Acs0605 Pulseless Extremity And Atheroembolism

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Acs0605 Pulseless Extremity And Atheroembolism

  1. 1. © 2007 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 6 VASCULAR SYSTEM 5 PULSELESS EXTREMITY AND ATHEROEMBOLISM — 1 5 PULSELESS EXTREMITY AND ATHEROEMBOLISM Sonny W.Tucker, Jr., M.D., Vicken N. Pamoukian, M.D., F.A.C.S., and Cynthia K. Shortell, M.D., F.A.C.S. Approach to the Acutely Ischemic Limb Pulseless Extremity (Acute Limb Ischemia) decision trees, or clinical pathways can help the clinician visualize Limb ischemia occurs when blood flow to an extremity is and evaluate multiple potential options that then serve as the basis inadequate. It is commonly the result of stenosis or occlusion of for selecting the path likely to yield the best outcome. a native vessel or bypass graft, and the symptoms are directly related to the duration and severity of the hypoperfusion. Acute CLINICAL EVALUATION limb ischemia (ALI) is a sudden reduction in limb perfusion that threatens the viability of an extremity [see Discussion, History Pathophysiology of ALI, below].The incidence of ALI in the gen- Because ALI is a clinical diagnosis, a eral population is approximately 1.7/10,000 per year.1 The clin- complete history is essential (unless it is ical presentation ranges from subtle to dramatic and is often unobtainable for some reason). complicated by various comorbid conditions typically seen in Generally, the dominant symptoms are patients with vascular diseases [see Table 1]. The goals of man- related to pain (usually the first manifes- agement include limb salvage, minimization of morbidity, and tation) or to loss of function. The onset prevention of death. However, given that no objective markers of and duration of symptoms should be limb viability are currently available, the initial determination of determined, and the location and the intensity of any changes whether a limb is likely to be viable must be made on clinical should be established. The pain of ALI is often not well localized grounds. and is unaffected by gravity. An effort should be made to deter- A study from the 1970s that comprised more than 3,000 mine whether the likely cause is embolic or thrombotic: pain of patients with ALI from 35 centers documented a mortality of 26% sudden onset suggests an embolic cause, whereas long-standing and an amputation rate of 37%.2 Since then, substantial progress pain before the acute event suggests a thrombotic cause [see in surgical management has been made and major technological Discussion, Etiology of ALI, below]. advances have occurred, but morbidity and mortality remain high, It is imperative to ask whether the patient experienced pain with death rates approximating 15% and amputation rates rang- before the current ischemic episode and whether the current ing from 10% to 30%.3 episode is the first. It is also important to ask about previous sur- Given the general frailty of ALI patients and the multiplicity of gical revascularization, as well as previous or current cardiac dis- available therapeutic options, it is prudent to take a methodical ease (e.g., myocardial infarction [MI], atrial fibrillation, or valvu- approach to the management of ALI. Making use of algorithms, lar disease), aneurysmal disease, or vasculitis. Finally, inquiries Table 1— Incidence of Medical Comorbidities in Patients 97 Presenting with ALI Incidence (%) Comorbidity Rochester Trial TOPAS-1 Trial TOPAS-2 Trial Total (N = 114) (N = 213) (N = 544) (N = 871) Cerebrovascular disease NR 15.4 11.5 11.6 Congestive heart failure NR 15.5 12.5 13.3 Coronary artery disease 56.1 47.1 42.5 45.4 Diabetes mellitus 28.1 36.7 29.0 30.8 Hypercholesterolemia 31.6 29.6 23.5 26.0 Hypertension 63.2 60.9 69.6 60.3 Malignancy NR 11.9 11.5 11.6 Tobacco history 51.8 79.3 77.5 74.6 NR—not reported TOPAS—Thrombolysis Or Peripheral Arterial Surgery
  2. 2. © 2007 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 6 VASCULAR SYSTEM 5 PULSELESS EXTREMITY AND ATHEROEMBOLISM — 2 Approach to the Acutely Ischemic Limb Patient presents with acute limb ischemia Obtain detailed history and perform careful physical exam. Assess limb viability (category I, II, or III). Order ECG and laboratory tests. Perform noninvasive cardiac evaluation: Doppler segmental pressures, ABI, duplex scan (if available). Initiate heparin anticoagulation: 18 U/kg bolus, followed by infusion of 80 U/kg to aPTT twice normal. Category I ALI Category IIa ALI Category IIb ALI Category III ALI Treat patient for Limb is marginally threatened. Limb is immediately threatened. Amputate limb. chronic limb ischemia. Perform urgent arteriography. Perform urgent arteriography. Evaluate Evaluate for • location and type of clot for • location and type of clot • duration • duration of ischemia • type of vascular of ischemia • type of vascular conduit conduit (native or bypass graft) (native or bypass graft) • patient status • patient status • safety of thrombolysis. • safety of thrombolysis. Perform percutaneous mechanical Perform surgical embolectomy. thrombectomy. or Perform thrombolysis with UK, t-PA, or rt-PA. Embolectomy is Embolectomy is successful unsuccessful Obtain completion Perform bypass of target angiogram. vessel. If revascularization is delayed, perform fasciotomy. Obstruction does not resolve Obstruction resolves Obstruction does not resolve Perform surgical embolectomy, If thrombosis rather than embolism Give intraoperative lytic therapy. as for category IIb (see above, right). seems likely, seek underlying lesion. If extensive lesion remains, perform bypass of target vessel. If revascularization is delayed, perform fasciotomy. Underlying focal lesion No underlying focal lesion is found is found Treat with angioplasty or Provide oral anticoagulation endovascular stenting. with warfarin and aspirin. If revascularization is delayed, perform fasciotomy.
  3. 3. © 2007 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 6 VASCULAR SYSTEM 5 PULSELESS EXTREMITY AND ATHEROEMBOLISM — 3 Table 2— Localization of Arterial Obstruction through Palpation of Peripheral Pulses97 Palpable Pulses Location of Possible Causes Femoral Popliteal Pedal Obstruction – – – Aortoiliac segment Aortoiliac atherosclerosis; embolus to common iliac bifurcation + – – Femoral segment Thrombosis, femoral atherosclerosis; common femoral embolus + ++ – Distal popliteal tibials Popliteal aneurysm with embolization + + – Distal popliteal tibials Popliteal embolus; popliteal/tibial atherosclerosis, diabetes should be made about previous atherosclerotic disease, current threatening ischemia.The extent of paralysis must be deter- risk factors for atherosclerosis (e.g., hypertension, smoking, dia- mined. The intrinsic muscles of the foot are affected by betes, tobacco abuse, hyperlipidemia, and stroke), and previous ischemia of the vessels around the ankle. Dorsiflexion and clotting episodes. plantar flexion of the foot are functions of muscles that rely The characteristic signs of ALI may be summarized as the six on blood supplied by the popliteal and superficial femoral Ps: Pulselessness, Pain, Pallor, Poikilothermia, Paresthesia, and arteries. Loss of dorsiflexion and plantar flexion indicates Paralysis. that blood flow is cut off at a higher level and signals that more tissue may be at risk. 1. Pulses should be palpated and documented. Any previous documentation should be noted and used for comparison. Staging of Limb Ischemia Careful evaluation of pulses will help localize the area of The primary goal of the clinical evaluation is to determine the arterial obstruction. When clot is fresh, its soft, semiliquid severity of the disease process so that appropriate management consistency allows the pulse to be translated at the level of can be rapidly instituted. To this end, the key question that must obstruction. Only when the thrombus becomes organized be answered is whether the limb is viable. In 1997, the Joint and densely compacted is the pulse lost at the site of occlu- Council of the Society for Vascular Surgery and the North sion. As an example, in a patient with obstruction at the American Chapter of the International Society for Cardiovascular popliteal artery, popliteal pulses remain palpable in the ear- Surgery developed reporting standards for ALI and stratified it lier stages of the process, but distal pulses are lost [see Table 2]. into three distinct categories on the basis of the severity of the dis- 2. Pain should be documented with regard to severity, area, ease process [see Table 3].4 and progression. In category I ALI, patients present with acute occlusion of an 3. Pallor may be seen in the early stages, followed by cyanosis. artery that is chronically narrowed.Therefore, abundant collater- 4. Poikilothermia may propagate the ischemic cascade als can be found, and the limb is viable. In category II ALI, the through its vasoconstrictive effects. The level of coolness ischemic limb is threatened but may be salvaged without the need and pallor is typically one level below the point of occlusion for an amputation if adequate revascularization can be achieved. on the arterial tree, and it should correlate with the pulses This category is further subdivided into categories IIa and IIb. or signals found. As always, baseline documentation should Category IIa includes patients with mild forefoot numbness or be done so that the progression or resolution of the process any lesion for which prompt revascularization of the limb achieves can be tracked. a good result. Category IIb includes patients with diminished 5. Paresthesia is an essential finding.The earliest sign of tissue sensation of the entire foot and weakness of calf muscles whose loss is the loss of light touch, two-point discrimination, limb is still salvageable but who require immediate revasculariza- vibratory perception, and proprioception, especially in the tion. In category III, ischemia is irreversible and amputation is first dorsal web space of the foot. required. Clinical features include permanent tissue loss, anes- 6. Paralysis, if present, is an indication of advanced limb- thesia, and paralysis of the limb. Table 3—Clinical Categorization of ALI4 Findings Doppler Signals Category Description/Prognosis Sensory Loss Muscle Weakness Arterial Venous I. Viable Not immediately threatened None None Audible Audible IIa. Marginally Salvageable if promptly treated Minimal (toes) or none None (Often) inaudible Audible threatened IIb. Immediately Salvageable with immediate More than toes, associated with Mild, moderate (Usually) inaudible Audible threatened revascularization rest pain III. Irreversible* Major tissue loss or permanent Profound, anesthetic Profound, paralysis (rigor) Inaudible Inaudible nerve damage inevitable *When presenting early, category IIb and category III may be difficult to differentiate.
