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Comorbidity
Cerebrovascular disease
15.4
11.5
11.6
NR
15.5
12.5
13.3
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
* The authors and editors gratefully acknowledge the contributions of the previous author, Sonny Tucker, MD, and Vicken
N. Pamoukian, MD, FACS, to the development and writing
of this chapter.
Financial disclosure information is located at the end of this chapter
before the references.
History
An early clinical evaluation is crucial for the diagnosis
and identification of the underlying etiology of the ALI.
A delay in treatment can result in limb loss, significant
morbidity, or death. Because ALI is a clinical diagnosis, a
complete history is essential (unless it is unobtainable
for some reason). Generally, the dominant symptoms are
related to pain (usually the first manifestation) or to loss
of motor or sensory function of the affected extremity. The
onset and duration of symptoms should be determined,
and the location and intensity of any changes should be
established. The pain of ALI is often not well localized and
is unaffected by gravity. An effort should be made to determine whether the likely cause is embolic or thrombotic: pain
of sudden onset suggests an embolic cause, whereas longstanding pain before the acute event suggests a thrombotic
cause [see Etiology of ALI, below].
It is imperative to ask whether the patient experienced
pain before the current ischemic episode and whether the
current episode is the first. The history should elicit the functional status of the affected extremity prior to the ischemic
event. It is also important to ask about previous vascular
procedures (including bypass or endovascular interventions), as well as previous or current cardiac disease (e.g.,
myocardial infarction [MI], atrial fibrillation, or valvular
disease), aneurysmal disease, or vasculitis. Finally, inquiries
should be made about previous atherosclerotic disease,
symptoms of claudication, rest pain, nonhealing ulcers,
current risk factors for atherosclerosis (e.g., hypertension,
smoking, diabetes, tobacco abuse, hyperlipidemia, and
stroke), and previous clotting episodes. The presence of
motor or sensory changes in the affected limb is very important in determining the urgency for revascularization.
Scientific American Surgery
DOI 10.2310/7800.2100
09/12
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Table 2
and pallor is typically one level below the point of occlusion on the arterial tree and should correlate with the
pulses or signals found. As always, baseline documentation should be done so that the progression or resolution
of the process can be tracked.
5. Paresthesia is an essential finding. The earliest sign of
tissue loss is the loss of light touch, two-point discrimination, vibratory perception, and proprioception, especially
in the first dorsal web space of the foot. Proprioception
and light touch sensation are lost early in ALI because
they are conducted by small myelinated neuron fibers,
whereas larger sensory nerves responsible for temperature, pain, and pressure are maintained unless ischemia
is prolonged.
6. Paralysis, if present, is an indication of advanced limbthreatening ischemia. The extent of paralysis must be
determined. The intrinsic muscles of the foot are affected
by ischemia of the vessels around the ankle. Dorsiflexion
and plantar flexion of the foot are functions of muscles
that rely on blood supplied by the popliteal and superficial femoral arteries. Loss of dorsiflexion and plantar
flexion indicates that blood flow is interrupted at a higher
level and signals that more tissue may be at risk. Once
motor function is lost, limb salvage is more challenging.
At this stage, skin mottling is more prominent and nonblanching, representing nonreversible ischemic changes.
Palpable Pulses
Femoral
Popliteal
Pedal
Aortoiliac segment
Location of Obstruction
Femoral segment
++
Possible Causes
Aortoiliac atherosclerosis; embolus to common iliac bifurcation
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Description/Prognosis
Doppler Signals
Sensory Loss
Muscle Weakness
Arterial
Venous
I. Viable
None
None
Audible
Audible
IIa. Marginally
threatened
None
(Often) inaudible
Audible
IIb. Immediately
threatened
Mild, moderate
(Usually) inaudible
Audible
III. Irreversible*
Profound, anesthetic
Profound, paralysis
(rigor)
Inaudible
Inaudible
*When presenting early, category IIb and category III may be difficult to differentiate.
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is a significant difference in blood pressure between the
proximal arterial tree and the distal extremity, which usually denotes an occlusive process. An ABI lower than 0.5
is seen in patients with critical ischemia. In these patients,
inspection of flow velocity waveform recording the pedal
arteries in conjunction with toe pressure measurement can
be used to determine the presence and degree of ischemia
if the severity of the ischemia is not limb threatening and
allows investigative studies. Next, segmental pressures are
obtained by placing cuffs at the ankle, below the knee, above
the knee, and on the thigh. Systolic blood pressures are
measured at each location, and any pressure drop greater
than 15 mm Hg is considered significant. When the venous
Doppler signal or hum is lost in addition to the arterial
Doppler signal, the ischemia is severe. However, the absence
of signals does not always signify an irreversibly threatened
limb.
