Добавил:
Sekretar
kiopkiopkiop18@yandex.ru
t.me/Prokururor I Вовсе не секретарь, но почту проверяю
Опубликованный материал нарушает ваши авторские права? Сообщите нам.
Вуз:
Предмет:
Файл:Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_3860_Библиотеки_им_академика_М_И_Перельмана
.pdf
https://t.me/med1917
K.S. Rholl and K. M. SterlingPeripheralVascular Disease
https://t.me/med1917
6
■■■
Clinical and Noninvasive Evaluation
of Peripheral Vascular Disease
KENNETH S. RHOLL and KEITH M. STERLING
Evolution in technology surrounding vascular disease has
resulted in increased treatment options for persons afflicted with peripheral vascular disease (PVD). Decreased
morbidity andmortality associated with newer procedures
have led to broadening of the indications for the treatment of these patients. Additionally, recentinnovations in
vascular imaging have enhanced the ability to detect vascular disease using less invasive techniques. Despite these
advances, optimal care of the patient with PVD still requires a balanced approach between conservative therapy
and more invasive procedures. Maintaining this balance
necessitates an ongoing process of evaluation of the disease process andits effects on the patient. The importance
of the clinical evaluation cannot be overstated. In many
cases, the clinical presentation may be straightforward
and a tentative diagnosis made on the basis of a directed
history and physical examination. In others, however, the
diagnosis may be less certain. Objective data supplied by
the noninvasive vascular laboratory can be of great use in
evaluating patients with suspected PVD, not only documenting the presence of disease but also providing information about the location, severity, and etiology of the
disease process. Conversely, data supplied by the noninvasive vascular laboratory should be viewed in the context of
the clinical presentation. Only then can appropriate decisions regarding therapeutic options be made.
Evaluation of the patient with PVD requires an understanding of the pathophysiology and natural history of
the disease. PVD is a disease of the aging population. Its
frequency increases rapidly with age, from 3 to 5%
in patients under 60 years of age to more than 20% in
patients over 75 years of age.
their activity level with advancing age; therefore most
1–5
Many patients decrease
cases of PVD in the general population are not symptomatic and pose no threat to the patient. An estimated
four of five patients with demonstrable PVD are asympto-
3–4
matic.
clinical manifestations, intermittent claudication being
the most frequent presenting symptom. It is important to
realize that PVD generally runs a benign course: 75% of
patients will stabilize (60%) or improve (15%) their clinical status without intervention following their initial presentation.
progression. Amputation is infrequent: Only 5 to 6% of
patients progress to this point over a 10-year period.
Patients who smoke cigarettes and who have diabetes
have a greater risk. Long-term follow-up of these patients
reveals an amputation rate of 20% or greater.
regular exercise and risk-factor control, however, most
patients will demonstrate significant improvement.
study of patients undergoing a supervised exercise program established not only clinical improvement but also
evidence of significant metabolic improvement after 12
weeks.
The risk factors for PVD are well known: hypertension,
smoking, diabetes mellitus, abnormal cholesterol levels,
obesity, and a strong family history.
risk than women, although this difference is reduced with
advancing age. The presence of concomitant vascular disease in other organ systems cannot be ignored. Increased
morbidity and mortality among patients with intermittent
claudication are well documented.
of patients with claudication die within 10 years of their
presenting symptoms, and two thirds of these patients will
have experienced a major cardiovascular event. A review
of patients undergoing treatment for PVD reveals a mor-
Other patients with PVD present with varying
6
Fewer than 25% will have significant clinical
1,8
9
1,3–5
Men are at higher
1–3,5–6,8,13–17
One third
6–7
With
9–12
A
55
56
https://t.me/med1917
K. S. Rholl and K. M. Sterling
tality rate even higher than the general population with
claudication: 5-year mortality rates are 25 to 40% and
10-year rates, 50 to 75%.
1,3,5,8,13
The vast majority of these
deaths are secondary to atherosclerotic heart disease. In
one study of patients who underwent vascular surgery, all
14 patients with diabetes mellitus and coronary artery
disease died within 5 years.
18
Similarly, in a second study,
all patients with diabetes mellitus who had undergone
aortofemoral reconstruction died within 5 years of sur-
19
gery.