  4. 4. © 2007 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 6 VASCULAR SYSTEM 5 PULSELESS EXTREMITY AND ATHEROEMBOLISM — 4 INVESTIGATIVE STUDIES dissections, and thrombi. In some centers, duplex ultrasound Additional diagnostic tests should be performed to support the technology has obviated the need for lengthy arteriograms and has clinical evaluation. An electrocardiogram should be obtained, and benefited patients by reducing ischemia time. if a cardiac source is suspected, a transesophageal echocardiogram should be obtained as well. A full set of laboratory tests, including Arteriography Arteriography remains the gold standard for a complete blood count and a platelet count, blood chemistries, diagnosis of ALI and may even be a primary tool in its manage- and coagulation profiles, should be ordered. In addition, chest and ment. It should not, however, be performed if doing so would keep abdominal x-rays should be done to look for obvious calcifica- a critically ischemic leg from receiving prompt surgical therapy. tions. If it appears that a hypercoagulable state may be causing Arteriography should be reserved for patients with viable limbs thrombosis, a hypercoagulability profile should be ordered. If, who can tolerate the additional delay before revascularization. however, a limb is acutely ischemic and exhibits clear motor or Arteriography should be performed from a site remote from the sensory deficits, diagnostic tests—other than an ECG and basic point of concern.Thus, if lytic therapy is to be administered, entry- hematologic and blood chemistry studies—should not be allowed site bleeding will be minimized. A complete angiogram that to delay treatment. includes the runoff vessels in the foot should be performed to establish the baseline degree of arterial disease and delineate the Evaluation of Arterial Tree anatomy of the inflow and outflow vessels. This information facil- An objective evaluation of the arterial tree should be performed itates subsequent planning for revascularization, should this step when feasible. If ischemia is particularly severe and long-lasting, a prove necessary. Digital subtraction angiography is preferred in full angiographic evaluation may not be possible; however, nonin- that it allows a reduced contrast load and lowers the incidence of vasive duplex studies and, if time permits, angiography should be contrast-associated renal injury.8,9 If the patient is allergic to the considered strongly in this setting. contrast agent or has renal insufficiency, CO2- or gadolinium- based angiography may be performed instead.These two modali- Doppler segmental pressures and ankle-brachial index ties have the advantage of minimizing nephrotoxicity, but they Evaluation of Doppler segmental pressures should begin at the yield poorer suprainguinal arterial visualization than standard con- level of the ankle and should include assessment of arterial signals trast angiography does.10,11 and venous hums. When arterial signals are found, the ankle- The arteriogram can provide useful clues for differentiating brachial index (ABI) should be measured. emboli from thrombi. In a patient with arterial embolism, there is The ABI is derived from the ankle systolic pressure and the often an identifiable source, there is rarely a history of claudica- brachial systolic pressure and is determined as follows.The systolic tion, contralateral and proximal pulses are normal, cutoff is sharp, pressure is measured in each arm, and the higher of the two mea- atherosclerosis is minimal, a few collateral vessels are present, and surements is taken to be the brachial systolic pressure. A cuff is a discrete clot is clearly visible on contrast studies. In a patient with then placed on each calf, and the examiner listens to signals in the arterial thrombosis, the thrombus has no identifiable source, there dorsalis pedis and posterior tibial arteries.The cuff is inflated until is a history of claudication with evidence of peripheral vascular the signal is no longer heard. At this point, the cuff is slowly disease, diffuse atherosclerotic vessel wall disease is present, cutoff released, and the systolic pressure is recorded at the point where is tapered and irregular, and there is ample collateral circulation. the signal is once again audible. Again, the higher of the two sys- tolic measurements is taken to be the ankle systolic pressure. The Other modalities Depending on availability within a given systolic ankle pressure is then divided by the brachial systolic pres- institution and the level of quality achievable within the institution, sure to yield the ABI. An ABI in the range of 0.9 to 1.0 is normal; either computed tomographic angiography (CTA) or magnetic however, the ABI can be falsely elevated if the distal arteries are resonance angiography (MRA) may be employed as alternative not compressible. When the ABI falls below 0.6, there is a signifi- means of evaluating the vasculature of the limb.These two modal- cant difference in blood pressure between the proximal arterial ities are less invasive than conventional angiography, but depend- tree and the distal extremity, which usually denotes an occlusive ing on the particular information being sought, they may yield process. Next, segmental pressures are obtained by placing cuffs at images of lower resolution than a standard angiogram, and they the ankle, below the knee, above the knee, and on the thigh. may be less diagnostically accurate. Nevertheless, as scanning Systolic blood pressures are measured at each location, and any technology continues to advance, the role of CTA and MRA in the pressure drop greater than 15 mm Hg is considered significant. evaluation of limb ischemia will continue to evolve. When the venous Doppler signal or hum is lost in addition to the arterial Doppler signal, the ischemia is severe. However, the MANAGEMENT absence of signals does not always signify an irreversibly threat- Until the middle of the 20th century, ened limb. when revascularization techniques were developed, amputation was the only Duplex ultrasonography Duplex scanning can be valuable treatment for acute lower-extremity for localizing the site of occlusion, especially in bypass grafts. ischemia. Today, however, the vascular Unfortunately, it is not always a practical option in acute circum- surgeon possesses an immense arma- stances, both because the machine is often unavailable in the mentarium for the treatment of this con- emergency setting and because the results of scanning are highly dition, ranging from emergency bypass operator dependent. However, in specialized centers where a to embolectomy or thrombectomy to duplex ultrasound machine is readily available and personnel are thrombolytic therapy [see 6:17 Infrainguinal Arterial Procedures and experienced in its use, a quick look at the suspected site may yield 6:19 Endovascular Procedures for Lower-Extremity Disease]. helpful information.5 In stenotic regions, the velocities measured ALI constitutes a clinical emergency. Rapid restoration of flow across the lesion are greatly increased.6,7 In addition, duplex ultra- to the extremity substantially reduces morbidity and mortality. sonography can be used to assess plaque morphology, stenoses, Accordingly, the clinician must be thoroughly familiar with the
  5. 5. © 2007 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 6 VASCULAR SYSTEM 5 PULSELESS EXTREMITY AND ATHEROEMBOLISM — 5 Thrombolytic Therapy therapeutic modalities available and capable of making an appropriate choice among them without undue delay.Whichever The use of thrombolytic agents to therapeutic modality is chosen for a given patient, several pri- treat chronic and acute arterial insuffi- mary measures should be undertaken to protect and optimize ciency dates back to the 1970s, when it the status of the extremity. Full, systemic anticoagulation (usual- was popularized by Dotter.20 Systemic ly with heparin unless contraindicated) should not be delayed. fibrinolytic therapy has not proved effec- The extremity should be placed in a dependent position, with tive and consequently has been sup- care taken to avoid extrinsic pressure on the limb. Temperature planted by intra-arterial (catheter-direct- fluxes should be minimized: cold induces vasoconstriction, and ed) thrombolysis, which yields signifi- heat increases tissue demand and metabolic and circulatory cantly better results. Still, the role of thrombolytic therapy for ALI demands. Finally, tissue oxygenation should be maximized via is somewhat controversial. In addition, such therapy requires a transfusion, improvement of cardiac function, and restoration of skilled team with considerable clinical expertise, typically includ- intravascular volume. ing a vascular surgeon, an interventional radiologist, and a well- Proper and timely preoperative preparation is crucial for pre- trained ancillary staff. The benefits of pharmacologic clot lysis venting rapid deterioration of the patient’s condition. Laboratory must always be weighed against those of surgical intervention and tests and radiologic studies are necessary, and a cardiology eval- the risk of bleeding associated with fibrinolysis. uation is often helpful. The ABI should be documented. Despite the use of fibrin-specific agents and catheter-directed Abnormalities in blood counts, electrolyte concentrations, and infusion, thrombolytic agents still exert systemic effects, most of coagulation profiles should be corrected. The duration of which are dose related. About 10% of patients receiving throm- ischemia should be noted and