Duplex ultrasonography Duplex scanning is a noninvasive imaging modality that can be valuable for localizing
the site of occlusion, especially in bypass grafts. In addition,
duplex ultrasonography has been useful in assessing the
patency of a single arterial segment (i.e., bypass graft or
stented superficial femoral artery). Unfortunately, it is not
always a practical option in acute circumstances, both
because the machine is often unavailable in the emergency
setting and because the results of scanning are highly
operator dependent. However, in specialized centers where
a duplex ultrasound machine is readily available and
personnel are experienced in its use, a quick look at the
suspected site may yield helpful information.10 In stenotic
regions, the velocities measured across the lesion are greatly
increased.11,12 Duplex ultrasonography can also be used to
assess plaque morphology, stenoses, dissections, and thrombi. In some centers, duplex ultrasound technology has obviated the need for lengthy arteriograms and has benefited
patients by reducing ischemia time.
Arteriography Arteriography remains the gold standard for diagnosis of ALI and may even be a primary tool
in its management. An important consideration is whether
the delay in performing arteriography can be tolerated in
patients with limb-threatening ischemia. In general, in
highly specialized centers, patients who require urgent
revascularization are evaluated with catheter-based arteriography in operating room angiosuites because it provides
detailed and accurate information regarding the etiology,
localization, and extent of the lesion as well as adequate
visualization of the distal arterial vascular tree without a
delay in therapy. In contrast, arteriography in formal
angiography suites should be reserved for patients with
viable limbs who can tolerate the additional delay before
revascularization and should not be performed if doing so
would keep a critically ischemic limb from receiving prompt
revascularization.
Arteriography should be performed from a site remote
from the point of concern. Thus, if lytic therapy is to be
administered, entry-site bleeding will be minimized. A
complete angiogram that includes the runoff vessels in the
foot should be performed to establish the baseline degree of
arterial disease and delineate the anatomy of the inflow and
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management
The major goal of therapy is reperfusion of the affected
extremity irrespective of underlying etiology. Until the middle of the 20th century, when revascularization techniques
were developed, amputation was the only treatment for
acute lower extremity ischemia. In the 1960s, the rates of
amputation and mortality flowing management of ALI were
as high as 50%.17 Today, however, the vascular surgeon
possesses an immense armamentarium for the treatment of
this condition, ranging from emergency bypass to embolectomy or thrombectomy to thrombolytic therapy. Clinical
outcome of the treatment is determined by the severity
of the presenting ischemia, the timing of its recognition,
and the treatment methods undertaken to reperfuse affected
extremity and to treat local and/or distal (systemic) reperfusion injury.
ALI constitutes a clinical emergency, and only a few emergency conditions carry the same potential for amputation,
morbidity, and mortality as ALI. Rapid restoration of flow
to the extremity substantially reduces morbidity and mortality. Accordingly, the clinician must be thoroughly familiar
with the therapeutic modalities available and capable of
making an appropriate choice among them without undue
delay. Whichever therapeutic modality is chosen for a given
patient, several primary measures should be undertaken
to protect and optimize the status of the extremity. Full,
systemic anticoagulation (usually with heparin unless contraindicated) should not be delayed. The extremity should
be placed in a dependent position, with care taken to avoid
extrinsic pressure on the limb. Temperature fluxes should
be minimized: cold induces vasoconstriction, and heat
increases tissue demand and metabolic and circulatory
demands. Finally, tissue oxygenation should be maximized
via transfusion, improvement in cardiac function, and restoration of intravascular volume. Dehydration is commonly
seen in these patients and is best treated with intravenous
administration of isotonic fluids (e.g., 0.9% NaCl). In a 1989
study, Berridge and colleagues demonstrated that the use of
continuous O2 inhalation during ALI may improve tissue
oxygenation before, during, and after definite treatment.18
Thus, patients with ALI should be given at least 24% O2 by
face mask to promote tissue oxygenation.
Proper and timely preoperative preparation is crucial for
preventing rapid deterioration of the patients condition.
As noted above, laboratory tests and radiologic studies are
necessary, and a cardiology evaluation is often helpful.
A central venous line should be inserted in patients with
cardiac impairment, and appropriate treatment of cardiac
arrhythmia and cardiac failure (or both) with antiarrhythmics and/or diuretics should not be delayed. Administration of fluids is beneficial to prevent nephrotoxicity due to
contrast administration. Special attention with fluid administration should be paid to patients with cardiac failure to
avoid volume overload. The ABI should be documented.
Abnormalities in blood counts, electrolyte concentrations,
and coagulation profiles should be corrected. The duration
of ischemia should be noted and any comorbid conditions
identified so that the examiner can determine the appropriate degree of monitoring required (e.g., arterial line or
pulmonary arterial catheter).
Anticoagulation
Heparin administration should be started as soon as the
diagnosis of ALI is entertained. Numerous studies have
shown that this measure decreases the morbidity and mortality associated with ALI and increases the limb salvage
rate. Heparin impedes the propagation of thrombus and,
in the instance of embolism, may help prevent additional
embolic events. Unfractionated heparin (5,000 IU) should
be administered intravenously immediately followed by
continuous heparin drip to maintain an activated partial
thromboplastin time (aPTT) ratio of more than 2.
Heparin acts at multiple sites in the normal coagulation
system, inhibiting reactions that lead to the clotting of blood
and the formation of fibrin clots both in vitro and in vivo.
