Embolism To The Lower Extremities

25/2/2018 Embolism to the lower extremities - UpToDate
Official reprint from UpToDate®

www.uptodate.com ©2018 UpToDate, Inc. and/or its affiliates. All Rights Reserved.
Embolism to the lower extremities
Author: Jonathan D Braun, MD

Section Editors: John F Eidt, MD, Joseph L Mills, Sr, MD
Deputy Editor: Kathryn A Collins, MD, PhD, FACS
All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jan 2018. | This topic last updated: Jan 02, 2018.
INTRODUCTION — Embolism to the lower extremities is caused by material that has traveled from elsewhere in
the body. The material that has lodged in the extremity decreases blood flow because of occlusion or severe
stenosis of the blood vessel. By understanding the breadth of that definition, the variables of "material" and
"elsewhere in the body" provide a way to systematically think through the various etiologies. In addition, a
systematic approach helps to avoid jumping to diagnostic conclusions based purely on what is common or what
may have been previously seen in practice.
The priorities of managing acute embolism to the lower extremities are first to address the ischemia and then to
institute measures to prevent further embolic events.
The clinical presentations, evaluation, diagnosis, and general management of embolism to the lower extremities
are reviewed here. Other causes of acute arterial occlusion to the lower extremities are reviewed elsewhere. (See
"Clinical features and diagnosis of acute limb ischemia".)
ETIOLOGY
Cardiac sources — The most commonly reported source of lower extremity emboli is the heart, accounting for 55
to 87 percent of events [1-3]. The main sources of embolism from the heart are thrombus from within the cardiac
chambers and debris shedding off valves (native, prosthetic). Rarely, cardiac tumor, most commonly atrial
myxoma, can also embolize [4].
Emboli from intracardiac thrombus usually come from the left atrium, often associated with atrial fibrillation.
Thrombus can also form in the left ventricle (eg, severe cardiomyopathy, post-myocardial infarction). In either
case, an area of relative stasis within the heart allows thrombus to form locally, which can dislodge and embolize
to virtually anywhere in the body, including the lower extremities. Intracardiac sources of thrombus are often fibrin
rich, with acute thrombus generally responding well to thrombolytic agents (eg, tissue plasminogen activator) [5].
(See "Atrial fibrillation: Risk of embolization" and "Left ventricular thrombus after acute myocardial infarction".)
The aortic or mitral valves can also be sources of emboli to the lower extremities. This may be from debris on
diseased native or prosthetic valves, vegetative growths from bacterial endocarditis, or nonbacterial vegetations
such as Libman-Sacks endocarditis in lupus [6,7]. As these types of embolic debris are not largely thrombotic in
nature, they do not respond well to thrombolysis. (See "Clinical manifestations and evaluation of adults with
suspected native valve endocarditis" and "Epidemiology, clinical manifestations, and diagnosis of prosthetic valve
endocarditis".)
https://www.uptodate.com/contents/embolism-to-the-lower-extremities/print?search=arterial%20thrombosis&usage_type=default&source=search_res… 1/20
When septic emboli from cardiac valves lodge in the lower extremity, they can cause local destruction of the
artery, abscess formation, and/or mycotic pseudoaneurysms in addition to the usual ischemic picture. (See
"Complications and outcome of infective endocarditis", section on 'Septic embolization' and "Overview of infected
(mycotic) arterial aneurysm".)
Aortic plaque — A diseased aortic wall with complex atherosclerotic plaque can also be a source of emboli.
Presumably following the rupture of the fibrous cap overlying an atherosclerotic plaque, luminal irregularities and
ulcerations result in a surface that is thrombogenic [8]. In addition to embolization of larger pieces of accumulated
thrombus, microembolization of cholesterol crystals can also occur. (See "Embolism from aortic plaque:
Thromboembolism" and "Embolism from atherosclerotic plaque: Atheroembolism (cholesterol crystal embolism)".)
Asymptomatic atherosclerotic disease of the aorta often seen incidentally on imaging studies (the so-called
"shaggy aorta syndrome") describes a condition that can lead to macrovascular or microvascular embolization (or
both) [9,10]. This can occur anywhere along the aorta, including the ascending aorta, aortic arch, descending
thoracic aorta, or abdominal aorta.
Another source of emboli from the aorta is thrombus that appears to be nearly free-floating with attachment at one
end to the wall of the aorta (also known as mural thrombus, mobile aortic thrombus, pedunculated aortic
thrombus) [11]. Sometimes these are found incidentally on imaging studies and other times during the evaluation
for an embolic source. When surgically removed, the attachment point appears often to originate from an intimal
irregularity/defect, suggesting that these may start from a ruptured plaque or other primary intimal defect.
Aortic and peripheral aneurysm — Blood flow within aortic aneurysms (thoracic or abdominal) is altered such
that mural thrombus frequently forms within the aneurysm sac. Unlike with rupture risk, there is no known
association of embolic potential of aortic aneurysms relative to their diameter. Although mural thrombus in an
aortic aneurysm is common, dislodgement of aortic thrombus is an uncommon but known source of embolization
to the lower extremities [12]. Embolism may be spontaneous, during manipulation of the aneurysm during open or
endovascular repair, or during arterial instrumentation for another reason. (See 'Instrumentation' below.)
Peripheral aneurysms such as femoral and popliteal aneurysms have a propensity to thrombose, which may
propagate to occlude the distal vasculature, or alternatively mural thrombus can embolize distally. (See "Femoral
artery aneurysm" and "Popliteal artery aneurysm".)
Although iliac artery aneurysms are more likely to be complicated by rupture, thrombosis with the potential for
embolism can occur. (See "Iliac artery aneurysm".)
Paradoxical embolism — A paradoxical embolus results from venous thrombus embolizing to the right heart and
then crossing into the arterial circulation through an intracardiac septal defect, or a right-to-left shunt in the
pulmonary circulation.
Although the most commonly described manifestation of paradoxical embolism is acute stroke, embolization
elsewhere in the peripheral arterial system has been described, including to the lower extremities. Because these
clots originate in the veins, they tend to be larger, and when they embolize to the lower extremities, they tend to
obstruct larger vessels.
A timely diagnosis of paradoxical embolism requires a high index of suspicion because it is quite rare due to the
low prevalence of the requisite structural defects required to allow crossing over from the venous to arterial
circulation.
Instrumentation — The incidence of lower extremity embolization as result of cardiac or peripheral interventions
(catheter based or surgical) is quite low, but it is important to consider as a potential etiology when evaluating an
embolic event. (See "Complications of diagnostic cardiac catheterization", section on 'Atheroembolism'.)
Endovascular intervention — Careful manipulation of wires, catheters, and treatment devices during
endovascular interventions is important to minimize damage from the intervention itself. Disruption of plaque or
thrombus can occur during any type of intervention, including diagnostic studies and stent or stent-graft
placement.
The incidence of iatrogenic embolization is not well known, but angiographically or clinically noted macroembolic
events are estimated to occur in 4 to 5 percent, with smaller, undetected microembolic events likely occurring at
much higher rates [13]. The clinical implications of microembolic events are not well known [14].
The intraprocedural embolic event may be recognized at the time of the procedure on completion imaging that
shows a new filling defect or loss of outflow vessels. Early recognition provides an opportunity to immediately
address the problem, with the goal of minimizing negative clinical effects, which can often be accomplished using
endovascular means. Embolization related to instrumentation can also occur in a delayed manner after the
intervention has been completed.
Arterial closure devices — A variety of arterial closure devices (suture-mediated closure, metal clip-mediated
closure, collagen or other soluble plugs) can be used at the end of endovascular procedures, usually with good
results [15]. Vessel thrombosis and/or distal embolization are potential complications of these devices, with
embolization occurring infrequently (<1 percent) [16-18].
Such complications are usually related to an unrecognized maldeployment of the device such that an external
component is deployed within the vessel wall or intraluminally. Although the component is generally designed to
dissolve over time, the timeframe is usually over weeks to months. Any narrowing of the vessel causing ischemia
will usually need to be addressed sooner.
CLINICAL PRESENTATIONS — The clinical presentation of lower extremity embolization varies depending upon
the source of the thrombus, the size of the embolic debris, and the ability of the extremity to compensate for
reduced flow related to the obstruction, which varies by the location of the obstruction. Some clinical presentations
increase suspicion for certain etiologies. Coexisting peripheral artery disease may alter the manner in which an
embolic event presents.
Emboli tend to lodge at arterial branch points where the caliber of vessels changes or at a site of narrowing from a
preexisting atherosclerotic plaque. In one of the largest series on embolic disease, lower extremity emboli
accounted for 63 percent of events, with the femoral artery affected most commonly (28 percent), followed by the
aortoiliac segment (18 percent), and then the popliteal segment (17 percent) [19].
Acute limb ischemia — The working definition of acute limb ischemia is based on the 2007 Inter-Society
Consensus for the Management of Peripheral Arterial Disease (TASC II), which describes acute limb ischemia as
"a quickly developing or sudden decrease in limb perfusion, usually producing new or worsening symptoms or