any comorbid conditions identi- bolytic therapy experience significant bleeding, including bleeding fied so that the examiner can determine the appropriate degree from both puncture and remote sites. Absolute contraindications of monitoring required (e.g., arterial line or pulmonary arterial to the use of lytic agents include recent surgery, recent stroke or catheter). brain tumor, pregnancy, a bleeding diathesis, recent trauma, and active bleeding [see Table 4]. Anticoagulation Heparin administration should be started as soon as the diag- Thrombolysis versus surgical treatment Three prospec- nosis of ALI is entertained. Numerous studies have shown that tive, randomized trials—the University of Rochester trial, the this measure decreases the morbidity and mortality associated Surgery versus Thrombolysis for Ischemia of the Lower Extremity with ALI and increases the limb salvage rate. Heparin impedes the (STILE) trial, and the Thrombolysis Or Peripheral Arterial propagation of clots and, in the instance of embolism, may help Surgery (TOPAS) trial—addressed the differences between prevent additional events. thrombolytic therapy and traditional surgery.21-24 Heparin acts at multiple sites in the normal coagulation system, inhibiting reactions that lead to the clotting of blood and the for- Rochester trial. This randomized, controlled single-center trial mation of fibrin clots both in vitro and in vivo. Small amounts of compared urokinase (UK) with surgery in patients with ischemia heparin, in combination with antithrombin (heparin cofactor), can of less than 7 days’ duration.21 At the end of 1 year, overall mor- inhibit thrombosis by inactivating activated factor X and inhibit- tality was lower in the thrombolysis group (25%) than in the ing the conversion of prothrombin to thrombin.12 Once active thrombosis has developed, larger amounts of heparin can inhibit further coagulation by inactivating thrombin and preventing the conversion of fibrinogen to fibrin. Heparin also prevents the for- Table 4 Contraindications to mation of a stable fibrin clot by inhibiting the activation of fibrin- Thrombolytic Therapy98 stabilizing factor.12-14 Heparin does not have fibrinolytic activity and therefore does Absolute contraindications not lyse existing clots. Heparin therapy can be complicated by Established cerebrovascular event (including TIAs) within past 2 mo thrombocytopenia, which has a reported incidence of 0% to Active bleeding diathesis 30%.15 If the thrombocyte count falls below 100,000/mm3 or if GI bleeding within past 10 days recurrent thrombosis develops, heparin should be discontin- Neurosurgery (intracranial, spinal) within past 3 mo ued.16,17 Patients receiving heparin may experience new thrombus Intracranial trauma within past 3 mo formation, either early or late, in association with this thrombocy- Major relative contraindications topenic phenomenon as a consequence of irreversible heparin- Cardiopulmonary resuscitation within past 10 days induced platelet aggregation (the so-called white clot syndrome). Major nonvascular surgery or trauma within past 10 days Uncontrolled hypertension: systolic BP > 180 mm Hg, diastolic BP This process may lead to severe thromboembolic complications, > 110 mm Hg including skin necrosis, gangrene of the extremities, MI, pul- Puncture of noncompressible vessel monary embolism, stroke, and, possibly, death.16,18,19 Accordingly, Intracranial tumor if new thrombosis develops in association with thrombocytopenia, Recent eye surgery heparin should be promptly discontinued and a suitable alterna- Minor relative contraindications tive (e.g., a direct thrombin inhibitor) used instead. Hepatic failure, particularly in patients with coagulopathy Periodic platelet counts, hematocrits, and tests for fecal occult Bacterial endocarditis blood are recommended during the entire course of heparin ther- Pregnancy apy, regardless of the route of administration. Bleeding time is usu- Diabetic hemorrhagic retinopathy ally unaffected by heparin. Clotting time is prolonged by full ther- TIA—transient ischemic attack apeutic doses of heparin, but in most cases, it is not measurably affected by low doses.
  6. 6. © 2007 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 6 VASCULAR SYSTEM 5 PULSELESS EXTREMITY AND ATHEROEMBOLISM — 6 surgery group (48%). The amputation rates were similar in the diagnostic and therapeutic angiography (including the use of two groups.Total hospital charges were comparable as well, which stents, balloon angioplasty, stent grafts, and thrombolysis) and suggests that at initial treatment, thrombolytic therapy is as costly finally for the performance of an emergency surgical procedure. A as surgery. Major bleeding was encountered in 11% of patients. discussion is undertaken with the patient to outline the course of treatment and to explain that indwelling catheters may have to be STILE trial. This randomized, controlled multicenter trial placed and that a stay in the ICU may be required. compared surgery with recombinant tissue plasminogen activator Access to the arterial system is gained via a single-wall puncture (rt-PA) and with UK.22 It was stopped early because of an increase technique [see 6:8 Fundamentals of Endovascular Surgery]; the risk in the number of patients with ongoing ischemia in the thrombol- of posterior-wall bleeding associated with a double-wall technique ysis groups. An ad hoc committee later determined that the reason is thereby avoided. Access should be obtained from a site as for this increase was the inclusion of chronically symptomatic remote from the intervention site as possible. Generally, this is patients in the study. In any case, the study clearly demonstrated accomplished by starting from the contralateral counterpart of the that patients with less than 14 days of ischemia had a lower ampu- target artery and going up and over the aortic bifurcation, then tation rate when treated with thrombolysis (11% versus 30%) but back to the ipsilateral artery. By removing the puncture site from that patients with more than 14 days of ischemia had a lower the site of catheter-directed thrombolysis, the incidence of bleed- amputation rate when treated with surgery. ing and formation of hematomas or pseudoaneurysms is reduced. After completion of the angiogram and delineation of the TOPAS trial. This randomized, controlled multicenter trial pathology, a guide wire is passed into the occluded area.We use a compared surgery with recombinant urokinase (r-UK) thrombol- 0.035 in. hydrophilic guide wire, which has a slippery, wet coating ysis in patients with ischemic symptoms of less than 14 days’ dura- that enables it to cross nonhydrophilic lesions. Once in place, the tion.23,24 At the end of 1 year, the amputation rates in the two wire is guided through the clot. A multiple-sidehole catheter is groups were similar. Bleeding complications were seen only in placed through the clot, and a hand-injection angiogram is per- patients undergoing thrombolysis, four of whom had intracranial formed to confirm that the catheter tip is in the true lumen. The hemorrhage. When additional end points were considered, the guide wire is then left within the catheter to occlude the tip, so that thrombolysis group was found to require significantly fewer major the lytic agent is infused through the sideholes preferentially. This interventions at the time of discharge and at 12 months. graded “coaxial” infusion technique allows the agent to reach the greatest possible surface area, maximizes the length of infusion, Recombinant tissue plasminogen activator versus urokinase. A and enables the surgeon to treat some of the longest bypass grafts. prospective, randomized multicenter trial evaluated local throm- If the guide wire–catheter system cannot be advanced into the bolysis with either rt-PA or UK in 234 patients with thrombotic clot, it is highly unlikely that thrombolysis will be successful. occlusions (223 native femoral or popliteal arteries, 11 bypass In many cases, mechanical thrombus removal, with or without grafts).25 Complete reperfusion occurred in 62% of the patients pulse spray, is employed initially, followed by continuous infusion treated with rt-PA and in 50% of the patients treated with UK. of a thrombolytic agent. In addition to lytic therapy, administra- However, bleeding was observed in 12.8% of rt-PA–treated tion of heparin is started (200 to 400 units I.V. or via sheath) to patients (including one instance of cerebral hemorrhage) and in prevent pericatheter thrombosis. Serial laboratory evaluation is 9.1% of UK-treated patients (none of whom experienced cerebral carried out to verify that the patient is not bleeding and that the bleeding). fibrinogen level is higher than 100 mg/dl. Serial follow-up arteri- ograms are obtained to monitor progress. It is critically important Current recommendations. Current data suggest, but do not that successful thrombolysis be followed by treatment, whether prove, that thrombolytic therapy is effective as initial therapy for endovascular or open, of any lesions uncovered during thrombol- patients with acute arterial and graft occlusions and no sensori- ysis; if it is not, reocclusion is inevitable. At the conclusion of motor deficits. Such an approach, however, is not suitable for thrombolysis and before intervention, the patient must be kept on patients with common femoral artery emboli, which should be a heparin drip (or on another anticoagulant) to prevent the for- treated surgically, and there are certain patients with sensorimotor mation of a new thrombus. The