Small amounts of heparin bind to the antithrombin III (AT),
causing conformational changes that result in profound AT
activation. The activated AT inhibits thrombosis by inactivating thrombin and several other proteins in the coagulation cascade, especially factor Xa.19 Once active thrombosis
has developed, heparin can inhibit further coagulation by
inactivating thrombin and preventing the conversion of
fibrinogen to fibrin. Heparin also prevents the formation
of a stable fibrin clot by inhibiting the activation of fibrinstabilizing factor.1921
Heparin does not have fibrinolytic activity and therefore
does not lyse existing clots. Heparin therapy can be complicated by heparin-induced thrombocytopenia (HIT), which
has a reported incidence of 0 to 30%.22 In HIT, the immune
system develops antibodies (mostly of IgG class) against
molecular complex heparin-platelet factor 4 (PF4).23 PF4 is
a cytokine released from activated platelets during platelet
aggregation phase of the coagulation process. Binding of
heparin to PF4 is required to trigger immune reaction and
subsequently induce HIT because heparin molecules alone
are not immunogenic. If the thrombocyte count falls below
100,000/L or if recurrent thrombosis develops, heparin
should be discontinued.24,25 Patients receiving heparin may
experience new thrombus formation, either early or late, in
association with this thrombocytopenic phenomenon as a
consequence of irreversible heparin-induced platelet aggregation (the so-called white clot syndrome). This process may
lead to severe thromboembolic complications, including
skin necrosis, gangrene of the extremities, MI, pulmonary
embolism, stroke, and, possibly, death.24,26,27 Accordingly,
if new thrombosis develops in association with thrombocytopenia, heparin should be promptly discontinued and a
suitable alternative (e.g., a direct thrombin inhibitor) used
instead. Periodic platelet counts, hematocrits, and tests for
fecal occult blood are recommended during the entire course
of heparin therapy, regardless of the route of administration.
As noted above, the anticoagulation effect should be monitored with the aPTT. Bleeding time is usually unaffected by
heparin. Clotting time is prolonged by full therapeutic doses
of heparin but, in most cases, is not measurably affected by
low doses.
Thrombolytic Therapy
The use of thrombolytic agents to treat chronic and
acute arterial insufficiency dates back to the 1970s, when
it was popularized by Dotter.28 All currently available
thrombolytic agents are plasminogen activators. They are
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characterized by different degrees of specificity directed at
the cleavage of a peptide bond in the plasminogen, converting it to plasmin. Plasmin subsequently cleaves fibrin
polymer, leading to thrombus dissolution. Thrombolytic
agents that are most frequently indicated for the treatment
of ALI include streptokinase (SK), urokinase (UK), and
tissue plasminogen activator (t-PA).
SK is derived from Streptococcus bacteria and was the first
thrombolytic agent to be described in 1933 by Tillett and
Garner.29 SK differs from other thrombolytic agents with
respect to the plasminogen-binding mechanism. To convert
plasminogen to plasmin, SK first needs to form a molecular
complex with plasminogen. This SK-plasminogen macromolecular complex activates a second plasminogen molecule to
form an active plasmin that will initiate subsequent dissolution of thrombus. It must be noted that SK is characterized
with a significant immunogenic potential. Patients with
exposure to SK have preformed SK antibodies that inactivate newly administered SK, making dosing of the SK a
challenge. Some authors suggest measurement of SK antibody titer prior to beginning SK therapy and titer-based
dosing of the SK.30
UK directly activates plasminogen to plasmin. The fibrinolytic potential of urine was first recognized and described
by Macfarlane and Pinot in 1947,31 but the active fibrinolytic
molecule was not extracted and named urokinase until
1952.32 Today, most UK is extracted from human neonatal
kidney cells or derived from recombinant techniques using
the murine hybridoma cell line (recombinant urokinase
[r-UK]).
t-PA is a fibrinolytic agent produced by endothelial cells.
It exhibits very high fibrin specificity and in plasma is
associated with little plasminogen activation. t-PA and plasminogen bind to fibrin at the site of the thrombus, leading
to a conformational change in both molecules that induces
the conversion of plasminogen to plasmin and dissolution
of the thrombus. Alteplase and duteplase are single- and
double-chain recombinant tissue plasminogen activator
(rt-PA), respectively. As mentioned above, they are clot
selective because they are more active on fibrin-bound
plasminogen than on free plasma fibrinogen. Tenecteplase
is a relatively novel molecule that is characterized with a
longer half-life and greater fibrin specificity and thus can
be administered as a single bolus rather than as continuous
infusion.
Systemic fibrinolytic therapy has not proved effective and
consequently has been supplanted by intra-arterial (catheterdirected) thrombolysis, which yields significantly better
results. The superiority of catheter-directed thrombolytic
therapy over systemic therapy was objectively established
by Berridge and colleagues in a randomized trial that
included 60 patients with acute or subacute arterial thrombosis treated with three different thrombolytic regimens:
intravenous rt-PA, intra-arterial rt-PA, or intra-arterial SK.33
Limb salvage at the 1-month follow-up was documented
in 80%, 60%, and 45% of patients treated with intra-arterial
rt-PA, SK, and intravenous rt-PA, respectively. Hemorrhagic
complications were documented in only one patient who
received intra-arterial rt-PA following catheter perforation.