signs, and often threatening limb viability" [20]. The duration of symptoms that distinguishes acute from chronic
limb ischemia is defined as <2 weeks [21-23].
Emboli from cardiac sources or paradoxical emboli tend to lodge in larger arteries and tend to occur in individuals
without peripheral artery disease. Symptoms are sudden and rapidly progressive. The severity of the initial
presentation corresponds to the degree of urgency needed for treatment [21].
Blue toe syndrome — Digital ischemia with intact large vessel circulation, also called the "blue toe” syndrome, is
a variation of acute limb ischemia, except that the size of the embolic material is small enough to travel into the
end arteries [24,25]. (See "Embolism from atherosclerotic plaque: Atheroembolism (cholesterol crystal
embolism)", section on 'Blue toe syndrome'.)
The patient will often have intact pedal pulses, but there is inadequate circulation to the individual toe(s). In
patients who do not have concomitant neuropathy or other sensory deficits, this condition is extremely painful.
The toe will often become discolored, hence this syndrome's moniker. The clinical course after the acute insult
varies, sometimes with complete resolution, other times with chronic pain/nerve damage but with preservation of
the toe, and at other times with progression to gangrene and need for toe amputation. Unless extensive, there is
minimal threat of major (above-ankle) amputation.
Subclinical progression to chronic ischemia — In contrast to acute limb ischemia, repeated emboli to the
lower extremities can manifest with a stepwise deterioration of distal arterial flow from individual embolic events
that have either no or mild symptoms.
Disruption of the lower extremity outflow circulation can become sufficiently severe to cause rest pain or tissue
loss. The resultant clinical presentation is similar to chronic peripheral artery disease but with an embolic rather
than atherosclerotic or other etiology [26,27]. (See "Clinical features and diagnosis of lower extremity peripheral
artery disease".)
Subclinical progression can appear clinically and is angiographically similar to other common pathologies that
predominantly affect the tibial vessels, such as patterns of peripheral artery disease in patients with diabetes or
renal failure, Buerger's disease, vasculitis, or repetitive arterial trauma.
Subclinical progression can be difficult to treat because the reduced arterial outflow limits the available treatment
options and durability of treatment.
CLINICAL EVALUATION — The clinical evaluation identifies the nature of the clinical presentation, grades the
severity of ischemia, and considers the potential sources of embolization, all of which are used to determine the
appropriate course of treatment and to institute treatment to prevent future embolic events. A systematic approach
is used to avoid missing potential embolic sources that can lead to recurrent embolism. The extent and timing of
the clinical evaluation largely depends on the nature of the clinical presentation. (See 'Clinical presentations'
above.)
● For acute limb ischemia, management of the limb takes priority over determining the source of the embolus.
The evaluation focuses primarily on what is necessary to make appropriate treatment decisions, namely
determining clinical severity, defining the anatomy, and identifying comorbidities that may influence treatment.
Identifying the suspected embolic source may need to be deferred until after treatment is begun.
● For other presentations (eg, subclinical progression, blue toe syndrome), acute treatment options may be
limited, and the emphasis is on preventing future embolic events.
History and physical — The history should evaluate risk factors associated with lower extremity embolism. (See
'Etiology' above.)
● A history of atrial fibrillation, valve replacement, structural heart defects, or known valvular problems may
point toward a potential cardiac source, but it must be kept in mind that for some people, cardiac disease may
be undiagnosed.
● For patients who are anticoagulated, it is important to identify the reason for anticoagulation and whether the
medication is being taken regularly and as prescribed, as well as when the last dose was taken. For patients
taking warfarin for atrial fibrillation, a nontherapeutic international normalized ratio (INR) increases the risk for
embolization. In a Veterans Administration study of over 34,000 patients with nonvalvular atrial fibrillation, low
INR (<2.0) increased the risk for systemic embolization (relative risk 6.3; 95% CI 4.4-8.9) [28].
● For patients with a history of peripheral artery disease, it is important to determine the baseline symptoms,
which may help determine the acuity of the current symptoms and, after treatment, whether there has been a
return to baseline. For patients with diabetes, a history of any baseline neurologic deficits is important.
● For the patient with a known history of aneurysmal disease or a family history of aneurysms, it is important to
consider all potential aneurysm sites. Aneurysm in one location increases the risk for aneurysms in other
locations. Patients with an abdominal aortic aneurysm have a prevalence of approximately 20 percent for
popliteal aneurysms, many of which may not be easily detected on physical exam [29]. Up to 80 percent of
patients with one peripheral aneurysm have multiple aneurysms, and in patients with a popliteal aneurysm,
the incidences of aortoiliac and bilateral popliteal aneurysms are approximately 60 and 50 percent,
respectively [30].
● The patient should also be asked about any recent catheterization procedures.
A thorough examination evaluates for signs of acute limb ischemia (six Ps) and any signs of chronic limb
ischemia. For the lower extremity, this involves evaluating the femoral, popliteal, dorsalis pedis, and posterior tibial
pulses bilaterally. (See "Clinical features and diagnosis of acute limb ischemia", section on 'Six Ps' and "Embolism
from atherosclerotic plaque: Atheroembolism (cholesterol crystal embolism)", section on 'Clinical manifestations'
and "Clinical features and diagnosis of lower extremity peripheral artery disease", section on 'Physical
examination'.)
Often in acute presentations, the history and physical examination may be all that is necessary to guide therapy.
As an example, an absent femoral pulse in the affected extremity but a normal or near-normal pulse examination
in the unaffected extremity in a patient with an appropriate history (eg, atrial fibrillation) may be all that is needed
to proceed to embolectomy. (See 'Approach to limb management' below.)
Classification of ischemia — Based on the clinical findings, the severity of acute ischemia should be
classified (table 1), which is important for guiding further evaluation and management [21,31]. (See "Classification
of acute and chronic lower extremity ischemia", section on 'Acute extremity ischemia' and "Classification of acute
and chronic lower extremity ischemia", section on 'Chronic extremity ischemia' and 'Approach to limb
management' below.)
Laboratory studies — Laboratory information is obtained initially to assess treatment risks and to serve as a
baseline for subsequent comparison. The patient will at least be started on anticoagulation and has a high
likelihood of being administered iodinated contrast for catheter-based arteriography or computed tomographic
(CT) angiography at some point during diagnosis and treatment. As such, we obtain a complete blood count,
basic metabolic panel, prothrombin time/international normalized ratio (PT/INR), and partial thromboplastin time
(PTT). For patients in whom thrombolysis will be considered, a baseline fibrinogen should be included with the
coagulation profile.
Vascular imaging — Whether or not to proceed with vascular imaging depends upon the suspected cause,
physical findings, and the severity of ischemia. For patients with acute lower extremity embolism, the history and
physical examination may be sufficient to provide the diagnosis and to initiate treatment. Whenever feasible, we
suggest obtaining CT angiography because it provides valuable information about the location of embolic debris
(image 1) and the amount and location of baseline atherosclerotic plaque burden, and it will detect aneurysmal
disease. Even in the setting of acute limb ischemia, CT angiography can usually be quickly accomplished while
preparing the patient for intervention. The information gained from CT angiography may also be helpful for
deciding whether to pursue open surgery or catheter-based intervention as well as aiding with the specifics of the
chosen approach. As an example, if an open approach would be favored, then arterial puncture for angiography,
which comes with its own risks, can be avoided. The benefits of CT angiography must be weighed against any
potential risks (eg, treatment delays, worsening renal function).
The objective is to obtain good imaging of the lower extremity vasculature as well as the abdominal and pelvic
inflow. Although complete vascular imaging would be desirable, it is often very difficult to get good-quality images
of the chest, abdomen, pelvis, and bilateral lower extremities with a single contrast bolus. In this setting,
evaluation of the chest can be deferred until the postoperative period, if still needed. (See 'Subsequent diagnostic
evaluation' below.)
Magnetic resonance (MR) angiography has limitations when evaluating acute embolic disease, one of which is the
additional time needed to complete the study. The extent of calcium within the walls of the vessels is particularly
relevant for deciding the best way to obtain proximal and distal control of the artery during open surgery. Calcium
is poorly visualized, and the spatial resolution may also be limited for evaluating ulcerative plaques or irregular
atheroma, but this can vary by available equipment and protocols.
INITIAL MANAGEMENT — Initial management of acute embolism to the lower extremities includes systemic
anticoagulation and intravenous fluid therapy, which can be started while awaiting evaluation by a specialist
trained to treat the lower extremity embolic event (typically a vascular surgeon). Medical risk assessment, which
may require consultation with medicine or cardiology services, should also be initiated to aid in selecting the best
option for treatment.
Anticoagulation — Systemic anticoagulation (intravenous heparin bolus followed by continuous intravenous