rate of successful reperfusion is deficits (e.g., those without any runoff) for whom the potential approximately 90% to 95% in most studies. benefits of thrombolysis outweigh the risks of delay. An important advantage of this selective approach is that it At present, acute thrombotic arterial occlusion in an occluded allows simultaneous angiographic definition of the nature of the bypass graft is the area where intra-arterial fibrinolysis may be occlusion (i.e., embolic or thrombotic) and of any vessel wall most useful, permitting better planning of the subsequent opera- abnormalities that would lead to rethrombosis if not corrected by tion and resulting in a less extensive procedure. Such therapy, means of surgery or balloon angioplasty. A major drawback to this however, does not necessarily yield improvements in major long- approach is that arterial catheterization is required for prolonged term end points. It is important to remember that thrombosis of periods (20 hours, on average), leading to major bleeding and femoral-popliteal or similar bypasses is related to early or late sur- thromboembolic complications in 6% to 20% of patients. gical stenosis and atherosclerosis and that restoring flow usually Therefore, the end points of thrombolytic therapy are (1) resolu- does not suffice to ensure continued patency. tion and reconstitution of flow through the obstruction, (2) absence of change in the occlusion of the vessel on angiography, Logistics of thrombolysis In patients with mild or no sen- and (3) bleeding complications. If it is determined that thrombol- sory deficits, angiography is performed first. Depending on the ysis is not progressing, it should be abandoned and surgical inter- location of the obstruction, the type of clot present, and the level vention undertaken. of patient risk, the patient may be offered thrombolysis as initial therapy. Thrombectomy In our practice, the patient is taken from the emergency depart- Percutaneous aspiration thrombectomy This technique ment to the angiography suite. Informed consent is obtained for uses a large, thin-walled catheter and a large syringe to remove an
  7. 7. © 2007 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 6 VASCULAR SYSTEM 5 PULSELESS EXTREMITY AND ATHEROEMBOLISM — 7 embolus or thrombus from a vascular conduit, whether native ves- period to soften the clot. The multiple-sidehole catheter is sel or graft. The catheter is placed as previously described [see advanced distally to the location of the clot, the guide wire is passed Logistics of Thrombolysis, above] and is parked immediately by through the lesion, and the catheter is passed over the wire into the the clot. Aspiration of the clot with the syringe is then attempted. substance of the clot. Infusion of the lytic agent is then started. If the clot is new, success is likely, but an old clot that is organized Repeat angiograms indicate whether the clot has dissolved or is will not be as amenable to removal. Percutaneous aspiration still present. If the clot is still apparent, repeat embolectomy is thrombectomy is most effective as an adjunct to catheter-directed attempted. If thrombosis rather than embolism is suspected, an thrombolysis.26,27 underlying lesion must be sought. In performing the embolecto- my, attention should be paid to the tactile sensations felt as the Percutaneous mechanical thrombectomy Percutaneous balloon is withdrawn. Such sensations give the operator a sense of mechanical thrombectomy (PMT) functions on the basis of a the disease process. When several deflations are needed and the hydrodynamic circulation. The basic concept is that a hydrody- withdrawal path of the balloon feels rough, a long-standing namic vortex is created around the tip of the PMT catheter. process (e.g., an atherosclerotic calcified vessel with anatomic dis- Thrombectomy is accomplished with the introduction of a pres- crepancies) is likely. surized saline jet stream through the directed orifices in the If there appears to be no residual clot after embolectomy, then distal tip of the catheter. The jets generate a localized low-pres- a completion angiogram is sufficient and the artery can be closed sure zone via the Bernoulli effect, which entrains and macerates primarily. Heparin is continued, and the patient is eventually thrombus. The saline and the fragmented thrombus are then switched to warfarin, which is continued for at least 6 months sucked back into the exhaust lumen of the catheter and out of the postoperatively. Finally, the location from which the embolus orig- body for disposal. inated is sought and appropriately treated. When an underlying This technique has proved beneficial when used in appropriate lesion is identified, a decision must be made as to whether it can settings and properly selected patients. Its efficacy depends on the be treated with angioplasty or stenting or whether a formal bypass age of the clot. Fresh thrombus is readily treated with PMT, but is required to correct the problem and salvage the limb. older clots are much less amenable to this technique and may have Key to the final management of these patients is assessment of to be treated with an adjunctive catheter-based modality (e.g., the lower extremities, especially the calves, for compartment syn- angioplasty, intra-arterial thrombolysis, or atherectomy).28-31 drome.To minimize the chances that an otherwise successful sur- gical operation may fail as a consequence of this syndrome, we Surgical Embolectomy and Revascularization typically perform intraoperative fasciotomies on the extremity if When a patient has significant sensory and motor deficits relat- profound ischemia has been present for several hours. ed to a profoundly ischemic limb, immediate surgical revascular- ization is indicated. The decision whether to accomplish this per- Cost Considerations cutaneously or surgically should be made expeditiously. Operating A retrospective study published in 1995 compared thromboly- room availability should be determined, the method of anesthesia sis with surgical thrombectomy as first-line therapy for ALI.32 should be chosen, and the technical details of the procedure Only the costs of the initial admission were documented. The should be planned. Heparin administration should be started average charge for the two treatments ranged from $20,000 to before the patient enters the OR. General anesthesia is the pre- $26,000. Economic analysis confirmed that the total economic ferred method of anesthesia. impact of thrombolysis approximated that of initial operative ther- For lower-extremity emboli, access to the femoral vessels should apy. The conclusion of the study was that there was no difference be obtained rapidly. The common, deep, and superficial femoral between an endovascular approach and an operative approach arteries are controlled proximally and distally with vessel loops, and with respect to cost. Thus, when acute treatment of ALI is being the common femoral artery is opened transversely. Catheter considered, cost should not be factored into the decision-making embolectomy of the superficial femoral, deep femoral, common process.32,33 femoral, and external iliac arteries is then performed. Differently sized embolectomy catheters are used, depending on the size of each artery. In our experience, a No. 3 catheter is usually suitable Atheroembolism for the deep femoral artery, a No. 4 for the superficial femoral Atheroembolism is a condition in which microscopic choles- artery, and a No. 5 for the common femoral and external iliac terol-laden debris travels from proximal arteries until it reaches arteries.The extracted clot is sent for pathologic evaluation.When the most distal arterial segments, typically in the skin of the lower the clot is believed to be in the distal vessels of the lower extremi- extremities and in the end-organs.34-37 This debris usually origi- ty, control of the popliteal artery and its trifurcation is obtained via nates from unstable plaque found at inflection points in the arte- a popliteal incision. A No. 3 catheter should be adequate at this site. rial tree, especially in the aorta.38,39 It may also originate from For upper-extremity emboli, a curvilinear incision is made that aneurysmal sacs either in the aorta or in the peripheral arteries. starts on the medial aspect of the upper arm, extends transversely CLINICAL EVALUATION across the antecubital fossa, and ends halfway down the middle of the lower arm [see 6:15 Upper-Extremity Revascularization Patients with atheroembolism usually present with focal toe Procedures].This incision allows control of the brachial, radial, and ischemia—the so-called blue toe syndrome—in conjunction with ulnar arteries. A No. 3 embolectomy catheter is typically used here. palpable pulses in the distal extremity [see Figure 1]. Acute pain of Several passes are done in each vessel until no more clot can be sudden onset is typically noted in the affected area.This pain can seen and there is brisk back-bleeding from the vessel.When no fur- often establish the exact timing of embolization. Cyanosis is pre- ther clot can be retrieved, a completion angiogram is obtained to sent either on the toe or over a more extensive area if the visualize the distal vessels and elucidate any anatomic pathology in atheroemboli were circulated throughout the extremity.40,41 When the native vessels. If distal clot is still present after the completion both lower extremities are involved, an aortic source of the angiogram, intraoperative thrombolysis can be employed for a brief microemboli is commonly found.