This was significantly lower when compared with six and
13 patients with hemorrhagic complications in patients
Table 4
Contraindications to Thrombolytic
Therapy165
Absolute contraindications
Established cerebrovascular event (including TIAs) within past
2 mo
Active bleeding diathesis
GI bleeding within past 10 days
Neurosurgery (intracranial, spinal) within past 3 mo
Intracranial trauma within past 3 mo
Major relative contraindications
Cardiopulmonary resuscitation within past 10 days
Major nonvascular surgery or trauma within past 10 days
Uncontrolled hypertension: systolic BP > 180 mm Hg, diastolic
BP 110 mm Hg
Puncture of noncompressible vessel
Intracranial tumor
Recent eye surgery
Minor relative contraindications
Hepatic failure, particularly in patients with coagulopathy
Bacterial endocarditis
Pregnancy
Diabetic hemorrhagic retinopathy
BP = blood pressure; GI = gastrointestinal; TIA = transient ischemic attack.
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was relatively low when cardiopulmonary complications
did not occur. The cumulative limb salvage rate was similar
in the two groups (82% at 12 months). Total hospital charges
were comparable as well, which suggests that at the initial
treatment, thrombolytic therapy is as costly as surgery. The
median in-hospital cost of treatment in the thrombolytic and
open surgery groups was $15,672 and $12,253, respectively.
Major bleeding was encountered in 11% of patients.
STILE (Surgery versus Thrombolysis for the Ischemic Lower
Extremity) trial This randomized, controlled, multicenter
trial was designed to evaluate catheter-directed thrombolysis versus surgery and to determine differences in outcomes
between rt-PA and UK in 393 patients.35 In this study, both
patients with chronic limb ischemia and patients with
ALI were included. Patients were not stratified based on the
duration of ischemia during randomization. The Data and
Safety Monitoring Committee stopped the trial early
because of an increase in the number of patients with ongoing ischemia in the thrombolysis groups. An ad hoc committee later determined that the reason for this increase was the
inclusion of chronically symptomatic patients in the study.
In any case, the study clearly demonstrated that patients
with less than 14 days of ischemia had a lower amputation
rate when treated with thrombolysis (11% versus 30%) but
that patients with more than 14 days of ischemia had a
lower amputation rate when treated with surgery. A subgroup analysis showed a significantly shorter time of lysis
in patients randomized to rt-PA when compared with
patients randomized to UK (8 hours versus 16 hours;
p = .01). Additional analysis did not show any difference in
safety and efficacy between rt-PA and UK.
TOPAS (Thrombolysis Or Peripheral Arterial Surgery) trial
The preliminary dose-ranging TOPAS trial compared surgery with r-UK thrombolysis in 213 patients with ischemic
symptoms of less than 14 days duration.36 At the end of 1
year, the amputation rates in the two groups were similar.
Bleeding complications were seen only in patients undergoing thrombolysis, four of whom (2.1%) had intracranial
hemorrhage. When additional end points were considered,
the thrombolysis group was found to require significantly
fewer major interventions at the time of discharge and at
12 months. Patients randomized to catheter-directed r-UK
received three different dosage regimens (2,000, 4,000,
or 6,000 IU/min for 4 hours followed by an infusion of
2,000 IU/min for additional 44 hours, for a maximum of
48 hours). The regimen of 4,000 IU/min seemed to be the
most effective when efficacy and safety were considered.
Complete lysis (defined as > 95% thrombus extraction) was
documented in 71% of patients randomized to a 4,000 IU/min
dosage regimen (mean infusion time 23 hours). In contrast,
complete lysis was achieved in 67% of patients who received
the 2,000 IU/min and 60% of patients who received the
6,000 IU/min dosage regimen. Hemorrhagic complications
were documented in 2%, 13%, and 16% of patients who
received the 4,000, 2,000, and 6,000 IU/min regimen, respectively. The 1-year mortality rates were not significantly
different between the surgical group and the 4,000 IU/min
r-UK group (14% versus 16%). Similarly, there was no significant difference in amputation-free survival rates between
these two groups (75% versus 65%).
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no apparent differences in 30-day clinical success, save that
the end point of 95% clot lysis occurred more rapidly in the
rt-PA group (p = .04). The authors also documented major
bleeding complications in five rt-PA patients and two UK
patients. As in the previous study, the authors of this trial
compared high doses of rt-PA (10 mg bolus followed by
5 mg/h for 24 hours) with relatively low doses of UK
(60,000 IU bolus followed by 240,000 IU/h for 2 hours, followed by 120,000 IU/h for 2 hours, followed by 60,000 IU/h
for 20 hours). Given widely disparate dosing regimens
between rt-PA and UK, the data from these trials must be
interpreted with caution because the data from several other
studies showed that bolus followed with high-dose infusion
of rt-PA reduced lysis time and increased the incidence of
hemorrhage compared with lower doses.41,42
Current recommendations Current data suggest, but do
not prove, that thrombolytic therapy is effective as initial
therapy for patients with acute arterial and graft occlusions
and no sensorimotor deficits. Such an approach, however,
is not suitable for patients with common femoral artery
emboli, which should be treated surgically, and there are
certain patients with sensorimotor deficits (e.g., those
without any runoff) for whom the potential benefits of
thrombolysis outweigh the risks of delay.