heparin infusion), along with intravenous fluid therapy (as needed), should be initiated as soon as the diagnosis of
embolism is made on clinical grounds, and before subsequent imaging [20,32]. Patients should remain
anticoagulated and monitored for progression of ischemia throughout any vascular imaging. (See "Heparin and
LMW heparin: Dosing and adverse effects", section on 'Dosing and monitoring'.)
Anticoagulation prevents further propagation of thrombus and inhibits thrombosis distally in the arterial and
venous systems due to low flow and stasis. Anticoagulation may result in clinical improvements that may
decrease the threat to the limb as collaterals open up and vasospasm improves, possibly allowing more time for
evaluation and treatment.
For some patients, systemic anticoagulation alone may serve as definitive treatment [33]. This strategy may be
useful for very-high-risk patients with viable limbs and some with marginally threatened limbs who have numerous
comorbidities or more pressing medical issues.
Medical risk assessment — The majority of patients with lower extremity embolism have underlying
cardiovascular disease. The severity of any underlying cardiac condition(s) may increase the risk of treatment and
limit the options available for restoring blood flow to the ischemic extremity. When time allows, preoperative
cardiac evaluation should be included in the management of these patients to assess surgical risk. (See
"Evaluation of cardiac risk prior to noncardiac surgery" and "Management of cardiac risk for noncardiac surgery".)
For patients who require emergency revascularization, a baseline electrocardiogram, chest radiography, and a
clinical history of the patient's level of activity (ie, whether or not the patient can perform >4 metabolic equivalents)
help stratify risk. An echocardiogram can usually be obtained following revascularization; however, if thrombolytic
therapy is being considered, obtaining an echocardiogram beforehand is useful to evaluate for mural thrombus.
APPROACH TO LIMB MANAGEMENT — While embolism to the lower extremities has a variety of potential
causes as well as treatment strategies, the approach to limb management strongly depends on the clinical
presentation, particularly the severity of limb ischemia at presentation (table 1) and duration of symptoms [22].
(See 'Classification of ischemia' above.)
Other factors that may play into decision making include the etiology and anatomy of the embolic occlusion, runoff
quality below the occlusion, patient comorbidities, prior operations, endovascular device availability, and
contingency plans in the event of treatment failure.
By severity of acute ischemia
Viable or marginally threatened extremity — For most patients with a viable or marginally threatened
extremity, based upon the outcomes of several randomized trials, we agree with major society guidelines that
support an initial attempt at thrombolysis for appropriately selected patients [22,32,34-36]. For viable limbs,
treatment can usually be approached urgently rather than as an emergency.
Clinical features that are useful for determining whether thrombolysis or surgical revascularization is the most
appropriate initial treatment include the following:
● Presumed etiology
● Lesion location and length
● Duration of symptoms
● Suitability of the patient for surgery
● Availability of autologous vein for bypass grafting
As examples, proximal thrombus (eg, aortoiliac, common femoral artery) may be more amenable to
thrombectomy. On the other hand, an embolus to a distal vessel (eg, tibial artery) may be best treated with
thrombolysis. In general, older thrombus (eg, from aneurysm sac) does not respond well to thrombolysis, and
thrombolysis has no effect on nonthrombotic material, so if either is strongly suspected, surgery may be the
preferred treatment. In patients who have previously undergone surgery, reoperative fields can make surgical
exposure more difficult, increasing the risk for complications. In addition, peripheral artery disease can make an
embolectomy more challenging. High-grade stenoses can make it difficult to pass embolectomy catheters, and
calcified plaque tends to pop the embolectomy balloon. Arterial dissection can also occur from the catheter
passing behind the plaque. Passing an embolectomy through a recent stent or vascular anastomosis increases
the risk of dislodging the stent or rupturing the vessel.
Thrombolysis is generally a safe and effective alternative to surgery for appropriately selected patients [37,38].
However, failure of thrombolysis can lead to progression of ischemia to a higher degree of limb threat that may
necessitate conversion to immediate surgical revascularization to reduce the risk of limb loss. Although the
success of thrombolytic therapy may be limited by the time required to dissolve thrombus and severity and
duration of ischemia, when subsequent revascularization is needed, the magnitude and complexity of the
procedure is frequently less for those receiving compared with not receiving prior thrombolytic therapy. (See 'By
etiology/anatomy' below and 'Intra-arterial thrombolysis' below and 'Open embolectomy' below.)
Immediately threatened extremity — For most patients with an immediately threatened extremity, surgical
revascularization is the most appropriate initial treatment. (See 'Open embolectomy' below.)
Patients with an immediately threatened limb are generally not good candidates for thrombolysis. Although
pharmacologic thrombolysis may successfully dissolve the embolus, the time required is usually too long for it to
be an acceptable alternative to surgery. Progression to an unsalvageable limb can occur in as little as four to six
hours if prompt revascularization is not performed. Thus, open embolectomy is preferred; however, some
clinicians may initiate thrombolysis in selected clinical circumstances, such as if the neurologic deficits are mild
and open revascularization represents an excessive risk for the patient. If thrombolysis is to be considered at all,
the limb needs be closely monitored to identify any signs of deterioration, which can happen quickly. In addition,
there needs to be expedient operating room availability in the event of clinical worsening to convert emergently to
open surgical revascularization for appropriate candidates.
Depending upon the duration and severity of the ischemia, a fasciotomy may be required to prevent the
development of compartment syndrome following reperfusion. (See "Acute compartment syndrome of the
extremities" and "Lower extremity fasciotomy techniques".)
Nonviable extremity — Patients with nonviable extremities should undergo prompt amputation. Vascular
imaging prior to surgery is usually not necessary, since the level of amputation is determined by clinical findings
and by the viability of tissues at the time of surgery. Every effort should be made to preserve as many joints as
possible to decrease the work of ambulating with a prosthetic, which improves the likelihood for successful
rehabilitation. Delays in amputation of a nonviable extremity can result in infection, myoglobinuria, acute renal
failure, and hyperkalemia. (See "Lower extremity amputation" and "Techniques for lower extremity amputation".)
By etiology/anatomy
● Suspected cardiac source – Emboli from cardiac sources tend to be large and lodge at the bifurcations of
major lower extremity vessels, such as the common femoral artery or aortic bifurcation. These patients often
do not have underlying vascular disease, present without a femoral pulse on the affected side, and have a
normal vascular exam on the contralateral side. These findings may be all that is needed prior to going to the
operating room. In this setting, open embolectomy is generally the best procedure, given that these emboli
are often are too large to aspirate and may have limited response to thrombolysis, though exceptions may
exist.
● Distal vessel occlusion/thrombosis – For patients who have little to no flow in the distal vessels on initial
arteriography, we suggest thrombolysis to improve outflow. Occlusion of the distal vessels can be the direct
result of embolization or can be due to low flow from a more proximally lodged embolus. The outflow may
thrombose to the extent that no suitable target is available for revascularization on initial arteriography.
Clearing distal thrombus may reveal treatment options that were not apparent on initial arteriography,
improving options for subsequent open and/or endovascular treatment.
● For patients whose history suggests that the embolic material is chronic thrombus (eg, mural thrombus from
aneurysm, aortic thrombus) or nonthrombotic material (eg, tumor, embolized device fragments), open
embolectomy or transcatheter embolectomy are better options compared with thrombolysis as these
materials are not likely to or simply will not respond to thrombolytic agents.
● For patients with recurrent embolism leading to subclinical progression, the suspected embolic source needs
to be found and treated. Revascularization is performed as needed based upon clinical symptoms and
anatomy, similar to the approach for chronic peripheral artery disease. (See "Treatment of chronic limb-
threatening ischemia".)
● Embolization during intervention – When distal embolization occurs during a peripheral intervention, it is
ideally identified at the index procedure and treated in the same setting. This can often be done by aspirating
the embolic material through a catheter (using a guiding catheter or specifically designed catheter for
removing emboli). Sometimes, applying low doses of tissue plasminogen activator (tPA; 2 to 4 mg) through
the catheter into the affected vessel can dissolve the embolized material, particularly when embolus is very
distal. Rarely, in larger vessels it may be necessary to place a stent to trap the embolized material against the
vessel wall to preserve luminal flow. (See 'Transcatheter embolectomy' below and 'Intra-arterial thrombolysis'
below.)
● Blue toe syndrome – The treatment of blue toe syndrome is predominantly medical, so it is important to
recognize it when it occurs; otherwise, the patient could be subjected to treatments that are ineffective. (See
"Embolism from atherosclerotic plaque: Atheroembolism (cholesterol crystal embolism)", section on