  8. 8. © 2007 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 6 VASCULAR SYSTEM 5 PULSELESS EXTREMITY AND ATHEROEMBOLISM — 8 Patient presents with apparent blue toe syndrome Signs and symptoms are not consistent Signs and symptoms are consistent with atheroembolism with atheroembolism Consider other diagnoses: • vasculitis Assess degree and extent of disease. • frostbite • chilblains • recreational drugs. Identify source of atheroemboli. Emboli are unilateral Emboli are bilateral Obtain duplex scan and angiogram. Perform CT or MRI. Obtain angiogram and intravascular sonogram. Patient has discrete source lesion Patient has diffuse atherosclerotic disease Place endovascular covered stent at lesion site. Disease is mild Disease is severe Assess level of operative risk. Patient is not good Patient is good operative candidate operative candidate Give antiplatelet therapy: •aspirin • clopidogrel Treat ischemic injury. Figure 1 Algorithm outlines workup of patient with blue toe syndrome as a result of Atheroemboli recur Atheroemboli do not recur atheroembolism. Perform surgical bypass or exclusion of target area. A complete vascular examination should be performed and with noncolor flow can also provide clues to the morphology of a pulses documented. Although a patent arterial tree is the rule, plaque.This is only true, however, in the extremity arteries.When emboli that are sufficiently small may travel through collateral the aorta is the suspected source of the emboli, computed tomog- channels. Palpation should be done to detect any aneurysmal dis- raphy, magnetic resonance imaging, or MRA is performed; these ease. A massive proximal atheroembolic event may affect the modalities provide better visualization of intraluminal disease. entire abdominal wall and both extremities, giving the appearance Arteriography also plays a useful role in identifying intraluminal of livedo reticularis. As the source of the atheroemboli ascends in pathology along the entire vascular tree. In addition, intravascular the arterial tree, more vital organs (e.g., the kidneys and the GI ultrasonography may be performed with the guide wire in place tract) may be damaged. and may help delineate the extent of the underlying disease. Manipulation of an intra-arterial catheter or clamping or surgi- MANAGEMENT cal manipulation of the arterial tree can also result in plaque dis- ruption. In these cases, the adverse effects are usually apparent If the atheroembolic events are minor and solitary, conservative immediately after the procedure. medical management is recommended. If, however, the emboli are recurrent or massive, a thorough evaluation should be initiat- INVESTIGATIVE STUDIES ed, followed by urgent treatment. Doppler examination may visualize unstable ulcerated plaques Medical management of atheroembolism consists primarily of or aneurysmal disease. Doppler segmental pressures may be used antiplatelet therapy and statin therapy. Given that most patients to identify the responsible lesion by localizing a significant drop in with atheroemboli are already receiving aspirin, addition of clopi- pressure and determining where the plaque is. Duplex imaging dogrel or ticlopidine is appropriate. The optimal agents for pre-
  9. 9. © 2007 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 6 VASCULAR SYSTEM 5 PULSELESS EXTREMITY AND ATHEROEMBOLISM — 9 venting recurrence of atheroembolism may prove to be lipid-low- ering drugs, particularly statins. Furthermore, given the goal of Table 5—Surgical Management preventing recurrence, all patients who continue to smoke should of Atheroembolism be counseled to attempt cessation, which is beneficial in curbing atherosclerosis. Aggressive treatment of diabetes is also warranted. Source of Emboli Treatment The role of warfarin therapy in treating atheroembolic disease Bypass of subclavian or axillary artery has not been established with certainty. Such therapy may even Upper extremity First rib or cervical rib resection aggravate the disease process by causing intraplaque hemorrhage and increased embolization.The Warfarin Aspirin Recurrent Stroke Aorta Focal disease: covered aortic stent Study (WARSS), a randomized multicenter study that included Diffuse disease: aortobifemoral bypass 2,206 patients who had recently experienced an ischemic stroke, Iliac artery Covered iliac stent found no evidence that warfarin is superior to aspirin for prevent- ing recurrent ischemic stroke or death within 2 years.42 The WARSS Popliteal artery Ligation and bypass of popliteal artery also found that there was a significant difference in bleeding risk between warfarin-treated patients and aspirin-treated patients. For patients with diffuse atherosclerotic disease, the mainstay of massive, an endovascular approach is attempted, involving the therapy is an antiplatelet regimen. Traditionally, an atheroembol- placement of a covered stent over the lesion.This approach is indi- ic source has been treated by surgical excision or by exclusion of cated for segments of the arterial tree where there are no collater- the disease process with a bypass graft, either of which provides a als, so that vital blood flow to organs is not hindered. If aneurys- good degree of safety from further embolization.43 With the mal disease is present, either conventional or endovascular thera- advent of endovascular surgery, however, the use of covered peutic approaches may be applied to exclude any source of stents, placed securely and precisely at the site of the offending emboli. In the case of thoracic aortic disease, covered stents may lesion, appears to be an increasingly effective and popular option be placed to push the plaque against the wall and prevent further [see Table 5].44,45 embolization. If suprarenal plaque cannot be treated with a stent- Our current approach to treating atheroembolism may be sum- ed graft, aortic ligation with an axillobifemoral bypass [see 6:12 marized as follows. The source lesion is first identified by means Aortoiliac Reconstruction] may be performed. Such treatment does of the modalities already discussed. If embolization is minor, not, however, protect the renal and visceral vessels, and these aspirin and clopidrogel are started. If embolization is recurrent or patients require lifelong strict antiplatelet therapy. Discussion Pathophysiology of ALI Knowledge of the varying degrees of ischemic tolerance helps in ALI begins when arterial embolization, local thrombosis, or determining the viability of the limb. arterial trauma results in occlusion of a peripheral artery or bypass HYPOPERFUSION-REPERFUSION STATE graft. The ischemic process may then develop slowly, over an Regardless of the cause, hypoperfusion leads to ischemic extended period, or quickly, over a few hours. A protracted course infarcts via various mechanisms. During the hypoperfusion state, leading to thrombosis allows collateral vessels to form, resulting in three major physiologic events occur. First, movement of blood the gradual onset of symptoms. When occlusion is acute, howev- through the vessels is slowed. As a result, the thrombus is able to er, as in trauma, embolization, or acute thrombosis of a vessel or a grow and propagate, occluding collateral vessels and further bypass graft, signs and symptoms of acute ischemia may become decreasing blood flow. Second, ischemic cells swell and accumu- rapidly apparent, including excruciating pain, mottling, cyanosis, late water. The resulting increase in pressure within a fixed space and, commonly, sensory and motor changes. The magnitude of between fascial structures creates an elevation of pressure within the ischemic injury is directly proportional to the duration of the compartment that further decreases flow and exacerbates the ischemia and the amount of tissue affected. injury. Third, the precapillary arteriolar cells swell, narrowing the The