Acute extremities ischemia Text, LNMI
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TOPIC: Classification of acute extremities ischemia. Clinical stages. Diagnosis. Differencial diagnosis. Methods of surgical treatment.
Acute Arterial Obstruction
The manifestations of acute arterial occlusion vary greatly, depending on the level and severity of the obstruction, timing from onset to presentation, and degree of chronic vascular disease and collateral circulation. The classic signs and symptoms of acute arterial occlusion include pain, pallor, pulselessness, paresthesias, and paralysis. Cutaneous manifestations are among the earliest in an acute occlusion. Pallor is seen initially and occurs with the loss of pulses. If timely revascularization does not take place, blistering of the skin may develop, followed by frank gangrene. Sensorimotor manifestations are among the most common symptoms in acute ischemia. Pain is noted early in the course of events; however, this may progress to numbness, which should not be mistaken as improvement. As ischemia progresses, nerve dysfunction may lead to sensory loss, followed by paralysis and muscle destruction resulting in paralysis; a late manifestation of ischemia in muscle is rigor, suggesting muscle death. The quality of pulses in the contralateral extremity can be very informative. It is uncommon for a patient with chronic vascular disease in one extremity to have full, strong, distal pulses in the other. A normal pulse exam in the contralateral leg suggests that the patient has had an acute event in the absence of chronic disease. This patient is unlikely to have developed significant collaterals, and expediency in obtaining revascularization is vital. The two major causes of acute arterial occlusion are emboli and thrombosis. An embolic source accounts for 80% of cases. The most common sites in the lower extremity for emboli to become lodged are, in descending order, the femoral, iliac, aorta, and popliteal arteries. Acute thrombosis, usually of a previously stenotic area in the setting of atherosclerosis, is the second most common cause of acute arterial occlusion. Thrombosis may also occur in the setting of low flow states such as congestive heart failure or hypotension, in hypercoagulable states, and in vascular grafts. The management of the patient with acute lowerextremity ischemia includes a thorough but expeditious history and physical, followed by optimization of hemodynamics and fluid balance. Unless a contraindication exists, most patients are heparinized. If the patient is thought to have potentially viable extremities, the lesion can be further delineated with arteriography. At this point a decision is made whether to treat the patient operatively or with an attempt at thrombolysis. If open surgery is chosen, the most common procedure is a catheter embolectomy, usually via a cutdown at the femoral or belowknee popliteal location. Alternatively, particularly in the setting of a thrombosed bypass graft, bypass reconstruction may be necessary. In an analysis of multiple series, the mortality and limb salvage rates were 12.6% and 78%, respectively, for the use of heparin alone in the setting of acute ischemia, 17% and 84% for thromboembolectomy alone, and 10.2% and 92% when the combination of perioperative heparin and catheter embolectomy was used.30 Postoperatively one should consider long-term anticoagulation as it may reduce the incidence of recurrent embolization from 21% to 7%.30 The comparison of lytic therapy and surgical therapy in the initial management of acute lower-extremity ischemia has been carefully studied in several multiinstitutional studies. In one study there was a significantly increased number of major adverse events in the thrombolysis group at 1 month as compared to the surgery-alone group. However, when patients were stratified to duration of ischemia, there were clear trends in favor of lysis in patients whose onset of ischemic symptoms was less than 14 days before presentation.31 An optimal situation in the setting of acute ischemia would be that of a patient with evidence of an acute thrombotic event who undergoes thrombolysis that clears the thrombus and reestablishes flow nonoperatively and also uncovers a culpable lesion which would be angioplastied or surgically reconstructed electively. Other principles of management of the patient with acute lower-extremity ischemia include careful monitoring postoperatively for metabolic derangements related to reperfusion such as acidosis and hyperkalemia, evaluation of the urine for myoglobin, and, if present, treatment with hydration, manitol, and bicarbonate to induce an alkaline diuresis. Additionally, if a limb has been ischemic for a significant time or develops elevated compartment pressures, one should have a low threshold for performing fasciotomy. Embolic events can also take the form of atheroemboli as atherosclerotic debris in a proximal artery dislodges and occludes distal arteries. The most common manifestation of this event is the blue toe syndrome. Blue toe syndrome consists of the sudden appearance of a cool, painful, cyanotic toe or forefoot in the often perplexing presence of strong pedal pulses and a warm foot. By far the most common source is the distal aorta, but atheromatous debris can embolize from anywhere along the aorta as well as from peripheral arteries such as the femoral or popliteal. These episodes portend both similar and more severe episodes in the future. Therefore, location and eradication of the embolic source is usually indicated.32
Section XI – ACUTE LIMB ISCHEMIA
Kenneth Ouriel, MD
Chapter 66 – Acute Limb Ischemia
KARTHIKESHWAR KASIRAJAN, MD, FACS KENNETH OURIEL, MD, FACS, FACC
Limb ischemia occurs when an extremity is deprived of adequate blood flow. Symptoms depend on the severity of hypoperfusion. The process can develop suddenly and, when the patient presents soon after its onset, the entity is said to represent acute limb ischemia. Acute limb ischemia is differentiated from those patients with an insidious onset of symptoms; these patients tend to present late and the phrase chronic limb ischemia is used to identify such a scenario. The extent of collateral flow across the site of occlusion often determines the severity of symptoms. Patients with long-standing atherosclerotic lesions often have adequate time to develop collateral channels; hence, arterial occlusion in these patients often may fall into the “chronic” category.