At present, acute thrombotic arterial occlusion in an
occluded bypass graft is the area where intra-arterial fibrinolysis may be most useful, permitting better planning of
the subsequent operation and resulting in a less extensive
procedure. Such therapy, however, does not necessarily
yield improvements in major long-term end points. It is
important to remember that thrombosis of femoropopliteal
or similar bypasses is related to early or late surgical stenosis
and atherosclerosis and that restoring flow usually does not
suffice to ensure continued patency.
Logistics of thrombolysis In patients with mild or no
sensory deficits, angiography is performed first. Depending
on the location of the obstruction, the type of clot present,
and the level of patient risk, the patient may be offered
thrombolysis as initial therapy.
In our practice, the patient is taken from the emergency
department to the angiography suite. Informed consent
is obtained for diagnostic and therapeutic angiography
(including the use of stents, balloon angioplasty, stent grafts,
and thrombolysis) and for the performance of an emergency
surgical procedure. A discussion is undertaken with the
patient to outline the course of treatment and to explain that
indwelling catheters may have to be placed and that a stay
in the intensive care unit may be required.
Access to the arterial system is gained via a single-wall
puncture technique; the risk of posterior wall bleeding
associated with a double-wall technique is thereby avoided.
Access should be obtained from a site as remote from the
intervention site as possible. Generally, this is accomplished
by starting from the contralateral groin of the target artery
and going up and over the aortic bifurcation and then back
to the ipsilateral artery. By removing the puncture site from
the side of catheter-directed thrombolysis, the incidence of
bleeding and formation of hematomas or pseudoaneurysms
is reduced.
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complications in 6 to 20% of patients. Therefore, the end
points of thrombolytic therapy are (1) resolution and
reconstitution of flow through the obstruction, (2) absence
of change in the occlusion of the vessel on angiography,
and (3) bleeding complications. If it is determined that
thrombolysis is not progressing, it should be abandoned and
surgical intervention undertaken.
Thrombectomy
Percutaneous aspiration thrombectomy This technique
uses a large-lumen, thin-walled catheter and a large syringe
(50 mL) to remove an embolus or thrombus from a vascular
conduit, whether native vessel or graft. The catheter is
placed as previously described [see Logistics of Thrombolysis, above] and is parked immediately adjacent to the clot.
Aspiration of the clot with the syringe is then attempted.
If the clot is new, success is likely, but an old clot that is
organized will not be as amenable to removal. Percutaneous
aspiration thrombectomy can be used as a stand-alone
procedure or together with thrombolysis (to reduce time of
procedure and to reduce dosage of the fibrinolytic agent).
However, it is most effective as an adjunct to catheterdirected thrombolysis.44,45
Percutaneous mechanical thrombectomy Based on their
mechanism of action, percutaneous thrombectomy devices
can be classified in several groups. Hydrodynamic (rheolytic) percutaneous mechanical thrombectomy (PMT) functions on the basis of a hydrodynamic circulation. The basic
concept is that a hydrodynamic vortex is created around the
tip of the PMT catheter. Thrombectomy is accomplished
with the introduction of a pressurized saline jet stream
through the directed orifices in the distal tip of the catheter.
The jets generate a localized low-pressure zone via the
Bernoulli effect, which fragments thrombus via a negative
pressure zone. The saline and the fragmented thrombus are
then sucked back into the exhaust lumen of the catheter
and out of the body for disposal. This technique has proved
beneficial when used in appropriate settings and properly
selected patients. Its efficacy depends on the age of the clot.
Fresh thrombus is readily treated with PMT, but older clots
are much less amenable to this technique and may have to
be treated with an adjunctive catheter-based modality (e.g.,
angioplasty, intra-arterial thrombolysis, or atherectomy).4649
Several clinical trials have validated the efficacy and safety
of PMT devices. Data from a multicenter trial involving 21
patients demonstrated that hydrodynamic PMT (AngioJet,
Possis Medical, Minneapolis, MN) can be effective, especially in high-risk patients who are unfit for open surgery
and in patients with a contraindication to thrombolytic therapy: 57% of patients in this trial had severe comorbidities
and 52% of patients had contraindication to thrombolytic
therapy.50 All patients presented to the hospital within 2
weeks of the development of limb-threatening ischemia.
Limb salvage was achieved in 95% of cases, and 6-month
limb salvage was documented in 89% of cases. Data from
several other studies showed that PMT treatment required
adjunctive thrombolytic therapy for complete thrombus
removal.5154 Dr. Ouriels group reported experience with
hydrodynamic PMT and adjunctive pharmacologic thrombolysis in 86 patients with acute (n = 65) and subacute
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occlusion.63 The mean length of the occlusion was 36.0
7.5 cm and was treated with mechanical thrombus fragmentation for 24.0 10.7 minutes. Data from this study showed
an average thrombus removal rate of 95% and no side
effects. In 2012, Daly and colleagues suggested that placing
a filter basket distal to the Trellis catheter should be considered in patients with a large clot burden and subsequently
anticipated incomplete thrombus dissolution to prevent
distal embolization after distal balloon deflation.64
In summary, the development and technical refinements
of percutaneous thrombectomy devices have provided several promising treatment modalities that have the potential
to reduce the morbidity and mortality associated with ALI.