pathophysiology of limb ischemia is related to the progres- lumina of distal arterioles, capillaries, and venules and again sion of tissue infarction and irreversible cell death. Compared with reducing blood flow. As a result, toxic metabolites accumulate other organs and tissues (e.g., the brain and the heart), the within the ischemic tissues. extremities are relatively resistant to ischemia. However, the vari- The reperfusion state that results when flow is restored can be ous tissue types of which an extremity is composed have different as detrimental to the ischemic extremity as the hypoperfusion state metabolic rates. The extent to which each cell type can tolerate was. During reperfusion, highly active oxygen metabolites are pro- ischemia depends on its metabolic rate. Bone and skin are the duced by neutrophils.47 These free radicals destroy cells by attack- most resistant to ischemia, nervous tissue is the least resistant, and ing the unsaturated bonds of fatty acids within the phospholipid muscle is somewhere in between. Although nerve tissue is the type membrane, thereby disrupting the cell membrane, allowing water that is most sensitive to ischemia, it is skeletal muscle, the major to enter the cell, and eventually causing cell lysis. Free radical scav- structural component of an extremity, that plays the largest patho- engers (e.g., mannitol and superoxide dismutase) have a slight physiologic role in the local and systemic effects of ALI. For mus- protective effect against reperfusion injury when given before cle tissue, 6 hours is the approximate upper limit of ischemic tol- large-scale release of these radicals.48,49 In addition, myoglobin erance; nervous tissue is affected well before this point.46 from injured muscle cells is released into the circulation and is
  10. 10. © 2007 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 6 VASCULAR SYSTEM 5 PULSELESS EXTREMITY AND ATHEROEMBOLISM — 10 cleared via the renal system. Myoglobin may cause renal failure and endothelial damage ensues.The endothelial damage activates through its direct toxic effect on the renal tubules and through the a repair process that results in intimal hyperplasia, which causes accumulation of casts in the tubules. further attraction of platelets and eventual thrombus formation. Creatinine phosphokinase levels may also increase to dramatic The process by which occlusion develops from an atheromatous levels once perfusion is reestablished. High concentrations of lac- plaque may be more important than the degree of stenosis within tic acid, potassium, thromboxane, and cellular enzymes are secret- the lumen.This would explain why acute occlusion occurs in ves- ed as a consequence of the rhabdomyolysis; these substances accu- sels with minimal (< 50%) stenosis: the contact between the ath- mulate in the ischemic limb and are released into the systemic cir- erosclerotic core and the bloodstream leads to platelet aggregation culation upon reperfusion.50 In one study that measured the and hence to eventual thrombosis. venous effluent from a series of patients with limb ischemia, the Occasionally, thrombosis of a native artery occurs without any pH was 7.07 and the mean potassium level 5.7 mEq/L 5 minutes obvious underlying pathologic condition. In such cases, a thor- after surgical embolectomy.51 ough investigation should be initiated into other causes of throm- Detrimental physiologic changes are seen when toxic oxygen bosis (e.g., hypovolemia, malignancy, hypercoagulable states, and metabolites are released systemically. Depression of myocardial blood dyscrasias). function, an increase in cardiac dysrhythmias, and loss of vascular tone may induce shock and even death.52 Bypass Graft Thrombosis Aggressive management of patients with peripheral arterial dis- ease has led to an increase in bypass graft procedures. As a result, Etiology of ALI graft thrombosis has become the leading cause of acute lower- The etiology of ALI can be divided into two distinct categories: extremity ischemia. In patients with native conduits, intimal thrombosis and embolism. A thorough evaluation must be per- hyperplasia and valvular hyperplasia are the two leading causes of formed to elucidate the precise cause of ischemia in each individ- graft failure.55 The situation is different in the prosthetic graft pop- ual patient. The two categories are each associated with specific ulation, where the inherent thrombogenicity of the graft material symptoms and signs [see Table 6]. Knowledge of these associations and kinking of the graft from crossing joints are believed to be the helps direct the clinician toward the most appropriate means of leading causes. These patients often have graft occlusions without accomplishing limb salvage in a given situation. any definable underlying lesion. Anastomotic irregularities can Thrombosis of a native vessel or bypass graft almost always also contribute to graft thrombosis.55 develops in conjunction with an underlying lesion in the vessel or EMBOLISM graft. The lesion usually has been present for some time, and the thrombosis occurs as a result of it. In contrast, embolic events Peripheral arterial embolization results in the sudden onset of occur in smaller-caliber vessels that are not diseased, with emboli extreme ischemia as the absence of collateral vessels compounds commonly resting at or immediately distal to branch points. the reduction in flow to the extremity.The heart is by far the most important source of spontaneous arterial emboli.The incidence of THROMBOSIS embolic phenomena increases as the population ages, with a cor- responding increase in the number of patients with significant car- Native Artery Thrombosis diac disease. Over the past 25 years, the incidence of embolization Native artery thrombosis is usually the end stage of a long- has doubled, from 23 to 51 per 100,000 admissions. Atheroscler- standing disease process of atheromatous plaque formation at spe- otic heart disease currently accounts for as many as 60% to 70% cific sites in the arterial tree. Atherosclerotic plaque begins with of all cases of arterial embolism.56,57 Atrial fibrillation and rheu- the slow deposition of lipids in the intima of the vessel and con- matic valvular disease account for the remaining 30% to 40%.56,58 tinues with the deposition of calcium, resulting in an atheroscle- With respect to peripheral emboli in particular, atrial fibrillation rotic core.53 This core is a highly thrombogenic surface that is currently associated with two thirds to three quarters of cases. encourages platelet aggregation, which results in disturbances of Transthoracic echocardiography is insensitive in visualizing atrial blood flow.54 The flow disturbances create a zone of separation, clots, especially in the left atrial appendage, which is the most stagnation, turbulence, and distorted velocity vectors. These fac- common cardiac source of emboli.59,60 Transesophageal echocar- tors cause low shear rates at inflection points in the arterial tree, diography, however, offers significantly better imaging of all four chambers and thus is considered the superior diagnostic test for suspected cardiac embolic sources.61-64 MI is the next most important cause of peripheral emboli. One Table 6—Differentiation of Embolism study from 1986 evaluated 400 patients and found that MI was a from Thrombosis causative factor in 20%.58 After an MI, a left ventricular wall thrombus is often seen, with or without a left ventricular wall Variable Embolism Thrombosis aneurysm; however, only 5% of such thrombi embolize and result in ischemia. 65-68 Other studies suggest that day 3 to day 28 is the Identifiable source Frequently detected None period during which the risk of embolization is highest for an Claudication Rare Frequent intracardiac thrombus.69 Evidence of ipsilateral and The ring portions of prosthetic cardiac valves are major intra- Physical findings Proximal and contralat- contralateral peripheral cardiac embolic sources before anticoagulation, as are biologic eral pulses normal vascular disease xenovalves, which do not require anticoagulation.70,71 Finally, Minimal atherosclero- Diffuse atherosclerotic disease; tumors (e.g., atrial myxomas) are occasional sources of peripheral Angiographic sis; sharp cutoff; few tapered and irregular cut- emboli.69 Cardiac vegetations from bacterial or fungal endocardi- findings collaterals; multiple off; well-developed collateral tis should be considered as possible sources of peripheral emboli occlusions circulation when I.V. drug abuse is suspected in a patient with no previous