Clearly, although intermittent claudication itself is
generally benign, the associated ramifications are markedly increased morbidity and mortality compared with
the general population, in large part as a result of the
effects of atherosclerotic disease on other organ systems,
mainly the coronary and cerebral vasculature. Risk-factor
modification should be a significant part, if not the mainstay, of any therapeutic regimen. Attempts to modify risk
factors should be initiated, beginning with patient evaluation.
■ Clinical Evaluation
Evaluation of the patient with suspected PVD should begin with a directed history and physical examination.
Much can be determined simply by listening to the patient’s description symtoms. Relevant details such as onset (gradual versus acute), character, location, and aggravating and relieving factors should be sought. Combining
the clinical history with findings extracted during physical examination will aid in determining the nature and
extent of the disease process.
History
Intermittent claudication, reported by about 70% of patients at initial presentation, is the most frequent complaint of patients with PVD.
Latin word claudicatio, meaning to limp) is defined as
muscular pain brought on by exercise and relieved by
rest. Onset is predictable in terms of the activity level
required to produce the symptoms. Similarly, the symptoms rapidly resolve with rest of the extremity. There is
generally no relation to position of the extremity. The
discomfort itself tends to be described by patients as a
“cramping” pain in the body of the muscle; however, the
perception may var y from patient to patient. The quality
of discomfort may range from a sharp searing or stabbing
pain to an aching discomfort. Others complain of numbness, heaviness, fatigue, or weakness. Vasculogenic claudication must be differentiated from other states, such as
neurogenic claudication and arthritis.
claudication or pseudoclaudication may be associated
with spinal stenosis. Therefore, there is generally less
predictability regarding onset with exercise. Interestingly,
2–5
Claudication (from the
20
Neurogenic
although these patients may be limited in their ability to
ambulate, they may experience no limitation with alternative forms of exercise, such as an exercise bicycle, because of the postural changes associated with the alternative exercises. Additionally, in contradistinction to
vascular claudication, relief frequently is delayed following cessation of exercise and may require additional
change in position.
20
Unfortunately, because both of
these diseases are increasingly common with advancing
age, they may coexist. Similarly, arthritic complaints, usually joint centered, may be confused with claudication.
Onset may occur after rather than during exercise, and
relief is delayed and often positional. The noninvasive
vascular laboratory with exercise testing can be extremely
useful in differentiating true vascular claudication from
other conditions.
Claudication characteristically develops in the muscles
of the calf, although other sites may be involved. In part
this relates to the heavy dependence on the calf muscles
during walking, frequently the only source of significant
exercise in the aging population. Distribution of disease
also plays a significant role. Although younger patients
affected by PVD frequently present with an aortoiliac
distribution, the femoropopliteal system more frequently
is involved in the older population.
4,21
In fact, multisegment disease is common in patients who have PVD symptoms. Because the effects of disease on perfusion are
hemodynamically cumulative as one progresses distally in
the arterial tree, it is reasonable that the calf muscles are
frequently the site of most significant ischemia when
walking. Other sites of claudication occasionally dominate. Young women frequently present with lesions involving the distal aorta and its bifurcation.
22
With proximal disease, patients may complain of symptoms
involving the buttocks or thighs.
21
Similarly, men with
disease in this distribution may experience erectile dysfunction. Conversely, foot claudication may be the presenting symptom in patients with isolated distal vessel
disease, such as Buerger’s disease.
23,24
Unusual character
or distribution of symptoms may be the cause of significant delay in diagnosis and treatment.
21
As the degree of ischemia worsens, the limitations imposed on the patient increase, and symptoms may occur
at rest. Ischemic rest pain occurs when perfusion of the
extremity is inadequate to meet the basic metabolic
needs of the tissues.
25
Because perfusion status is extremely tenous at this point, small changes in perfusion
brought about by positional changes may either alleviate
or aggrevate symptoms. The patient may describe the
need to hang the distal extremity over the edge of the bed
at night for symptomatic relief provided by the gravitational advantage in perfusion. Frequently, the patient
may need to get up at night to “walk off” the pain, seemingly a contradiction. Minor trauma to the extremity with
this level of impaired perfusion may result in tissue break-
down or cutaneous ulceration. A small cut or blister that
https://t.me/med1917
is generally an innocuous event in the otherwise healthy
patient may become a limb-threatening lesion. Similarly,
with significant ischemia, cellulitis can progress rapidly
despite adequate antimicrobial treatment. Revascularization of these extremities is critical to long-term limb salvage and, depending on the clinical situation, should not
be delayed. Further decrease in perfusion invariably will
lead to tissue loss. Although tissue damage at this point
may be irreversible, limb salvage still can be attained with
revascularization and wound care.