'Treatment'.)
TECHNIQUES
Intra-arterial thrombolysis — Prior to initiating thrombolysis, patients should be screened for contraindications to
thrombolytic therapy [35]. Severe complications of thrombolysis include intracranial hemorrhage, which has high
mortality, and major gastrointestinal bleeding, which is potentially life-threatening.
Thrombolytic therapy can be initiated in a hybrid operating room suite, a standard operating room with portable C-
arm capabilities, or an interventional suite. Whenever thrombolysis is performed, it is important to have an
operating room available in the event that ischemia progresses during thrombolysis, the treatment fails, or
bleeding occurs that requires operative intervention.
A Cochrane review that included five trials evaluated the best approach to thrombolytic therapy when this form of
treatment is chosen [39,40]. Comparisons were available between tissue plasminogen activator (tPA),
streptokinase, and urokinase. This review concluded that intra-arterial tPA may be more effective at improving
patency compared with intra-arterial streptokinase [40,41]. Three other studies comparing tPA and urokinase
found that although intra-arterial tPA led to more rapid initial lysis, these agents appeared to be equally effective in
terms of treated vessel patency, and no significant differences were found for rates of limb salvage, bleeding
complications, or death [42-44]. For urokinase, higher dose (8 mg/hour versus 2 or 4 mg/hour) and forced infusion
techniques resulted in more rapid thrombolysis, but bleeding risk appeared to be increased, and clinical outcomes
were no different [45].
Our approach to lower extremity thrombolysis is as follows:
● To obtain access with minimal trauma, which is always important during percutaneous intervention but is
particularly so in cases when a thrombolytic agent will be infused, we recommend ultrasound guidance to
assist arterial puncture to ensure a single stick into the artery (typically common femoral) and to avoid
puncturing the back wall (ie, a "through-and-through" stick), which increases the likelihood of access site
bleeding/hematoma.
● Once the access is established and an arterial sheath has been placed, a wire is used to cross the site of
thrombosis intraluminally; subintimal passage of wires and catheters should be avoided. The thrombolytic
agent is generally infused though a multi-sidehole infusion catheter that is placed over the wire within the
extent of the thrombus. The multi-sidehole catheter must be long enough to encompass the length of the
involved segment.
● Once the catheter has been positioned, we generally bolus 4 to 10 mg of tPA (alteplase) through the catheter
on the table and then initiate a drip of 1 mg/hour through the catheter with a simultaneous infusion of
intravenous heparin (400 units/hour) through the side port of the sheath. After securing the catheters, the
patient is transferred to an intensive care unit to monitor the limb for potential worsening limb ischemia,
bleeding, compartment syndrome, or other complications (eg, acute neurologic changes).
● We obtain serial labs to monitor for bleeding risk as well as for the possible development of thrombocytopenia
or hypofibrinogenemia. We obtain hemoglobin, hematocrit, platelets, partial thromboplastin time, and
fibrinogen every six hours. An increased risk for bleeding has been correlated with reduced fibrinogen levels
after intravenous stroke thrombolysis [46]; however, in a review of catheter-directed intra-arterial or
intravenous thrombolysis, there were no differences in major bleeding events when comparing patients with
low (<150 mg/dL) versus higher fibrinogen levels [47].
● For fibrinogen <200 mg/dL, we generally reduce the rate of infusion by one-half, and if the fibrinogen falls
below 150 mg/dL, we hold the infusion for one hour, and then recheck fibrinogen levels. If fibrinogen levels
are low and there is concern for bleeding, fresh frozen plasma or cryoprecipitate can be transfused, but this is
rarely needed.
● For evidence of significant bleeding, the infusion is stopped. Low-dose heparinized saline can generally be
continued to prevent rethrombosis of clot that has already lysed.
● The need for ongoing infusion, possible repositioning of the catheter, or another course of therapy is
determined by repeat arteriography (daily or in response to clinical changes). If needed, the infusion can be
continued up to two to three days, as long as the extremity is not threatened.
Pharmacomechanical thrombolysis involves the additional use of some sort of mechanical force to assist in
breaking up the clot. The mechanism differs among the various devices and includes pulsed spray, rotating wire,
ultrasound energy, or other mechanisms to break up the thrombus [48,49]. The segment being treated is generally
also initially laced with a thrombolytic agent. Some devices can also be used as a mechanical thrombectomy
device alone, if there are contraindications to thrombolysis. The goal of pharmacomechanical thrombolysis is to
reduce the overall thrombolysis time as well as overall dose of the lytic agent. Some advocate using a distal filter
when performing pharmacomechanical thrombolysis to prevent propagation of smaller emboli distally, while others
would manage such events with either catheter thrombectomy or infusion of intra-arterial thrombolysis.
Open embolectomy — One of the main advantages of open embolectomy is that blood flow is generally restored
quite quickly. However, revascularization may be accompanied by adverse cardiac events due to sudden release
of acid and potassium from the ischemic tissue.
For patients with large emboli that lodge at/near the femoral bifurcation, an open embolectomy is an expedient
solution that can be performed on almost any patient. If comorbidities increase the risk for general anesthesia, a
femoral cutdown and embolectomy can be performed under regional or local anesthesia.
Either a transverse or longitudinal incision can be made over the common femoral artery. If the vessel is soft and
healthy, a transverse arteriotomy is made for embolectomy, which prevents luminal narrowing on repair. If the
artery is diseased, we generally prefer to use the longitudinal incision because it provides greater flexibility for
additional exposure if a concomitant endarterectomy and patch angioplasty becomes necessary.
From the single arteriotomy, Fogarty balloon catheters can be passed proximally into the iliac artery and distally
into the superficial and deep femoral arteries, and often down to the popliteal artery. A #5 Fogarty is often
sufficient for the common femoral and iliac arteries, and a #4 Fogarty is typically used in the superficial femoral
artery, although smaller or larger catheters may be necessary as the circumstances dictate. To embolectomize
down to the popliteal artery from the groin, a #3 Fogarty catheter will often be necessary. Once strong inflow and
backbleeding are obtained with clean passes of the Fogarty embolectomy catheters, intraoperative completion
arteriography is performed to evaluate the adequacy of distal blood flow. Intraoperative administration of a
thrombolytic agent directly into the distal vessels may be necessary if small emboli are still present in the runoff
vessels.
If needed, additional exposures of the below-knee popliteal artery at the tibial trifurcation and/or distal tibial/pedal
vessels can be used to ensure adequate flow. Passing embolectomy catheters into tibial vessels requires extreme
care as these vessels are easily injured. A #2 Fogarty is generally used for tibial vessels. Very distal thrombus can
sometimes be treated with localized intra-arterial tPA injection. Spasm of otherwise healthy vessels or dissection
of the arteries can occur with embolectomy. If spasm is suspected, intra-arterial administration of a vasodilator
such as nitroglycerin or papaverine will often resolve the issue. If a dissection is flow limiting, angioplasty and/or
stenting may be required.
If embolectomy fails, bypass grafting may become necessary, although for purely embolic events without baseline
peripheral artery disease, this is rarely necessary. For immediately threatened limbs, prosthetic graft (ie,
polytetrafluoroethylene [PTFE]) is often chosen to avoid the time needed for vein harvest, which expedites
restoration of blood flow with the tradeoff of decreased expected patency. Individual surgeons need to weigh the
risks and benefits for each patient based on the clinical scenario.
Transcatheter embolectomy — Techniques have been developed for using guiding catheters to engage
thrombus and directly aspirate embolus that occurs, primarily during an intervention. Other options for
https://www.uptodate.com/contents/embolism-to-the-lower-extremities/print?search=arterial%20thrombosis&usage_type=default&source=search_re… 10/20
percutaneous, catheter-based thrombus extraction are emerging for clinical use. These are particularly useful for
cases of intraprocedural embolization of plaque/thrombus large enough to lodge in major runoff vessels or in
cases where there is a contraindication to the use of thrombolytic agents. In addition, a device based on the same
system that has been used for neuro-rescue in acute strokes is also available with catheter sizes and lengths for
treating lower extremity emboli, even those occurring distally [50]. Retrospective studies are based on case
reports/series without prolonged follow-up; however, data from acute ischemic stroke treatment suggest some
benefit compared with thrombolysis [51]. Better studies and definitive data are needed for the peripheral
vasculature, but this represents a potential area of innovation for embolism treatment.
PREVENTING FUTURE EMBOLIC EVENTS — After managing the acute ischemic insult, further evaluation and
treatment focuses on preventing recurrent embolic events. Once the acute limb issues have been attended to, the
subsequent diagnostic evaluation is focused on identifying the suspected embolic source. Once the source is
known, treatment may involve additional intervention to remove or exclude the source from the circulation, or use
of adjunctive medical therapies.
Subsequent diagnostic evaluation
Echocardiography — Echocardiography is an integral part of the subsequent evaluation to determine the