Due to the lack of level 1 data from randomized, prospective, controlled clinical trials, regarding the superiority of
one currently available percutaneous thrombectomy device
over another, the decision regarding which treatment
modality is most appropriate is based on the individual
patients characteristics and on the judgment of an experienced vascular surgeon.
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this is most easily accomplished in the antecubital fossa.
A curvilinear (lazy S) incision is made that starts on the
medial aspect of the upper arm, extends transversely across
the antecubital fossa, and ends halfway down the middle of
the lower arm. The brachial artery is exposed deep to the
bicipital aponeurosis, and a transverse arteriotomy is made
proximal to the bifurcation. This incision allows control
of the brachial, radial, and ulnar arteries. A 3 French embolectomy catheter is typically used here. If the pulse is not
present, the catheter should be passed proximally into the
brachial artery first. This is followed by selective embolectomy down the radial and ulnar arteries. Regardless of the
clot location, several passes of the balloon catheter are made
in each vessel until no more clot can be retrieved and there
is brisk back-bleeding from the vessel. A completion angiogram is obtained to visualize the distal vessels and elucidate
any anatomic pathology in the native vessels. If distal clot is
still present after the completion angiogram, intra-arterial
thrombolysis can be employed for a brief period to soften
the clot. The multiple sidehole catheter is advanced distally
to the location of the clot, the guide wire is passed through
the lesion, and the catheter is passed over the wire into
the substance of the clot. Infusion of the lytic agent is then
started. Repeat angiograms indicate whether the clot has
dissolved or is still present. If the clot is still apparent, repeat
embolectomy is attempted. If completion arteriography
shows successful embolectomy, the arteriotomy is closed
using interrupted 6-0 polypropylene suture.
If thrombosis rather than embolism is suspected, an
underlying lesion must be sought. Failure to establish inflow
via brachial embolectomy should prompt angiographic
evaluation of the axillary and subclavian arteries for aneurysm or occlusion. A proximal occlusion of the subclavian
artery is most expeditiously treated by stenting via the
exposed brachial artery when possible. However, axillary
and subclavian aneurysms are often associated with chronic
compression by a cervical rib in the thoracic outlet and
should be repaired through a separate incision.
Several technical points of balloon embolectomy deserve
emphasis. In performing the embolectomy, attention should
be paid to the tactile sensations felt as the inflated balloon is
withdrawn. Such sensations give the operator a sense of the
disease process. When several deflations are needed and the
withdrawal path of the balloon feels rough, a long-standing
process (e.g., an atherosclerotic calcified vessel with anatomic discrepancies) is likely. If there appears to be no
residual clot after embolectomy, then a completion angiogram is sufficient and the artery can be closed primarily. In
cases where the source of embolus is not identified or the
source cannot be corrected, the patient should be considered
for long-term anticoagulation. Heparin is continued into the
postoperative period, and the patient is eventually switched
to warfarin, which is continued for at least 6 months postoperatively. Data from several studies have demonstrated that
postoperative anticoagulation treatment reduces the risk of
recurrent thromboembolic events, especially in patients with
atrial fibrillation.6769 In a study that included 287 patients
with acute thromboembolic lower extremity ischemia,
Campbell and colleagues demonstrated that recurrent limb
ischemia and amputation were less common in patients who
received warfarin anticoagulation initially than in patients
Cost Considerations
A retrospective study published in 1995 compared thrombolysis with surgical thrombectomy as first-line therapy for
ALI.71 Only the costs of the initial admission were documented. The average charge for the two treatments ranged
from $20,000 to $26,000. Economic analysis confirmed that
the total economic impact of thrombolysis approximated
that of initial operative therapy. The conclusion of the study
was that there was no difference between an endovascular
approach and an operative approach with respect to cost. A
more recent study by Korn and colleagues retrospectively
analyzed 100 consecutive cases of acute and subacute lower
extremity ischemia in 85 patients treated with UK thrombolysis.72 The authors documented that the cost of initial
hospitalization for thrombolysis approximated $18,500 per
patient and concluded that thrombolysis can be as or more
costly than traditional surgery. These data show that when
acute treatment of ALI is being considered, cost should not
be factored into the decision-making process. The choice of
treatment strategy should be based on the availability of the
equipment, the experience of the surgeon, and the evidence
regarding the safety and efficacy of the procedure for each
case.