Symptoms of chronic limb ischemia generally have an
insidious onset, although patients frequently relate the
onset to some event in their lives. As might be expected,
patients presenting with rest pain usually relate a long
history of worsening claudication before, seeking medical help. Ischemia, however, may present in an acute
fashion, often with abrupt onset of severe pain in the calf
or foot. Depending on the severity of the ischemia, the
patient may complain of paresthesias or numbness rather
than pain or describe sudden onset of coolness and discoloration with either cyanosis or pallor. Motor function
also may be impaired; the patient may be unable to move
the foot or toes. Generally, the symptoms are so sudden
and severe that medical attention is sought immediately.
If there is delay in presentation, however, the acute, severe symptoms may subside to some degree because collateral beds gradually supply some reperfusion to the
affected limb. Alternatively, without improved perfusion,
clinical status may deteriorate rapidly, with tissue breakdown and the development of gangrenous changes.
Acute ischemia may be secondary to an embolic or
thrombotic event. Emboli can occur anywhere in the
arterial tree but frequently lodge at sites of arterial division where vessel caliber is reduced suddenly. Large emboli may adhere to the aortic bifurcation, affecting both
lower extremities. The common femoral bifurcation and
the popliteal trifurcation are two additional frequent sites
of emboli, each presenting with a different distribution of
ischemia. Occasionally, microembolization will occur to
the most distal vascular beds. The sudden appearance of
one or more painful, discolored toes in the presence of
palpable pedal pulses, called the “blue toe syndrome,” is
characteristic of atheroembolization to the digital arteries (Fig. 6-1).
26
In general, this condition is thought to
represent embolization from a proximal ulcerated atherosclerotic lesion. Depending on the severity of the
proximal lesion, there may be an antecedent histor y of
claudication. Occasionally, a similar presentation occurs
secondary to a proximal critical stenosis without demonstrable ulceration. Presumably, small thromboemboli account for the distal arterial occlusions. A thorough history may reveal prior episodes of distal embolization.
Even in the presence of palpable pulses, distal embolization warrants further investigation of the source of em-
Peripheral Vascular Disease 57
FIGURE 6-1. A 48-year-old man presented with the acute
onset of a painful discolored fifth toe. A focally ischemic digit in
the face of normal pulses is characteristic of the “blue toe
syndrome.” Note the normal cutaneous features, hair distribution and venous distention indicating lack of chronic ischemia.
boli. Many of the inciting lesions are treatable by percutaneous techniques.
Thrombosis as a cause of acute ischemia may involve
native vessels or bypass grafts. If there is thrombosis of a
vessel with preexisting stenosis, careful questioning frequently will yield a preceding history of claudication. The
differentiation of in situ thrombosis of a diseased vessel
from embolic occlusion of an otherwise healthy vessel
carries different prognostic and therapeutic implications.
Thrombectomy is much less likely to be successful if the
underlying vessel is diseased; thrombolysis and angioplasty may represent an attractive alternative. In addition
to stenotic disease, aneurysmal disease is particularly susceptible to sudden thrombosis and or embolization.
27,28
Acute ischemia secondary to popliteal artery thrombosis
should lead to aninvestigation ofthe underlying artery (as
well as the contralateral artery) to exclude aneurysmal
disease. A similar picture may be encountered with popliteal entrapment with or without associated aneurysm
formation. Again, examination of the contralateral
extremity is crucial, because the disease is frequently bilateral. Bypass grafts frequently fail without prior clinical
symptoms, and a history of claudication may not be encountered. Routine graft surveillance is therefore thought
58
https://t.me/med1917
K. S. Rholl and K. M. Sterling
to be warranted to avoid the consequences of graft fail-
29,30
ure.
Further interrogation regarding the involvement of
vascular disease in other organ systems should be undertaken. As previously noted, cardiovascular and cerebrovascular events account for most of the mortality in this
patient population. The presence of significant disease
involving these organ systems may alter the therapeutic
approach to the patient. Risk factors should be elucidated, and initial efforts at risk-factor modification begun. Family history is important not only for its prognostic value, but it also occasionally aids in determining the
source of disease. A family history of thrombotic events
may suggest a hypercoagulable state, although this is
found infrequently. These events more often involve the
venous system but occasionally result in arterial emboli or
thrombosis, particularly following instrumentation, such
as arterial catheterization or vascular surgery. Surgical
history, particularly as it pertains to the vascular system,
should be outlined in detail. Prior grafts may alter significantly both diagnostic and therapeutic approaches.