  11. 11. © 2007 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 6 VASCULAR SYSTEM 5 PULSELESS EXTREMITY AND ATHEROEMBOLISM — 11 side, and becomes an arterial embolus.82-84 About 5% to 10% of emboli remain unidentified despite a thorough diagnostic evalua- tion85,86; some of these are now being attributed to hypercoagula- ble states.87 Incidence Axillary The increase in the number of endovascular interventions (4.5%) being performed has affected the overall incidence patterns for Aorta arterial embolism, with a greater number of embolic episodes now (9.1%) arising from endovascular procedures. A 1996 study found that 45% of all atheroemboli were iatrogenic and that the majority of Common these originated during manipulation of the abdominal aorta, the lliac iliac artery, or the femoropopliteal artery, with the remainder orig- (13.6%) inating during surgery.88 Emboli usually lodge at arterial bifurca- Brachial tions and thus cause hypoperfusion of more than one vessel. Axial (9.1%) External lliac limb vessels account for 60% to 80% of clinically significant (3.0%) embolic events, with the remainder divided between cerebral ves- Radial (1.2%) sels (20%) and upper-extremity vessels (10% to 20%).58,69,89 The most common site for embolic lodgment is the common femoral bifurcation [see Figure 2]. The aortoiliac region is the next most Ulnar Common common site, followed closely by the popliteal artery.52,57,58,69,90,91 (1.2%) Femoral The presence of normal pulses in the contralateral leg in a (34.0%) patient with an ischemic leg should elicit an aggressive workup to rule out a cardiac embolic source and may be a clue that the occlusive event is embolic rather than thrombotic. Superficial Femoral (4.5%) Upper-Extremity Emboli Acute ischemia of the upper extremity is usually caused by Popliteal embolism, usually from an intracardiac source. Subclavian (14.2%) aneurysms, arteriovenous fistulae, upper-extremity arterial bypasses, and iatrogenic manipulation of the arteries are rare caus- es.92 As noted (see above), emboli lodge at bifurcations within the arterial tree. In the upper extremity, the bifurcation of the brachial artery into the radial and ulnar arteries is the most common lodg- Anterior Posterior ment site, followed by the takeoff of the deep brachial artery. Tibial Tibial (2.8%) (2.8%) Adequate exposure of all three arteries can be obtained via an elongated S-shaped incision that runs medially to laterally across the elbow joint. Other Causes Figure 2 Depicted are the most common sites of arterial Sepsis and cardiogenic shock result in a low-flow state that embolic occlusions. places patients at high risk for thrombosis. Certain vasoconstric- tors and recreational drugs are also associated with lower-extrem- ity thrombosis.93,94 Patients with these conditions usually present history of cardiac disease.72,73 with bilateral extremity ischemia.Vasculitides (e.g.,Takayasu) may Noncardiac sources account for 5% to 10% of peripheral also cause extremity ischemia.95 emboli. The majority of these involve downstream atherosclerotic The hypercoagulable states (e.g., antithrombin deficiency, arterial disease (e.g., aneurysms or unstable plaques).74-77 Foreign antiphospholipid syndrome, protein C and S deficiencies, activated objects (e.g., missiles) and tumors (e.g., melanoma) can also protein C resistance, and hyperprothrombinemia) are the most embolize if they gain access to the arterial tree.78-81 Paradoxical common disorders associated with acute arterial thrombosis.96 embolization occurs when a venous thrombus crosses from right The contribution of these states to ALI, with usually devastating to left via an atrial or ventricular route, gains access to the arterial consequences, is increasingly being recognized. References 1. Davies B, Braithwaite BD, Birch PA, et al: Acute 4. Rutherford RB, Baker JD, Ernst C, et al: 6. Mazzariol F, Ascher E, Hingorani A, et al: Lower- leg ischaemia in Gloucestershire. Br J Surg 84:504, Recommended standards for reports dealing with extremity revascularization without preoperative 1997 lower extremity ischemia: revised version. J Vasc contrast arteriography in 185 cases: lessons 2. Blaisdell FW, Steele M, Allen RE: Management of Surg 26:517, 1997 learned with duplex ultrasound arterial mapping. acute lower extremity arterial ischemia due to 5. Katzenschlager R, Ahmadi A, Atteneder M, et al: Eur J Vasc Endovasc Surg 19:509, 2000 embolism and thrombosis. Surgery 84:822, 1978 Colour duplex sonography-guided local lysis of 7. Hingorani AP, Ascher E, Marks N: Duplex arteri- 3. Dormandy J, Heeck L,Vig S: Acute limb ischemia. occlusions in the femoro-popliteal region. Int ography for lower extremity revascularization. Semin Vasc Surg 12:148, 1999 Angiol 19:250, 2000 Perspect Vasc Surg Endovasc Ther 19:1, 2007
  12. 12. © 2007 WebMD, Inc. All rights reserved. ACS Surgery: Principles and Practice 6 VASCULAR SYSTEM 5 PULSELESS EXTREMITY AND ATHEROEMBOLISM — 12 8. Kim D, Porter DH, Brown R, et al: Renal artery tomy for peripheral major arterial lesions. Angiol duction and myocardial depression. Surg Gynecol imaging: a prospective comparison of intra-arterial Vasc Surg 5:1, 1999 Obstet 157:500, 1983 digital subtraction angiography with conventional 30. Dick A, Neuerburg J, Schmitz-Rode T, et al: 51. Fischer R, Fogarty T, Morrow A: A clinical and angiography. Angiology 42:345, 1991 Declotting of embolized temporary vena cava filter biochemical observation of the effect of transient 9. Lindholt JS: Radiocontrast induced nephropathy. by ultrasound and the AngioJet: comparative femoral artery occlusion in man. Surgery 68:233, Eur J Vasc Endovasc Surg 4:296, 2003 experimental in vitro studies. Invest Radiol 33:91, 1970 10. Kerns SR, Hawkins IFJ, Sabatelli FW: Current 1998 52. Green RM, DeWeese J, Rob CG: Arterial status of carbon dioxide angiography. Radiol Clin 31. Douek PC, Gandjbakhche A, Leon MB, et al: embolectomy before and after the Fogarty North Am 33:15, 1995 Functional properties of a ‘prototype rheolytic catheter. Surgery 77:24, 1975 11. Waver FA, Pentecoast MJ,Yellin AE, et al: Clinical thrombectomy catheter’ for percutaneous 53. Stary HC, Chandler AB, Dinsmore RE, et al: A applications of carbon dioxide/digital subtraction thrombectomy—in vitro investigations. Invest definition of advanced types of atherosclerotic arteriography. J Vasc Surg 13:266, 1991 Radiol 29:547, 1994 lesions and a histological classification of athero- 12. Bjork I, Lindahl U: Mechanism of the anticoagu- 32. Ouriel K, Kolassa M, DeWeese JA, et al: Economic sclerosis: a report from the committee on vascular lant action of heparin. Mol Cell Biochem 48:161, implications of thrombolysis or operation as the lesions of the council on arteriosclerosis, American 1982 initial treatment modality in acute peripheral arte- Heart Association. Circulation 92:1355, 1995 rial occlusion. Surgery 118:810, 1995 13. Hirsh J, Dalen J, Deykin D, et al: Heparin, mecha- 54. Fernandez-Ortiz A, Badimon JJ, Falk E, et al: nism of action, pharmacokinetics, dosing consider- 33. Korn P, Khilnani NM, Fellers JC, et al: Characterization of the relative thrombogenicity of ation, monitoring, efficacy