source of the embolus. Obtaining this study can generally be performed after the intervention for acute ischemia
and should not delay treatment.
Echocardiography can detect the presence of residual thrombus in the left atrium as well as evaluate for possible
valvular pathology. If valvular vegetations are strongly suspected, a transesophageal echocardiogram (TEE) may
be required given better sensitivity and specificity. (See "Transesophageal echocardiography in the evaluation of
the left ventricle" and "Echocardiographic evaluation of the atria and appendages".)
TEE can also identify thoracic aneurysmal disease and aortic plaque and can provide dynamic visualization of
mobile aortic thrombus or plaque that could be the source of distal embolization. (See "Embolism from aortic
plaque: Thromboembolism", section on 'Echocardiography' and "Echocardiographic evaluation of the thoracic and
proximal abdominal aorta".)
Vascular imaging — For those in whom vascular imaging was not completed, we obtain imaging (or
completion imaging) to evaluate the aorta for potential embolic sources, from its origin to the femoral bifurcation,
once it is safe to do so. (See "Embolism from aortic plaque: Thromboembolism" and "Embolism from
atherosclerotic plaque: Atheroembolism (cholesterol crystal embolism)" and "Clinical manifestations and diagnosis
of thoracic aortic aneurysm", section on 'Imaging diagnosis'.)
Treatment
Operative treatment of suspected source — If valvular vegetations are diagnosed as the cause of the
embolic event, valve replacement is strongly considered to prevent future embolic events, as well as to remove a
potential source of infection. (See "Surgery for left-sided native valve infective endocarditis".)
Aneurysmal disease and large vessel atheroma/thrombus as etiologies of embolism can be treated with exclusion
of the segment involved or open surgical bypass grafting. Open aortic aneurysm repair and aortobifemoral bypass
have excellent durability. (See "Open surgical repair of abdominal aortic aneurysm".)
Open aortic thromboendarterectomy may be an option for patients with symptomatic mobile aortic thrombus,
particularly for those located at or near the visceral segment of the abdominal aorta [52]. Although the optimal
treatment strategy is not known for certain, intervention may offer better long-term outcomes. In one review
comparing surgery with anticoagulation for mural thrombus in minimally atherosclerotic aortas, patients who had
the thrombus removed had lower rates of persistent thrombus/recurrence (5.7 versus 26.4 percent) and lower
rates of recurrent peripheral artery embolization (9.1 versus 25.7 percent compared with anticoagulation alone)
[53]. (See "Embolism from aortic plaque: Thromboembolism", section on 'Surgery'.)
For patients with popliteal aneurysm as the source of embolization, lower extremity bypass and exclusion of the
aneurysm provide a durable revascularization. The patency rates for popliteal artery bypass are largely dependent
on the quality of the available outflow [26,27]. (See "Surgical and endovascular repair of popliteal artery
aneurysm", section on 'Surgical bypass'.)
Endovascular exclusion of suspected source — Techniques for endovascular treatment of aneurysmal and
occlusive disease have been used for treating suspected sources of embolic disease to the lower extremities.
Compared with open procedures, the general advantages include less pain, faster recovery time, and less
perioperative morbidity and mortality. A combination of open and endovascular approaches can sometimes be
used to treat multiple areas suspected to be sources of embolus [9].
Endovascular stent grafts have been used to exclude thoracic or abdominal aortic and popliteal sources of lower
extremity embolization. At all sites, adequate sealing above and below the affected area is necessary. When a
stent-graft is used to cover an area that is suspected of having been an embolic source, it is important to avoid
manipulations that may cause intraprocedural embolization. (See "Endovascular repair of the thoracic aorta" and
"Endovascular repair of abdominal aortic aneurysm".)
To obtain vascular access during these procedures, open exposure of the femoral vessels has the advantage of
being able to flush out debris that may have become dislodged during the conduct of the case prior to repairing
the arteriotomy.
Surveillance imaging protocols following endovascular repair need to be followed as endoleaks or other late
complications of endovascular intervention can occur.
Medical therapies — We agree with multidisciplinary guidelines that recommend oral anticoagulation to
prevent recurrent embolism after embolectomy [32]. Most patients will need to be anticoagulated for at least three
months. For patients who do not have a surgically correctible cause of their embolic event, the benefits versus risk
of anticoagulation need to be considered.
Patients with ongoing atrial fibrillation and a prior embolic event are at a significantly increased risk of stroke or
other embolic event and often warrant lifelong anticoagulation unless there is some other compelling factor. (See
"Atrial fibrillation: Anticoagulant therapy to prevent embolization".)
Statins and antiplatelet agents such as aspirin appear to reduce the risk of atheroembolic events and are
generally recommended for patients with coronary artery disease equivalents (ie, peripheral artery disease,
aneurysmal disease). Regimens for developing plaque regression for reduced embolic events in the aorta are
being investigated [54]. (See "Prevention of cardiovascular disease events in those with established disease or at
high risk" and "Embolism from aortic plaque: Thromboembolism", section on 'Medical therapy'.)
MORBIDITY AND MORTALITY — It is difficult to compare published results of the treatment of acute embolism
resulting in ischemia because of different methods used to describe the severity of ischemia and differences in the
duration of ischemia. However, it is clear that, in spite of optimal therapy, acute embolism is associated with high
rates of morbidity and mortality [55,56]. Limb loss rates as high as 30 percent and hospital mortality as high as 20
percent have been quoted in surgical series [57-59]. A majority of amputations are above the knee.
Cardiopulmonary complications account for the majority of the deaths, underscoring the severity of the baseline
medical condition of the typical patient. Approximately 15 to 20 percent of patients die within one year after
presentation, usually from the medical illnesses that predisposed them to acute limb ischemia [60].
SUMMARY AND RECOMMENDATIONS