Unusual graft anatomy or occlusive disease can interfere
with angiographic and therapeutic approaches. Prior harvesting of the saphenous vein may limit surgical alternatives.
Current medications, particularly those with vascular effects, such as anticoagulants and vasoconstricting
agents, should be recorded. Drug interactions and side
effects are not infrequent and may have consequences
for therapeutic endeavors. Specific inquiry must be made
regarding certain drugs (e.g., nicotine patches) because
often the patient does not perceive these agents as being
medication
Physical examination
With the clinical history in mind, a directed physical
examination should be performed to evaluate the patient’s vascular status. The investigation should include a
basic cardiovascular examination as well as an evaluation
of the possible effects of vascular disease on the extremities. Ausculatation of the heart is performed to exclude
arrhythmias such as atrial fibrillation and significant murmurs. The carotid arteries, abdomen, and pelvis, including the femoral arteries, are auscultated for the presence
of bruits. A thorough assessment of peripheral pulses by
palpation includes both upper and lower extremities.
Pulses should be recorded as absent, diminished, normal,
or hyperdynamic bilaterally. If a pulse is absent by palpation, its presence should be ascertained by using a handheld Doppler device. Although the dorsalis pedis pulse
may be absent by palpation in up to 12% of the normal
population, absence of the posterior tibial pulse is a
strong indicator of disease.
soft tissue edema or open ulceration may confound the
4
The presence of significant
process of palpation; again, Doppler evaluation may be
necessary. Palpation also should be used to investigate
possible aneur ysmal disease at common sites of formation including the abdominal aorta, common femoral
arteries, and popliteal arteries (the most frequently ignored site). Blood pressures obtained from both upper
extremities should be recorded as part of the vascular
examination.
Inspection of the extremities is performed to evaluate
for signs of acute and chronic arterial insufficiency. In
addition to pulse evaluation, this should encompass inspection of the quality of the skin, the distribution of hair
on the extremities, cutaneous temperature, capillary refill
and neuromuscular function, each as it relates to the presence of vascular disease. Chronic arterial insufficiency
leads to trophic skin changes with thin, shiny skin, particularly in the pretibial region.
11
Loss of normal hair
distribution occurs from the distal calf and dorsum of the
foot. Nails may become thickened and brittle. With increasing severity of chronic ischemia, dependent rubor
may be present owing to relatively fixed vasodilation in
the distal arteriolar and capillary beds. With the patient in
a sitting or erect position, the foot and distal calf are
ruborous, whereas in the supine position, particularly
with the extremity elevated, the extremity appears pale.
Temperature changes, which are more pronounced in
the acutely ischemic limb, may be present in chronic ischemia, particularly if the limb is left without the thermal
protection of a sock or blanket for a brief period. Comparison of proximal to distal and side-to-side is made.
Capillary refill is evaluated by applying gentle pressure to
the skin or nail bed, followed by release and observation
of the return of the normal pinkish color. Capillary refill,
normally 1 to 2 seconds, becomes increasingly delayed
with the severity of the ischemia. As ischemia progresses
and the limb becomes threatened, sensor y and muscular
function are affected. These changes are generally most
pronounced in acute, severe ischemia. With chronic ischemia, muscle mass begins to atrophy, accounting for
much of the weakness encountered. Finally, inspection
should include a thorough evaluation of skin integrity.
Tissue breakdown, ulceration, and frank gangrene may
occur with severe ischemia. Ulceration tends to occur at
pressure points in the distal extremities, including the
regions around the malleoli, heels, heads of the metatarsals, and toes. Frequently undetected without careful inspection are lesions between the toes. Detection of tissue
breakdown is extremely important because these lesions,
untreated, may become infected and life threatening. Ischemic ulcerations tend to be dry, punched-out lesions
with well defined borders (Fig. 6-2). Usually little erythema is found unless infection is present. These ulcerations should be differentiated from venous ulcers, which
tend to be weeping, indurated lesions around the distal
calves (Fig. 6-3). Associated cutaneous changes of venous
FIGURE 6-2. A 68-year-old woman presented with a chronic
https://t.me/med1917
ulcerated lesion along the anterior aspect of her shin. The
lesion is well defined, dry and shows little associated erythema. The surrounding skin is atrophic with a paucity of hair.