PATHOPHYSIOLOGY
Acute limb ischemia may occur as the result of embolization or in-situ thrombosis. Emboli originate from the heart in more than 90% of cases and normally lodge at the site of an arterial bifurcation such as the distal common femoral or popliteal arteries. The decreasing prevalence of rheumatic heart disease underlies a diminishing proportion of embolic versus thrombotic causes for acute limb ischemia. When embolization occurs, it usually does so in the setting of atrial fibrillation or acute myocardial infarction, when portions of atrial or ventricular mural thrombus detach and embolize to the arterial tree. It is often difficult to distinguish embolus from thrombosis, but embolic occlusions should be suspected in patients with the following features: (1) acute onset where the patient is often able to accurately time the moment of the event; (2) prior history of embolism; (3) known embolic source, such as cardiac arrhythmias; (4) no prior history of intermittent claudication; and (5) normal pulse and Doppler examination in the unaffected limb.
Thrombosis as an etiology for acute limb ischemia is a much more diverse category than embolization. With the increased use of peripheral arterial bypass grafts for chronic limb ischemia, and noting the finite patency rate of any bypass graft conduit, it is not surprising that acute graft occlusion is now the most frequent cause of acute lower extremity ischemia in most centers. Symptoms may be less dramatic than embolic occlusion, depending on the extent of collateral flow across the site of occlusion. In addition to the presence of collateral channels, the location of the occlusion may also play a critical role in the severity of limb ischemia. For example, occlusion of the popliteal artery results in profound limb ischemia, since it is the only artery crossing at the level of the knee. By contrast, occlusion of the anterior tibial artery is often asymptomatic because the posterior tibial and peroneal arteries can function as alternate parallel channels to supply the foot.
Irrespective of the etiology of ischemia, the end result is the build-up of toxic byproducts within the ischemic tissue bed. These toxins include the free radicals, which are oxygen-derived, chemically reactive molecules that are responsible for the injury that occurs after ischemia and reperfusion. Ischemia induces leakage of protein and fluid from the capillary bed, resulting in tissue edema. Hydrodynamic pressure in the extravascular space rises to a level that competes with venous outflow, perpetuating a vicious cycle that can eventually impede arterial inflow. At first, this process occurs at a microscopic level, but it may progress to the development of high tissue pressures at a regional level and the clinical entity known as the compartment syndrome. The development of a compartment syndrome is hastened by the abrupt reperfusion of a previously ischemic tissue bed, a phenomenon that explains the relatively frequent need for fasciotomy after lower extremity surgical revascularization for severe limb ischemia.