Atheromatous Embolization
Atheroembolism is a condition in which microscopic
cholesterol-laden debris travels from proximal arteries to
reach the most distal arterial segments, typically in the skin
of the lower extremities.7376 This debris usually originates
from unstable plaque found at inflection points in the
arterial tree, especially in the aorta.77,78 It may also originate
from aneurysmal sacs either in the aorta or in the peripheral
arteries. The atheromatous embolization can also be a manifestation of a multisystem disorder associated with high
mortality and morbidity rates. Although it was first reported
more than a century ago (in 1862) by German pathologist
Panum,79 this disorder still remains poorly recognized
and underdiagnosed by many practitioners. Much of the
confusion can be attributed to the numerous clinical manifestations that are apparent across many different medical
specialties, making the differential diagnosis broad and the
diagnosis challenging. The confusion has been compounded
by the inexact nomenclature that permeates the medical
literature. Unfortunately, archaic terms such as blue toe
syndrome, purple toe syndrome, cholesterol embolism,
vasc
cholesterol crystal embolization, multiple cholesterol
emboli syndrome, or the pseudovasculitic syndrome are
still frequently used by some specialists.8085 Based on data
from autopsy studies, the estimated incidence of atheromatous embolization is relatively low and ranges from 0.15
to 3.4%.8688 However, data from several clinical studies
demonstrated that the incidence is much higher in older
patients with atherosclerosis, especially in patients with
known atherosclerosis who underwent arteriography or
cardiac and/or vascular surgical procedures.8993 Thurlbeck
and Castleman found that 17 of 22 patients (77.3%) who died
after open abdominal aortic aneurysm repair had evidence
of atheromatous embolization on a postmortem examination.93
clinical evaluation
A high index of suspicion for atheromatous embolization
should be present in all patients with unexplained MI,
stroke, acute renal failure, mesenteric ischemia, cutaneous
ischemic manifestations, or limb ischemia, especially following vascular or cardiac surgery, as well as angiographic or
endovascular procedures. Patients with atheroembolism of
the extremity usually present with focal toe ischemia, the
so-called blue toe syndrome, in conjunction with palpable
pulses in the distal extremity [see Figure 1]. Acute pain of
sudden onset is typically noted in the affected area. The pain
can often establish the exact timing of embolization. Cyanosis is present either on the toe or over a more extensive area
if the atheroemboli were circulated throughout the extremity.94 When both lower extremities are involved, the source
of the microemboli is commonly found above the aortic
bifurcation. Unilateral manifestation implies that atheroemboli most likely originated distal to the bifurcation. The
descending thoracic, suprarenal, and infrarenal aortas are
common sources of atheromatous embolization to the lower
extremities and to the visceral and renal arteries.
A complete vascular examination should be performed
and pulses documented. Although a patent arterial tree is
the rule, emboli that are sufficiently small may travel through
collateral channels. Palpation should be done to detect
any aneurysmal disease. A massive proximal atheroembolic
event may affect the entire abdominal wall and both extremities, giving the appearance of livedo reticularis.
Livedo reticularis is the most common (present in > 50%
of all patients) cutaneous manifestation of atheromatous
embolization.95 It must be noted that livedo reticularis is
not pathognomonic for atheromatous embolization as it can
be seen in patients with several other disorders, including
antiphospholipid antibody syndrome, systemic lupus
erythematosus, cryoglobulinemia, and macroglobulinemia.
It can also be seen in healthy young women96 and in patients
taking steroids. Livedo reticularis results from delayed
venous drainage of the skin secondary to embolic obstruction of capillaries, venules, and small arteries. It frequently
involves the lateral aspect of the toes, feet, soles, and
calves.97.98 Less frequently, it is seen on the buttocks or trunk.
As the source of the atheroemboli ascends in the arterial
tree, more vital organs (e.g., the kidneys and the gastrointestinal tract) may be damaged. Manipulation of an intraarterial catheter, surgical manipulation of the arterial tree,
or clamping in an area of disease can also result in plaque
vasc
Disease is mild
Disease is severe
Assess level of operative risk.
Patient is good
operative candidate
Atheroemboli recur
vasc
Treatment
Upper extremity
Aorta
Iliac artery
Popliteal artery
Hypoperfusion-Reperfusion State
The severity of ALI symptoms is directly related to
the duration of ischemia and the effects of reperfusion.
Hypoperfusion (ischemia)-reperfusion injury occurs in the
settings of reversible diminished or absent blood supply to
a tissue followed by the return of oxygenated blood flow.
Regardless of the cause of the ischemia, hypoperfusion leads
to ischemic infarcts via various mechanisms. In addition to
diminished delivery of O2 to tissues during the hypoperfusion state, three major physiologic events occur. First, movement of blood through the vessels is slowed. As a result,
the thrombus is able to grow and propagate, occluding
collateral vessels and further decreasing blood flow. Second,
ischemic cells swell and accumulate water. The resulting
increase in pressure within a fixed space between fascial
structures creates an elevation of pressure within the
compartment that further decreases flow and exacerbates
the injury. Third, the precapillary arteriolar cells swell,
narrowing the lumina of distal arterioles, capillaries, and
venules and again reducing blood flow. As a result, biotoxic
products of anaerobic metabolism accumulate within the
ischemic tissues distal to the occlusion with resultant
tissue edema, which, if left uncorrected, may progress to
compartment syndrome.