Although unusual in position, the lesion is characteristic of an
ischemic ulcer.
stasis are frequently present with brawny edema and
brownish discoloration of the skin. Dilated superficial
varicosities also may be in the region of a venous ulcer.
The physical examination in acute limb ischemia may
be quite different from that of chronic disease. Initially,
pulses are severely diminished to absent because collaterals have had little time to form. The underlying skin
and hair distribution are frequently normal, although in
the case of acute graft occlusion, the stigmata of chronic
disease may have previously developed. Color change
may be pronounced, with the distal ischemic portion of
the extremity having a blanched or marbled appearance
in the more severe cases. Differential temperature of the
Peripheral Vascular Disease 59
affected extremity is usually pronounced. The level of
temperature change should be recorded as well as
marked on the extremity. As the ischemic process
evolves, a well-defined line of demarcation develops between the perfused proximal extremity and the ischemic
distal portion. As collateral perfusion increases following
the acute episode, this line of demarcation tends to move
distally. Capillar y refill may be markedly delayed or absent. Evaluation of motor and sensory function is critical
in these patients because it aids in the determination of
limb viability. Sensory changes range from none to complete anesthesia. Patients with threatened but reversible
ischemia frequently note dysethesia or paresthesia of the
affected extremity. The presence of diabetes may confuse the issue because peripheral neuropathy is frequently present.
31
Comparison with the contralateral extremity should be performed in all patients but is
particularly useful when an underlying neuropathy is
present. Similarly, muscle function ranges from normal
to paralysis; weakness is a sign of the threatened limb.
Generally, tissue breakdown is not present at initial presentation owing to the acuity of the process. Without revascularization, however, the threatened to irreversible
limb may progress rapidly to frank gangrenous changes.
When present, these changes may represent a contraindication to revascularization, particularly if infection is
present, owing to the milieu of toxic substances that may
be released from the affected limb.
To provide consistency in the evaluation and reporting
of the ischemic limb, a system of grading extremities has
been developed for both acute and chronic limb ischemia
(Table 6-1) using clinical findings and objective criteria
that may be provided by the vascular laboratory.
32–35
In
addition to prognostic implications, therapeutic decisions
can be made consistently using these standardized categories. For instance, percutaneous thrombolytic treatment
of the acutely threatened limb may be appropriate in
many cases. If the clinical status of the extremity declines
rapidly, with loss of sensory and motor function, there is
frequently insufficient time for thrombolytic agents to
restore perfusion, and surgical revascularization may be
more appropriate. The goal of the clinical evaluation of
the patient is to document the vascular status of the
patient, providing a basis for any therapeutic decision,
whether conservative or invasive.
FIGURE 6-3. A 58-year-old black man presented with chronic
cutaneous ulceration around the medial malleolus. The reddish
brown discoloration of the skin and the distribution around the
ankle are typical of chronic venous stasis changes.
Noninvasive Vascular Testing
Although the importance of the clinical evaluation cannot
be overstated, objective data supplied by the noninvasive
vascular laboratory can be of great use in the evaluation of
patients with suspected PVD, not only documenting the
presence of disease but also providing information as to
the location, severity, and etiology of the disease process.
For instance, there may bea paucity of physical findings in
60 K. S. Rholl and K. M. Sterling
https://t.me/med1917
TABLE 6-1. Clinical categories of limb ischemia (31–35)
Acute limb ischemia
Category Description Capillary refill Motor impairment impairment Doppler Doppler
Viable Not immediately threatened Intact None None Audible, Audible
Threatened Salvageable if promptly Intact, slow Mild Mild Inaudible Audible
Irreversible Major tissue loss, Absent (marbling) Profound, paralysis Profound, Inaudible Inaudible
Grade Category Clinical description Objective criteria
I 1 Mild claudication Treadmill completed, postexercise AP ⬎50 mm Hg but⬎25 mm Hg
II 4 Ischemic rest pain Resting AP ⱕ40mm Hg, flat or barely pulsatile metatarsal
III 5 Minor tissue loss, nonhealing ulcer, focal Resting AP ⱕ to 60 mm Hg, ankle or metatarsal plethysmography
a
Treadmill at 2 mph with a 12% grade for 5 min. AP = Ankle pressure.