and safety. Chest Thrombolysis for native arterial occlusions of the atherosclerotic plaque components: implications 102:337S, 1992 lower extremities: clinical outcome and cost. J Vasc for consequences of plaque rupture. J Am Coll Surg 33:1148, 2001 Cardiol 23:1562, 1994 14. Salzman EW, Deykin D, Shapiro RM, et al: Management of heparin therapy: controlled 34. Carvajal JA, Anderson WR, Weiss L, et al: 55. Ouriel K, Shortell CK, Green RM, et al: prospective trial. N Engl J Med 292:1046, 1976 Atheroembolism: an etiologic factor in renal insuf- Differential mechanisms of failure of autogenous ficiency, gastrointestinal hemorrhages, and periph- and non-autogenous bypass conduits: an assess- 15. Walenga JM, Frenkel EP, Bick RL: Heparin- eral vascular diseases. Arch Intern Med 119:593, ment following successful graft thrombolysis. induced thrombocytopenia, paradoxical throm- 1967 Cardiovasc Surg 3:469, 1995 boembolism, and other adverse effects of heparin- type therapy. Hematol Oncol Clin North Am 35. Karmody AM, Jordan FR, Zaman SM: Left colon 56. Abbott W, Maloney R, McCabe C, et al: Arterial 7:259, 2003 gangrene after acute mesenteric artery occlusion. embolism: a 44 year perspective. Am J Surg Arch Surg 111:972, 1976 143:460, 1982 16. Warkentin TE, Bernstein RA: Delayed-onset heparin-induced thrombocytopenia and cerebral 36. Gore L, Collins DP: Spontaneous atheromatous 57. Fogarty T, Daily P, Shumway N, et al: Experience thrombosis after a single administration of unfrac- embolization: review of the literature and a report with balloon catheter technique for arterial tionated heparin. N Engl J Med 348:1067, 2003 of 16 additional cases. Am J Clin Pathol 33:416, embolectomy. Am J Surg 122:231, 1971 1960 17. Kelton JG: Heparin-induced thrombocytopenia: 58. Paneta T, Thomson J, Talkington C, et al: Arterial an overview. Blood Rev 16:77, 2002 37. Ramirez G, O’Neill WM, Lambert R, et al: embolectomy: a 34 year experience with 400 cases. Cholesterol embolization: a complication of Surg Clin North Am 66:339, 1986 18. Rice L, Attisha WK, Drexler A, et al: Delayed- angiography. Arch Intern Med 118:534, 1966 onset heparin-induced thrombocytopenia. Ann 59. Shresta N, Moreno F, Narcisco F, et al: Two Intern Med 136:210, 2002 38. Williams GM, Harrington D, Burdick J, et al: dimensional echocardiographic diagnosis of left Mural thrombus of the aorta: an important, fre- atrial thrombus in rheumatic heart disease: a clini- 19. Napolitano LM,Warkentin TE, Almahameed A, et quently neglected cause of large peripheral emboli. copathologic study. Circulation 67:341, 1983 al: Heparin-induced thrombocytopenia in the crit- Ann Surg 194:737, 1981 ical care setting: diagnosis and management. Crit 60. Schweizer P, Bardos F, Erbel R: Detection of left Care Med 34:2898, 2006 39. Khatibzadeh M, Mitusch R, Stierle U, et al: Aortic atrial thrombi by echocardiography. Br Heart J atherosclerotic plaques as a source of systemic 45:148, 1981 20. Dotter C: Selective clot lysis with low-dose strep- embolization. J Am Coll Cardiol 27:664, 1996 tokinase. Radiology 111:31, 1974 61. Daniel W, Mugge A:Transesophageal echocardiog- 40. Falanga V, Fine MJ, Kapoor WN: The cutaneous raphy. N Engl J Med 332:1268, 1995 21. Ouriel K, Shortell C, DeWeese JA, et al: A com- manifestations of cholesterol crystal embolization. parison of thrombolytic therapy with operative Arch Dermatol 122:1194, 1986 62. Husain A, Alter M: Transesophageal echocardiog- revascularization in the initial treatment of acute raphy in diagnosing cardioembolic stroke. Clin peripheral arterial ischemia. J Vasc Surg 19:1021, 41. Karmody AM, Powers SR, Monaco VJ, et al: “Blue Cardiol 18:705, 1995 1994 toe syndrome”: an indication for limb salvage surgery. Arch Surg 111:1263, 1976 63. Seward J, Khandheria B, Oh J, et al: Trans- 22. Weaver FA, Comerota AJ, Youngblood M, et al: esophageal echocardiography: technique, anatom- Surgical revascularization versus thrombolysis for 42. Mohr JP, Thompson JL, Lazar RM, et al: A com- ic correlations, implementation, and clinical appli- non-embolic lower extremity native artery occlu- parison of warfarin and aspirin for the prevention cations. Mayo Clin Proc 63:649, 1988 sions: results of a prospective randomized trial.The of recurrent ischemic stroke. N Engl J Med 345:1444, 2001 64. Rubin B, Barzilai B, Allen B, et al: Detection of the STILE investigators: Surgery versus Thrombolysis source of arterial emboli by transesophageal for Ischemia of the Lower Extremity. J Vasc Surg 43. Keen RR, McCarthy WJ, Shireman PK, et al: echocardiography: a case report. J Vasc Surg 24:513, 1996 Surgical management of atheroembolism. J Vasc 15:573, 1992 23. Ouriel K, Veith FJ, Sasahara AA: Thrombolysis or Surg 21:773, 1995 65. Loop F, Effler D, Navia J, et al: Aneurysms of the peripheral arterial surgery: phase I results. TOPAS 44. Dougherty MJ, Calligaro KD: Endovascular treat- left ventricle: survival and results of a ten-year sur- investigators. J Vasc Surg 23:64, 1996 ment of embolization of aortic plaque with covered gical experience. Ann Surg 178:399, 1973 24. A comparison of recombinant urokinase with vas- stents. J Vasc Surg 36:727, 2002 66. Hellerstein H, Martin J: Incidence of thromboem- cular surgery as initial treatment for acute arterial 45. Kumins NH, Owens EL, Oglevie SB, et al: Early bolic lesions accompanying myocardial infarction. occlusion of the legs. Thrombolysis or Peripheral experience using the Wallgraft in the management Am Heart J 33:443, 1947 Arterial Surgery (TOPAS) investigators. N Engl J of distal microembolism from common iliac artery Med 338:1105, 1998 pathology. Ann Vasc Surg 16:181, 2002 67. Keely E, Hillis L: Left ventricular mural thrombus after acute myocardial infarction. Clin Cardiol 25. Mahler F, Schneider E, Hess H: Recombinant tis- 46. Blebea J, Kerr JC, Franco CD, et al: Technetium 19:83, 1996 sue plasminogen activator versus urokinase for 99m pyrophosphate quantitation of skeletal mus- local thrombolysis of femoropopliteal occlusions: a cle ischemia and reperfusion injury. J Vasc Surg 68. Asinger R, Mikell F, Elsperger J: Incidence of left prospective, randomized multicenter trial. J 8:117, 1998 ventricular thrombosis after acute transmural Endovasc Ther 8:638, 2001 myocardial infarction. N Engl J Med 305:297, 47. Quinones-Baldrich WJ, Chervu A, Hernandez JJ, 1981 26. Morgan R, Belli AM: Percutaneous thrombecto- et al: Skeletal muscle function after ischemia: “no my: a review. Eur Radiol 12:205, 2002 reflow” versus reperfusion injury. J Surg Res 51:5, 69. Darling R, Austen W, Linton R: Arterial embolism. 1991 Surg Gynecol Obstet 124:106, 1967 27. Zehnder T, Birrer M, Do DD, et al: Percutaneous catheter thrombus aspiration for acute or subacute 48. Ricci MA, Graham AM, Corbisiero R, et al: Are 70. Perier P, Bessou J, Swanson J, et al: Comparative arterial occlusion of the legs: how much thrombol- free radical scavengers beneficial in the treatment evaluation of aortic valve replacement with Starr, ysis is needed? Eur J Vasc Endovasc Surg 20:41, of compartment syndrome after acute arterial Bjork, and porcine valve prostheses. Circulation 2000 ischemia? J Vasc Surg 9:244, 1989 72:140, 1985 28. Crain MR: Percutaneous mechanical thrombolysis 49. Ouriel K, Smedira NG, Ricotta JJ: Protection of 71. Pipkin R, Buch W, Fogart T: Evaluation of aortic and thrombectomy.Tech Vasc Interv Radiol 1:235, the kidney after temporary ischemia: free radical valve replacement with porcine xenograft without 1998 scavengers. J Vasc Surg 2:49, 1985 long-term anticoagulation. J Thorac Cardiovasc 29. Demin VV, Zeienin VV, Zheludkov AN, et al: Initial 50. Mathieson MA, Dunham BM, Huval WV, et al: Surg 71:179, 1976 experience of transcutaneous rheolytic thrombec- Ischemia of the limb stimulates thromboxane pro- 72. Kitts D, Bongard F, Klein S: Septic embolism

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