of the degree of stenosis, it is recommended that at least two modalities be used to confirm the degree of stenosis. Diagnostic cerebral angiography is reserved for cases where carotid artery stenting (CAS) is to be done.
Digital subtraction angiography of the carotid bifurcation showing severe carotid stenosis and a large ulceration.
See Chapter 24 for a discussion of the medical management of occlusive cerebrovascular disease.
Large studies have shown a 5-year reduction in stroke rate from 11.5% to 5.0% with surgical treatment of asymptomatic carotid stenosis that is greater than 60%. Patients with asymptomatic carotid stenosis may benefit from carotid intervention if their risk for intervention is low and their expected survival is longer than 5 years. The CREST2 NIH-sponsored trial is determining the validity of these recommendations for intervention since there has been improvements in conservative therapy, including the use of statins.
Mild to moderate disease (30–50% stenosis) indicates the need for ongoing monitoring and aggressive risk factor modification. Patients with carotid stenosis that suddenly worsens are thought to have an unstable plaque and are at particularly high risk for embolic stroke.
Large randomized trials have shown that patients with TIAs or strokes from which they have completely or nearly completely recovered will benefit from carotid intervention if the ipsilateral carotid artery has a stenosis of more than 70% (Figure 12–1), and they are likely to benefit if the artery has a stenosis of 50–69%. In these situations, carotid endarterectomy (CEA) and CAS have been shown to have a durable effect in preventing further events. In symptomatic patients, intervention should ideally be planned within 2 weeks since delays increase the risk of a second event.
High-grade (90%) stenosis of internal carotid artery, with ulceration (arrow). (Used, with permission, from Dean SM, Satiani B, Abraham WT. Color Atlas and Synopsis of Vascular Diseases. McGraw-Hill, 2014.)
The most common complication from carotid intervention is cranial nerve injury while the most dreaded complication is stroke due to embolization of plaque material. The American Heart Association’s recommendations for upper limits of acceptable combined morbidity and mortality for these interventions is 3% for patients with asymptomatic carotid stenosis, 5% for those with TIAs, and 7% for patients with previous stroke. Results that are not as good as these guidelines will jeopardize the therapeutic benefit of carotid intervention.
A. Carotid Endarterectomy
In the 2010 CREST study the stroke risk for CEA was 2.3%. CEA also carries transient 1–2% risk cranial nerve injury (usually the vagus). There is also the risk of postoperative neck hematoma, which can cause acute compromise of the airway. Coronary artery disease is a comorbidity in most of these patients. Myocardial infarction rates after CEA are approximately 5%.
B. Angioplasty and Stenting
CAS had a stroke risk of 4.1% in the 2010 CREST study; patients over 70 years of age as well as women had higher stroke rates with CAS than with CEA. However, the risk of myocardial infarction was lower with CAS compared to CEA (1.1% vs 2.3%). CAS does avoid both cranial nerve injury and neck hematoma. However, emboli are more common during carotid angioplasty and stenting in spite of the use of embolic protection devices, although newer devices may reduce embolic risk. In cases of restenosis after previous carotid intervention, CAS is an excellent choice since the risk of embolization is low and the risk of cranial nerve injury with surgery is high.
Twenty-five percent of patients presenting with carotid stenosis and a TIA or small stroke will have further brain ischemia within 18 months with most of the events occurring within the first 6 months. Historically, patients with asymptomatic carotid stenosis are believed to have an annual stroke rate of just over 2% but this may be lower in the statin era. Prospective ultrasound screening at least annually is recommended in asymptomatic patients with known carotid stenosis because approximately 10% of asymptomatic patients have evidence of plaque progression per year which increases stroke risk. Concomitant coronary artery disease is common and is an important factor in these patients both for perioperative risk and long-term prognosis. Aggressive risk factor modification should be prescribed for patients with cerebrovascular disease regardless of planned intervention.
Asymptomatic or symptomatic patients with a carotid stenosis of more than 80% and patients with carotid stenosis of less than 80% with symptoms of a TIA or stroke should be referred to a vascular specialist for consultation.
et al; CREST Investigators. Long-term results of stenting versus endarterectomy for carotid-artery stenosis. N Engl J Med. 2016 Mar 17;374(11):1021–31.
et al; CREST Investigators. Stenting versus endarterectomy for treatment of carotid-artery stenosis. N Engl J Med. 2010 Jul 1;363(1):11–23.
et al. Outcomes after carotid artery stenting in medicare beneficiaries, 2005 to 2009. JAMA Neurol. 2015 Mar;72(3):276–86.
et al; VISSIT Trial Investigators. Effect of a balloon-expandable intracranial stent vs medical therapy on risk of stroke in patients with symptomatic intracranial stenosis: the VISSIT randomized clinical trial. JAMA. 2015 Mar 24–31;313(12):1240–8.
VISCERAL ARTERY INSUFFICIENCY (INTESTINAL ANGINA)
ESSENTIALS OF DIAGNOSIS
Severe postprandial abdominal pain.
Weight loss with a “fear of eating.”
Acute mesenteric ischemia: severe abdominal pain yet minimal findings on physical examination.