treated
amputation required (rigor) anesthetic
regardless of treatment
Chronic limb ischemia
0 Asymptomatic; no hemodynamically Normal result of treadmilla/ stress test
significant lesion
below normal
2 Moderate claudication Symptoms between categories 1 and 3
3 Severe claudication Treadmill test cannot be completed, postexercise AP⬍50 mm Hg
plethysmography, toe pressure ⬍30 mm Hg
gangrene with diffuse pedal edema flat or barely pulsatile, toe pressure ⬍40 mm Hg
6 Major tissue loss, extending above Same as for category 5
transmetatarsal level, functional foot not
salvageable
Sensory Arterial Venous
ankle pressure
⬎ 30 mm Hg
many patients with intermittent claudication. The absence of peripheral pulses is an unreliable finding. Patients with high levels of activity may be severely limited
despite the presence of palpable peripheral pulseson resting examination. Therefore, a diagnosis of intermittent
claudication is sometimes difficult, with history and physical examination having false-positive and false-negative
36
rates in the range of 44% and 19%, respectively.
The
noninvasive laboratory can provide objective data regarding the presence or absence of disease in patients whose
complaints suggest claudication. Frequently, the ability of
the noninvasive vascular laboratory to provide correlation
of the diseaseprocess with the patient’s symptomatology is
of equal importance, especially in patients whose clinical
presentation may not fit the classical description of vascular disease. The information provided is therefore vital to
the success of any management, whether conservative or
invasive.
In addition to the evaluation of the patient with suspected intermittent claudication, indications for noninvasive vascular testing include documentation of disease
in the severely ischemic extremity, nonhealing ulcers,
assessment of potential wound or amputation healing,
vasospastic disorders, entrapment syndromes, trauma,
and evaluation of other lower-extremity complaints. Before any intervention is undertaken, an initial evaluation
can be invaluable in procedural planning, serving also
as a baseline against which the results of the intervention
can be gauged. The vascular noninvasive examination is
extremely useful in monitoring the status of the disease
process, documenting the stability or progression of disease, and allowing correlation with changes in the patient’s clinical status. Traditionally, the most important
task of the noninvasive laboratory has been documentation of physiologic changes occurring with PVD and correlation of this information with the patient’s symptoma-
37
tology.
More recently, however, noninvasive testing has
been performed for anatomic mapping, possibly eliminating the contrast angiogram for certain patients.
38,39
Vascular testing, therefore, may be divided into examinations that provide primarily physiologic information
and those that provide primarily anatomic information.
Because it is not cost effective to perform every modality
available in the noninvasive laboratory on every patient,
consideration should be given to the desired information, using modalities that can provide this information
best and most efficiently. If intervention is considered,
most patients will proceed to angiography, and anatomic
testing may be redundant. Physiologic testing, by evaluating the overall perfusion of the extremity, may be more
useful in allowing one to decide whether intervention is
indeed warranted. When specific anatomic questions are
Peripheral Vascular Disease 61
https://t.me/med1917
present, anatomic testing such as duplex imaging or
magnetic resonance angiography (MRA) may provide
this information. The expansion of the modalities available in vascular testing allows tailoring of the examination to fit the needs of the clinician and patient.
Ankle brachial indices
Measurement of arterial blood pressures at the ankle with
comparison branchial pressure constitutes the simplest
noninvasive screening test for PVD. Ankle brachial indices (ABIs) are determined by measuring the systolic pressure from both the dorsalis pedis and the posterior tibial
arteries at each ankle and dividing by the higher of the
two brachial pressures. In normal subjects, the ABIs
should be approximately 1.0, with values of less than 0.95
suggesting the presence of vascular disease.
33,37,40,41
The
degree of depression of the ABI correlates fairly well with
the severity of the disease. Although there is significant
variability, ABIs in the range of 0.75 to 0.9 correspond to
mild, often single-segment (e.g., aortoiliac or femoropopliteal) disease. Patients, if active, may experience symptoms of mild claudication. ABIs in the range of 0.5 to 0.75
are indicative of moderate ischemia; two arterial segments are frequently involved. Depending on the level of
activity, the clinical picture may range from asymptomatic
to fairly severe claudication. ABIs below 0.5 usually indicate multisegment disease (frequently with multiple occlusions) and generally are associated with severe claudication that may approach rest pain. Below 0.3, ischemia
is severe and tissue breakdown is likely. Absolute ankle
pressures of less than 50 mm Hg also are associated with
severe ischemia and likely tissue breakdown.