DIAGNOSIS
Acute limb ischemia is a clinical diagnosis. Patients complain of numbness and pain in the extremity, progressing in severe cases to motor loss and muscle rigidity. Examination reveals the absence of palpable pulses, and the location of the pulse deficit allows one to predict the site of arterial occlusion. The “5 Ps” have been used as a mnemonic to remember the presentation of a patient with acute limb ischemia—paresthesia, pain, pallor, pulselessness, and paralysis. In some cases, a sixth P is added—poikilothermia, meaning equilibration of the temperature of the limb to that of the ambient environment (coolness). The process is sometimes confused with deep venous thrombosis by an inexperienced observer. Although a deep venous thrombosis may manifest as limb ischemia when severe (phlegmasia cerulea dolens), profound lower extremity edema is uncommon in pure arterial ischemia. Occasionally, a patient with arterial ischemia and pain at rest keeps the extremity in a dependent position and edema may develop; such a scenario may be apparent if an adequate history is obtained. Pain may either be constant or elicited by passive movement of the involved extremity. History should include a description of the duration, location, intensity, and suddenness of the onset of pain and change over time. Embolic occlusions are usually quite sudden and of great intensity, such that patients often present within a few hours of onset. The past history should state whether or not the patient has a history of intermittent claudication, previous leg bypass or other vascular procedures, and history suggestive of embolic sources such as cardiac arrhythmias and aortic aneurysms. General atherosclerotic risk factors (smoking, hypertension, diabetes, hyperlipidemia, family history of cardiac or vascular events) should be recorded because these can be predictors of thrombosis.
In an effort to classify the extent of acute ischemia for standardization reporting of outcome, the Society for Vascular Surgery/International Society for Cardiovascular Surgery (SVS/ISCVS) (now SVS) ad hoc committee was established and published what has now come to be known as the Rutherford criteria, after Dr. Robert Rutherford, the lead author of the article. The following three classes were defined:
Class 1: the limb is viable and remains so even without therapeutic intervention
Class 2: the limbs are threatened and require revascularization for salvage
Class 3: those limbs that are irreversibly ischemic and infarction has developed such that salvage is not possible
As examples, a patient with a palpable femoral pulse but an absent popliteal pulse is likely to have a superficial femoral artery occlusion. Absence of a femoral pulse signifies disease above the inguinal ligament, within the iliac arterial segment or the aorta itself. Patients with common femoral artery emboli maintain an easily palpable femoral pulse, sometimes even augmented with a “water-hammer” characteristic, until such time as the absence of outflow in the external iliac artery causes this vessel to thrombose and the femoral pulse to disappear. Patients with popliteal emboli, by contrast, usually have a palpable popliteal pulse but no palpable pulses below (dorsalis pedis or posterior tibial). Finally, a patient with leg ischemia secondary to a popliteal aneurysm usually demonstrates a very large and easily palpable popliteal pulse, concurrent with severe calf and foot ischemia. The popliteal pulse is maintained in these patients as a result of the events leading to occlusion—the aneurysm is associated with serial embolic events to the three crural vessels, occluding them one by one until, at the time of the last occlusion, the leg becomes ischemic. The aneurysm itself, however, remains palpable owing to the somewhat static column of blood and absent outflow.
Even the most astute clinician sometimes has difficulty in discerning his or her own digital pulse from the patient’s pedal pulse. For this reason, the use of a Doppler instrument is advantageous to document flow within the smaller arteries and, most important, to provide an objective and quantitative assessment of the extent of arterial insufficiency through the calculation of a Doppler-derived ankle-brachial index (ABI). Normally, the ABI is greater than 1.0. The index is decreased to 0.40 to 0.80 in patients with claudication and to lower levels in patients with pain at rest or tissue loss. The ABI may be normal in some patients with mild arterial narrowing; treadmill exercise has been used in these cases to increase the sensitivity of the test. Patients with diabetes mellitus or renal failure may have calcific lower leg arteries, rendering them incompressible and causing a falsely elevated ABI; in these cases a toe-brachial pressure index can be measured and is more predictive of significant arterial disease.] In some centers, transcutaneous oxygen tension has also been used to assess the severity of peripheral arterial occlusion as well as to predict the most appropriate level of amputation.
Characteristic Ankle-Brachial Indices in Patients Presenting with Lower Limb Ischemia
CLINICAL CATEGORY
ANKLE-BRACHIAL INDEX
Normal
>0.97 (usually 1.10)
Claudication
0.40–0.80
Rest pain
0.20–0.40
Ulceration, gangrene
0.10–0.40
Acute ischemia
Usually <0.10
The anatomic level of the arterial stenoses can be predicted from palpation of pulses in the femoral, popliteal, and ankle regions. For example, patients with disease confined to the superficial femoral artery have a normal femoral pulse but no palpable popliteal or ankle pulses below, whereas patients with aortoiliac disease have absent femoral pulses as well. Doppler segmental pressures are also useful in defining the level of involvement; a drop in pressure of 30 mm Hg or more ...
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