Acute visceral artery insufficiency results from either embolic occlusion or primary thrombosis of at least one major mesenteric vessel. Ischemia can also result from nonocclusive mesenteric vascular insufficiency, which is generally seen in patients with low flow states, such as heart failure, or hypotension. A chronic syndrome occurs when there is adequate perfusion for the viscera at rest but ischemia occurs with severe abdominal pain when flow demands increase with feeding. Because of the rich collateral network in the mesentery, generally at least two of the three major visceral vessels (celiac, superior mesenteric, inferior mesenteric arteries) are affected before symptoms develop. Ischemic colitis, a variant of mesenteric ischemia, usually occurs in the distribution of the inferior mesenteric artery. The intestinal mucosa is the most sensitive to ischemia and will slough if underperfused. The clinical presentation is similar to inflammatory bowel disease. Ischemic colitis can occur after aortic surgery, particularly aortic aneurysm resection or aortofemoral bypass for occlusive disease, when there is a sudden reduction in blood flow to the inferior mesenteric artery.
1. Acute intestinal ischemia
Patients with primary visceral arterial thrombosis often give an antecedent history consistent with chronic intestinal ischemia. The key finding with acute intestinal ischemia is severe, steady epigastric and periumbilical pain with minimal or no findings on physical examination of the abdomen because the visceral peritoneum is severely ischemic or infarcted and the parietal peritoneum is not involved. A high white cell count, lactic acidosis, hypotension, and abdominal distention may aid in the diagnosis.
2. Chronic intestinal ischemia
Patients are generally over 45 years of age and may have evidence of atherosclerosis in other vascular beds. Symptoms consist of epigastric or periumbilical postprandial pain lasting 1–3 hours. To avoid the pain, patients limit food intake and may develop a fear of eating. Weight loss is universal.
Characteristic symptoms are left lower quadrant pain and tenderness, abdominal cramping, and mild diarrhea, which is often bloody.
B. Imaging and Colonoscopy
Contrast-enhanced CT is highly accurate at determining the presence of ischemic intestine. In patients with acute or chronic intestinal ischemia, a CTA or MRA can demonstrate narrowing of the proximal visceral vessels. In acute intestinal ischemia from a nonocclusive low flow state, angiography is needed to display the typical “pruned tree” appearance of the distal visceral vascular bed (eFigure 12–11). Ultrasound scanning of the mesenteric vessels may show proximal obstructing lesions.
A: Preoperative visceral arteriogram showing severe stenosis of the celiac and superior mesenteric arteries. B: The postoperative visceral arteriogram shows wide patency of the celiac and superior mesenteric arteries after transaortic endarterectomy. The inset shows the atherosclerotic stenotic lesions removed by endarterectomy. (Reproduced, with permission, from Way LW [editor]. Current Surgical Diagnosis & Treatment, 10th ed. Originally published by Appleton & Lange. Copyright © 1994 by The McGraw-Hill Companies, Inc.)
In patients with ischemic colitis, colonoscopy may reveal segmental ischemic changes, most often in the rectal sigmoid and splenic flexure where collateral circulation may be poor.
A high suspicion of acute intestinal ischemia dictates immediate exploration to determine bowel viability. If the bowel remains viable, bypass using a prosthetic conduit can be done either from the supra-celiac aorta or common iliac artery to the celiac and the superior mesentery artery. In cases where bowel viability is questionable or bowel resection will be required, the bypass can be done with autologous vein to avoid the use of prosthetic conduits in a potentially contaminated field. Angioplasty and stenting of the arteries can be used but does not avoid a surgical evaluation of bowel viability.
In chronic intestinal ischemia, angioplasty and stenting of the proximal vessel may be beneficial depending on the anatomy of the stenosis. Should an endovascular solution not be available, an aorto-visceral artery bypass is the preferred management. The long-term results are highly durable. Visceral artery endarterectomy is reserved for cases with multiple lesions where bypass would be difficult.
The mainstay of treatment of ischemic colitis is maintenance of blood pressure and perfusion until collateral circulation becomes well established. The patient must be monitored closely for evidence of perforation, which will require resection.
The combined morbidity and mortality rates are 10–15% from surgical intervention in these debilitated patients. However, without intervention both acute and chronic intestinal ischemia are uniformly fatal. Adequate collateral circulation usually develops in those who have ischemic colitis, and the prognosis for this entity is better than chronic intestinal ischemia.
Any patient in whom there is a suspicion of intestinal ischemia should be urgently referred for imaging and possible intervention.
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et al. Chronic mesenteric ischemia outcome analysis and predictors of endovascular failure. J Vasc Surg. 2016 Jun;63(6):1582–7.
ACUTE MESENTERIC VEIN OCCLUSION
The hallmarks of acute mesenteric vein occlusion are postprandial pain and evidence of a hypercoagulable state. Acute mesenteric vein occlusion presents similarly to the arterial occlusive syndromes but is much less common. Patients at risk include those with paroxysmal nocturnal hemoglobinuria; protein C, protein S, or antithrombin deficiencies; or the JAK2 mutation. These lesions are difficult to treat surgically, and thrombolysis is the mainstay of therapy. Aggressive long-term anticoagulation is required for these patients.