vasc
Thrombosis
Native artery thrombosis Native artery thrombosis
represents the end stage of a long-standing disease process
of atheromatous plaque formation at specific sites in the
arterial tree. Atherosclerotic plaque begins with the slow
deposition of lipids in the intima of the vessel and continues
with the deposition of calcium, resulting in an atherosclerotic core.118 This core has a highly thrombogenic surface
that encourages platelet aggregation, which results in disturbances of blood flow.119 The flow disturbances create
a zone of separation, stagnation, turbulence, and distorted
velocity vectors. These factors cause low shear rates at
inflection points in the arterial tree, and endothelial damage
ensues. The endothelial damage activates a repair process
that results in intimal hyperplasia, which induces further
attraction of platelets and eventual thrombus formation. The
process by which occlusion develops from an atheromatous
plaque may be more important than the degree of stenosis
within the lumen. This would explain why acute occlusion
occurs in vessels with minimal (< 50%) stenosis: atheromatous plaque not only reduces blood flow but also represents
an irregular surface within the arterial lumen that is prone
to thrombus formation. The contact between the atherosclerotic core and the bloodstream leads to platelet aggregation
and hence to eventual thrombosis. Occasionally, thrombosis
of a native artery occurs without any obvious underlying
pathologic condition. In such cases, a thorough investigation
should be initiated into other causes of thrombosis (e.g.,
hypovolemia, malignancy, hypercoagulable states, and
blood dyscrasias).
Bypass graft thrombosis Aggressive management of
patients with peripheral arterial disease has led to an
increase in bypass graft procedures. As a result, graft
thrombosis has now become the leading cause of acute
lower extremity ischemia. Some patients have graft occlusions without any definable underlying lesion, but most
have a definable lesion. In patients with native conduits,
intimal hyperplasia leading to the narrowing of the vein
graft and valvular hyperplasia are the two leading causes of
graft failure.120 The situation is different in the prosthetic
Embolism
Thrombosis
Identifiable source
Frequently detected
None
Claudication
Rare
Frequent
Physical findings
Angiographic findings
vasc
graft population where the graft failure is attributed to
one of the following: thrombogenicity of the graft material,
kinking of the graft from crossing joints, anastomotic intimal
hyperplasia, and progression of atherosclerotic disease
proximal or distal to the graft. Among these, anastomotic
irregularities probably represent the most common cause
of graft thrombosis.111 Data from the most recent studies
suggest that geometric remodeling of the native conduits
and decreased vein graft adaptation to the arterial environment are caused by mediators of inflammation.121 Fortunately,
diminished blood flow in the graft can be detected before
graft thrombosis occurs. Establishing a policy of routine
ultrasound surveillance after bypass procedure and prompt
revision of an identified vein graft stenosis is important; if
an advanced lesion is not corrected, graft thrombosis leads
to acute ischemic events with the possibility of limb loss.
Advanced vein graft stenosis should be repaired using open
surgical or endovascular techniques prior to occlusion.
Most short lesions (< 2 cm in length) can be corrected by
percutaneous transluminal angioplasty (PTA). Longer or
more complex lesions should be treated with vein patch
angioplasty or a short bypass.
Embolism
Peripheral arterial embolization results in the sudden
onset of severe ischemia as the absence of collateral vessels
compounds the reduction in flow to the extremity. The heart
is by far the most common source of spontaneous arterial
emboli, accounting for about 90% of cases. The incidence of
embolic phenomena has increased as the population has
aged, with a corresponding increase in the number of
patients with significant cardiac disease. Over the past
25 years, the incidence of embolization has doubled, from 23
to 51 per 100,000 admissions. Atherosclerotic heart disease
currently accounts for as many as 60 to 70% of all cases of
arterial embolism.122,123 Atrial fibrillation and rheumatic valvular disease account for the remaining 30 to 40%.113,124 With
respect to peripheral emboli in particular, atrial fibrillation
is currently responsible for 65 to 75% of cases. Transthoracic
echocardiography is insensitive in visualizing atrial clots,
especially in the left atrial appendage, which is the most
common cardiac source of emboli.125,126 Transesophageal
echocardiography, however, offers significantly better imaging of all four chambers and thus is considered the superior
diagnostic test for suspected cardiac embolic sources.127130
MI is the next most important cause of peripheral emboli.
One study from 1986 evaluated 400 patients and found that
MI was a causative factor in 20%.115 A left ventricular wall
thrombus is often seen after an acute MI, with or without a
left ventricular wall aneurysm; however, only 5% ultimately
embolize and result in peripheral ischemia.131134 Other
studies suggest that day 3 to day 28 is the period during
which the risk of embolization is highest for an intracardiac
thrombus.135
Other cardiac sources of peripheral emboli include the
ring portions of prosthetic cardiac valves and biologic
xenovalves. Chronic anticoagulation is recommended for
prosthetic valves, but the biologic xenovalves do not require
anticoagulation.136,137 Cardiac tumors (e.g., atrial myxomas)
are rare sources of peripheral emboli.126 Cardiac vegetations
from bacterial or fungal endocarditis should be considered
vasc
Axillary
(4.5%)
Aorta
(9.1%)
Common
lliac
(13.6%)
Brachial
(9.1%)
External
lliac
(3.0%)
Radial
(1.2%)
Ulnar
(1.2%)
Common
Femoral
(34.0%)
Superficial
Femoral
(4.5%)
Popliteal
(14.2%)
Anterior
Tibial
(2.8%)
Figure 2
Posterior
Tibial
(2.8%)
vasc
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