● Clinical manifestations of acute embolism to the lower extremities can range from isolated digital ischemia to
profound acute global limb ischemia. Some patients will experience a subclinical progressive loss of outflow
vessels from recurrent embolism leading to a chronic peripheral artery disease (PAD)-like picture. (See
'Clinical presentations' above.)
● A variety of etiologies can potentially lead to embolization of the lower extremities, and understanding these
should guide an efficient and thorough clinical evaluation, treatment, and source control. (See 'Etiology'
above.)
● The history and physical examination may be sufficient to determine the most likely etiology and to initiate
treatment. Whenever feasible, we suggest obtaining computed tomographic (CT) angiography because it
provides valuable information about the location of the disease and level of baseline atherosclerotic plaque
burden. Even in the setting of acute limb ischemia, CT angiography can usually be quickly accomplished
while preparing the patient for intervention, but imaging can be deferred if it will delay treatment. (See
'Vascular imaging' above.)
● For those who present with acute limb ischemia, anticoagulation with a heparin drip and intravenous fluid
therapy should be immediately initiated prior to making plans for intervention. These can be started while
awaiting evaluation by a specialist trained to treat the embolic event. (See 'Initial management' above.)
● Options for managing lower extremity embolism include open embolectomy, thrombolysis, and transcatheter
thrombectomy. Factors such as anatomy, degree of limb threat, runoff, suspected etiology, and patient factors
will guide the choice of one over the other. (See 'Approach to limb management' above.)
• For patients without a femoral pulse who have a normal vascular exam on the contralateral side, open
embolectomy is generally the best procedure, though exceptions may exist.
• For patients who have embolized or thrombosed their tibial runoff, initial thrombolytic therapy may
improve outflow, leading to better options for open and/or endovascular treatment.
• For patients whose history suggests that the embolic material is chronic thrombus (eg, mural thrombus
from aneurysm, aortic thrombus) or nonthrombotic material (eg, tumor, embolized device fragments),
open embolectomy or transcatheter embolectomy are better options compared with thrombolysis.
● Once the acute limb issues have been attended to, the subsequent diagnostic evaluation is focused on
identifying the suspected embolic source, typically using echocardiography or additional vascular imaging.
Once the source is known, additional intervention to remove or exclude the source from the circulation is
generally preferred over anticoagulation alone. For patients with coronary heart disease equivalents,
treatment with aspirin and statins should be a component of their medical therapy. (See 'Preventing future
embolic events' above and 'Medical therapies' above.)
Use of UpToDate is subject to the Subscription and License Agreement.
REFERENCES
1. Becquemin JP, Kovarsky S. Arterial emboli of the lower limbs: analysis of risk factors for mortality and
amputation. Association Universitaire de Recherche en Chirurgie. Ann Vasc Surg 1995; 9 Suppl:S32.
2. Dag O, Kaygın MA, Erkut B. Analysis of risk factors for amputation in 822 cases with acute arterial emboli.
ScientificWorldJournal 2012; 2012:673483.
3. Hu HD, Chang Q, Chen Z, et al. [Management and prognosis of acute arterial embolism: a multivariable
analysis of 346 patients]. Zhonghua Yi Xue Za Zhi 2011; 91:2923.
4. Coley C, Lee KR, Steiner M, Thompson CS. Complete embolization of a left atrial myxoma resulting in acute
lower extremity ischemia. Tex Heart Inst J 2005; 32:238.
5. Molina CA, Montaner J, Arenillas JF, et al. Differential pattern of tissue plasminogen activator-induced
proximal middle cerebral artery recanalization among stroke subtypes. Stroke 2004; 35:486.
6. Sorajja P, Mack M, Vemulapalli S, et al. Initial Experience With Commercial Transcatheter Mitral Valve
Repair in the United States. J Am Coll Cardiol 2016; 67:1129.
7. Galyfos G, Giannakakis S, Kerasidis S, et al. Infective endocarditis as a rare cause for acute limb ischemia.
World J Emerg Med 2016; 7:231.
8. Zhang WW, Abou-Zamzam AM, Hashisho M, et al. Staged endovascular stent grafts for concurrent
mobile/ulcerated thrombi of thoracic and abdominal aorta causing recurrent spontaneous distal
embolization. J Vasc Surg 2008; 47:193.
9. Illuminati G, Bresadola L, D'Urso A, et al. Simultaneous stent grafting of the descending thoracic aorta and
aortofemoral bypass for "shaggy aorta" syndrome. Can J Surg 2007; 50:E1.
10. Hollier LH, Kazmier FJ, Ochsner J, et al. "Shaggy" aorta syndrome with atheromatous embolization to
visceral vessels. Ann Vasc Surg 1991; 5:439.
11. Fueglistaler P, Wolff T, Guerke L, et al. Endovascular stent graft for symptomatic mobile thrombus of the
thoracic aorta. J Vasc Surg 2005; 42:781.
12. Baxter BT, McGee GS, Flinn WR, et al. Distal embolization as a presenting symptom of aortic aneurysms.
Am J Surg 1990; 160:197.
13. Lam RC, Shah S, Faries PL, et al. Incidence and clinical significance of distal embolization during
percutaneous interventions involving the superficial femoral artery. J Vasc Surg 2007; 46:1155.
14. Spiliopoulos S, Theodosiadou V, Koukounas V, et al. Distal macro- and microembolization during subintimal
recanalization of femoropopliteal chronic total occlusions. J Endovasc Ther 2014; 21:474.
15. Robertson L, Andras A, Colgan F, Jackson R. Vascular closure devices for femoral arterial puncture site
haemostasis. Cochrane Database Syst Rev 2016; 3:CD009541.
16. Rao S, Kaul P, Stouffer GA. Successful aspiration of Mynx vascular closure device sealant that embolized to
the popliteal artery. J Invasive Cardiol 2013; 25:E172.
17. Choi DH, Kim MJ, Yoo CJ, Park CW. Nitinol clip distal migration and resultant popliteo-tibial artery occlusion
complicating access closure by the StarClose SE vascular closure system. J Neurointerv Surg 2017; 9:e5.
18. Jud P, Portugaller R, Bohlsen D, et al. Successful Retrieval of an Embolized Vascular Closure Device
(Angio-Seal(®)) After Peripheral Angioplasty. Cardiovasc Intervent Radiol 2017; 40:942.
19. Abbott WM, Maloney RD, McCabe CC, et al. Arterial embolism: a 44 year perspective. Am J Surg 1982;
143:460.
20. Norgren L, Hiatt WR, Dormandy JA, et al. Inter-Society Consensus for the Management of Peripheral
Arterial Disease (TASC II). J Vasc Surg 2007; 45 Suppl S:S5.
21. Rutherford RB, Baker JD, Ernst C, et al. Recommended standards for reports dealing with lower extremity
ischemia: revised version. J Vasc Surg 1997; 26:517.
22. Gerhard-Herman MD, Gornik HL, Barrett C, 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; 135:e726.
23. Writing Committee to Develop Clinical Data Standards for Peripheral Atherosclerotic Vascular Disease,
Creager MA, Belkin M, et al. 2012 ACCF/AHA/ACR/SCAI/SIR/STS/SVM/SVN/SVS key data elements and
definitions for peripheral atherosclerotic vascular disease: a report of the American College of Cardiology
Foundation/American Heart Association Task Force on Clinical Data Standards (Writing Committee to
Develop Clinical Data Standards for Peripheral Atherosclerotic Vascular Disease). Circulation 2012;
125:395.
24. Ahmadi F, Zabihiyeganeh M, Abdollahi M. Coil embolization of persistent sciatic artery pseudoaneurysm
presenting as blue toe syndrome, a rare case. Indian J Surg 2013; 75:316.
25. Kim MG, Kim SJ, Oh J, et al. Blue toe syndrome treated with sympathectomy in a patient with acute renal
failure caused by cholesterol embolization. Kidney Res Clin Pract 2013; 32:186.
26. Pulli R, Dorigo W, Troisi N, et al. Surgical management of popliteal artery aneurysms: which factors affect
outcomes? J Vasc Surg 2006; 43:481.
27. Serrano Hernando FJ, Martínez López I, Hernández Mateo MM, et al. Comparison of popliteal artery
aneurysm therapies. J Vasc Surg 2015; 61:655.
28. Nelson WW, Wang L, Baser O, et al. Out-of-range INR values and outcomes among new warfarin patients
with non-valvular atrial fibrillation. Int J Clin Pharm 2015; 37:53.
29. Tuveson V, Löfdahl HE, Hultgren R. Patients with abdominal aortic aneurysm have a high prevalence of
popliteal artery aneurysms. Vasc Med 2016; 21:369.
30. Dent TL, Lindenauer SM, Ernst CB, Fry WJ. Multiple arteriosclerotic arterial aneurysms. Arch Surg 1972;
105:338.
31. Suggested standards for reports dealing with lower extremity ischemia. Prepared by the Ad Hoc Committee
on Reporting Standards, Society for Vascular Surgery/North American Chapter, International Society for
Cardiovascular Surgery. J Vasc Surg 1986; 4:80.
32. Alonso-Coello P, Bellmunt S, McGorrian C, 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; 141:e669S.
33. Blaisdell FW, Steele M, Allen RE. Management of acute lower extremity arterial ischemia due to embolism
and thrombosis. Surgery 1978; 84:822.
34. Ouriel K, Veith FJ, Sasahara AA. A comparison of recombinant urokinase with vascular surgery as initial
treatment for acute arterial occlusion of the legs. Thrombolysis or Peripheral Arterial Surgery (TOPAS)
Investigators. N Engl J Med 1998; 338:1105.
35. Results of a prospective randomized trial evaluating surgery versus thrombolysis for ischemia of the lower
extremity. The STILE trial. Ann Surg 1994; 220:251.
36. Hirsch AT, Haskal ZJ, Hertzer NR, et al. ACC/AHA 2005 Practice Guidelines for the management of patients
with peripheral arterial disease (lower extremity, renal, mesenteric, and abdominal aortic): a collaborative
report from the American Association for Vascular Surgery/Society for Vascular Surgery, Society for
Cardiovascular Angiography and Interventions, Society for Vascular Medicine and Biology, Society of
Interventional Radiology, and the ACC/AHA Task Force on Practice Guidelines (Writing Committee to
Develop Guidelines for the Management of Patients With Peripheral Arterial Disease): endorsed by the
American Association of Cardiovascular and Pulmonary Rehabilitation; National Heart, Lung, and Blood
Institute; Society for Vascular Nursing; TransAtlantic Inter-Society Consensus; and Vascular Disease
Foundation. Circulation 2006; 113:e463.
37. Huettl EA, Soulen MC. Thrombolysis of lower extremity embolic occlusions: a study of the results of the
STAR Registry. Radiology 1995; 197:141.
38. Berridge DC, Kessel DO, Robertson I. Surgery versus thrombolysis for initial management of acute limb
ischaemia. Cochrane Database Syst Rev 2013; :CD002784.
39. Kessel DO, Berridge DC, Robertson I. Infusion techniques for peripheral arterial thrombolysis. Cochrane
Database Syst Rev 2004; :CD000985.
40. Robertson I, Kessel DO, Berridge DC. Fibrinolytic agents for peripheral arterial occlusion. Cochrane
Database Syst Rev 2013; :CD001099.
41. Berridge DC, Gregson RH, Hopkinson BR, Makin GS. Randomized trial of intra-arterial recombinant tissue
plasminogen activator, intravenous recombinant tissue plasminogen activator and intra-arterial streptokinase
in peripheral arterial thrombolysis. Br J Surg 1991; 78:988.
42. Mahler F, Schneider E, Hess H, Steering Committe, Study on Local Thrombolysis. Recombinant tissue
plasminogen activator versus urokinase for local thrombolysis of femoropopliteal occlusions: a prospective,
randomized multicenter trial. J Endovasc Ther 2001; 8:638.
43. Meyerovitz MF, Goldhaber SZ, Reagan K, et al. Recombinant tissue-type plasminogen activator versus
urokinase in peripheral arterial and graft occlusions: a randomized trial. Radiology 1990; 175:75.
44. Schweizer J, Altmann E, Stösslein F, et al. Comparison of tissue plasminogen activator and urokinase in the
local infiltration thrombolysis of peripheral arterial occlusions. Eur J Radiol 1996; 22:129.
45. Ouriel K, Kandarpa K, Schuerr DM, et al. Prourokinase versus urokinase for recanalization of peripheral
occlusions, safety and efficacy: the PURPOSE trial. J Vasc Interv Radiol 1999; 10:1083.
46. Matosevic B, Knoflach M, Werner P, et al. Fibrinogen degradation coagulopathy and bleeding complications
after stroke thrombolysis. Neurology 2013; 80:1216.
47. Lee K, Istl A, Dubois L, et al. Fibrinogen Level and Bleeding Risk During Catheter-Directed Thrombolysis
Using Tissue Plasminogen Activator. Vasc Endovascular Surg 2015; 49:175.
48. Schrijver AM, van Leersum M, Fioole B, et al. Dutch randomized trial comparing standard catheter-directed
thrombolysis and ultrasound-accelerated thrombolysis for arterial thromboembolic infrainguinal disease
(DUET). J Endovasc Ther 2015; 22:87.
49. Leung DA, Blitz LR, Nelson T, et al. Rheolytic Pharmacomechanical Thrombectomy for the Management of
Acute Limb Ischemia: Results From the PEARL Registry. J Endovasc Ther 2015; 22:546.
50. Gandini R, Merolla S, Chegai F, et al. Foot Embolization During Limb Salvage Procedures in Critical Limb
Ischemia Patients Successfully Managed With Mechanical Thromboaspiration: A Technical Note. J
Endovasc Ther 2015; 22:558.
51. McDonald JS, Brinjikji W, Rabinstein AA, et al. Conscious sedation versus general anaesthesia during
mechanical thrombectomy for stroke: a propensity score analysis. J Neurointerv Surg 2015; 7:789.
52. Verma H, Meda N, Vora S, et al. Contemporary management of symptomatic primary aortic mural thrombus.
J Vasc Surg 2014; 60:1524.
53. Fayad ZY, Semaan E, Fahoum B, et al. Aortic mural thrombus in the normal or minimally atherosclerotic
aorta. Ann Vasc Surg 2013; 27:282.
54. Kawahara T, Nishikawa M, Kawahara C, et al. Atorvastatin, etidronate, or both in patients at high risk for
atherosclerotic aortic plaques: a randomized, controlled trial. Circulation 2013; 127:2327.
55. Eliason JL, Wainess RM, Proctor MC, et al. A national and single institutional experience in the
contemporary treatment of acute lower extremity ischemia. Ann Surg 2003; 238:382.
56. Earnshaw JJ, Whitman B, Foy C. National Audit of Thrombolysis for Acute Leg Ischemia (NATALI): clinical
factors associated with early outcome. J Vasc Surg 2004; 39:1018.
57. Yeager RA, Moneta GL, Taylor LM Jr, et al. Surgical management of severe acute lower extremity ischemia.
J Vasc Surg 1992; 15:385.
58. Duval S, Keo HH, Oldenburg NC, et al. The impact of prolonged lower limb ischemia on amputation,
mortality, and functional status: the FRIENDS registry. Am Heart J 2014; 168:577.
59. Wolosker N, Kuzniec S, Gaudêncio A, et al. Arterial embolectomy in lower limbs. Sao Paulo Med J 1996;
114:1226.
60. Creager MA, Kaufman JA, Conte MS. Clinical practice. Acute limb ischemia. N Engl J Med 2012; 366:2198.
Topic 112120 Version 2.0
GRAPHICS
Classification of acute extremity ischemia
Viable Threatened Nonviable
Pain Mild Severe Variable
Capillary refill Intact Delayed Absent
Motor deficit None Partial Complete
Sensory deficit None Partial Complete
Arterial Doppler Audible Inaudible Inaudible
Venous Doppler Audible Audible Inaudible
Treatment Urgent work-up Emergency surgery Amputation
From Rutherford RB, Semin Vasc Surg 1992; 5:4.
Graphic 75112 Version 3.0
Femoral artery emboli on CT scan
A transverse CT scan through the pelvis (A) shows nonocclusive thrombus in the left superficial femoral and deep femoral
arteries (circle). (B) is a magnified view of (A) and shows nonocclusive thrombus in the SFA (arrowhead) and in the DFA
(arrow). (C) is a magnified sagittal reformat of the CT scan and shows the thrombus straddling the bifurcation (dashed
arrow) and extending into the SFA (arrowhead) and DFA (arrow).
CT: computed tomography; SFA: superficial femoral artery; DFA: deep femoral artery.
Graphic 98593 Version 2.0
Contributor Disclosures
Jonathan D Braun, MD Nothing to disclose John F Eidt, MD Nothing to disclose Joseph L Mills, Sr,
MD Grant/Research/Clinical Trial Support: Voyager Trial [Peripheral artery disease (Rivoxaraban)].
Consultant/Advisory Boards: Innomed [Peripheral artery disease (Femoral artery stent)]. Equity Ownership/Stock
Options: NangioTx [Peripheral artery disease (Self-assembling nanotubules)]. Other Financial Interest: Elsevier;
Rutherford [Vascular surgery (Rutherford and Comprehensive Vascular and Endovascular Surgery
textbooks)]. Kathryn A Collins, MD, PhD, FACS Nothing to disclose
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are
addressed by vetting through a multi-level review process, and through requirements for references to be
provided to support the content. Appropriately referenced content is required of all authors and must conform to
UpToDate standards of evidence.
Conflict of interest policy

Embolism To The Lower Extremities - UpToDate

Uploaded by

Document Information

Original Title

Copyright

Available Formats

Share this document

Share or Embed Document

Sharing Options

Did you find this document useful?

Is this content inappropriate?

Copyright:

Available Formats

Embolism To The Lower Extremities - UpToDate

Uploaded by

Copyright:

Available Formats

25/2/2018 Embolism to the lower extremities - UpToDate

Official reprint from UpToDate®

Author: Jonathan D Braun, MD

Anticoagulation — Systemic anticoagulation (intravenous heparin bolus followed by continuous intravenous

By severity of acute ischemia

● Lesion location and length

● Suitability of the patient for surgery

● Availability of autologous vein for bypass grafting

mortality, and major gastrointestinal bleeding, which is potentially life-threatening.

Our approach to lower extremity thrombolysis is as follows:

Subsequent diagnostic evaluation

Echocardiography — Echocardiography is an integral part of the subsequent evaluation to determine the

SUMMARY AND RECOMMENDATIONS

Use of UpToDate is subject to the Subscription and License Agreement.

Topic 112120 Version 2.0

Classification of acute extremity ischemia

Viable Threatened Nonviable

Pain Mild Severe Variable

Capillary refill Intact Delayed Absent

Motor deficit None Partial Complete

Sensory deficit None Partial Complete

Arterial Doppler Audible Inaudible Inaudible

Venous Doppler Audible Audible Inaudible

Treatment Urgent work-up Emergency surgery Amputation

From Rutherford RB, Semin Vasc Surg 1992; 5:4.

Graphic 75112 Version 3.0

Femoral artery emboli on CT scan

Graphic 98593 Version 2.0

Conflict of interest policy

You might also like