33,40
Measurement of ABIs represents a simple, reproducible
screening test for arterial disease, requiring only minimal
equipment, namely a handheld Doppler unit and a
sphygmomanometer. A significant drawback to ABIs is
the insensitivity of the technique to mild disease. An
active person may have normal resting ABIs but may
develop limiting ischemia with exercise. Moreover, pressures may be artificially elevated in patients with calcific,
noncompliant vessels, as is frequently seen in diabetic
patients with medial sclerosis. ABIs greater than 1.0 are
commonly seen in diabetic patients despite fairly severe
ischemia demonstrable by other techniques.
31,37
The
presence of bilateral upper-extremity arterial disease may
also result in artificially elevated ABIs. Finally, other than
laterality, there is no anatomic information provided. Despite these limitations, determination of ABIs should be
part of any physical examination for PVD.
Segmental limb pressures
Determination of segmental limb pressures (SLP) in the
lower extremities adds some anatomic information to that
provided by ABIs. Initially, ankle pressures are measured
for both the posterior tibial and the dorsalis pedis arteries.
The stronger pulse (higher systolic pressure) then is used
for determination of SLPs. Measurements then are performed using a series of blood-pressure cuffs along both
lower extremities. In the three-cuff technique, cuffs are
placed at the midthigh, calf, and ankle levels; with the
four cuff technique, the thigh is divided into high-thigh
and low-thigh measurements. Systolic pressures are determined asthe cuffs aresequentially inflated and deflated at
each level while monitoring the stronger pedal pulse distally. Cuffs appropriate to the size of the extremity should
be used to avoid artificially high measurements in large
extremities. Although ideally, using larger cuffs for the
thighs, the artifactual elevation of pressures measured by
cuff would be avoided and SLPs in a patient without PVD
all would be equivalent to the brachial pressure, thigh
pressures tend to be overestimated by at least 30 mm Hg,
particularly in patients with a more obese body habi-
37,40
tus.
Intraarterial pressure measurements have demonstrated that actual systolic arterial pressure in the iliac
and femoral arteries is about equal to branchial pressures.
Familiarity with the body habitus of the patient being
examined and the equipment and cuffs used in the laboratory is therefore critical. With this knowledge, appropriate compensation for this artifact can be made and the
potential error in diagnosis avoided. SLPs are compared
from proximal to distal in each extremity as well as from
side to side. In general, a segmental drop in pressure
between any two segments of greater than 20 to30 mm Hg
is indicative of stenotic disease in the underlying seg-
37,40
ment.
Similarly, a difference of greater than 15 to 20
mm Hg from side to side suggests significant disease at or
above the cuff in the extremity with the lower measurement. Advantages of SLPs include limited equipment requirements and an element of anatomic specificity in the
detection of disease. Similar to the determination of ABIs,
however, medial sclerosis again can result in artificial elevation of pressure measurements. In diabetic patients, in
whom healing potential is frequently the greatest concern, measurement of toe pressures may aid in this concern. Because digital arteries are generally less affected by
medial sclerosis and therefore the measurement of pressure more accurate. In general an absolute toe pressure of
greater than 50 mm Hg and a toe brachial index of 0.6 or
greater is normal. Absolute toe pressure of at least 30 mm
Hg is ordinarily required for healing.
37,42
Another significant disadvantage of SLPs is the inability to differentiate
an occlusion from a stenosis. Although occlusive disease
generally resultsin a larger pressure reductionthan stenotic disease, collateral circulation may diminish this differential. This determination may be critical in a patient with
intermittent claudication who may be a candidate for percutaneous revascularization but may not meet the criteria
for a surgical procedure. Despite these limitations, deter-
62 K. S. Rholl and K. M. Sterling
https://t.me/med1917
A
C
FIGURE 6-4. Physiologic noninvasive arterial examination from a 62-year-old man presenting with complaints of bilateral calf
aching when walking. A: Resting segmental limb pressures are normal bilaterally with ankle brachial indices (ABIs) greater than
1.0. Note the side-to-side symmetrically and the gradual decline from high thigh to ankle. B: Doppler waveform analysis is also
normal with triphasic waveforms throughout both lower extremeties. C: Resting volume plethysmography recordings demonstrate normal perfussion throughout the lower exremeties. Note the progression in amplitude from the high thigh to the calf. Side
to side, there is symmetry with normal morphology throughout the lower extremities. D: The patient was exercised on a treadmil
with a 12% grade at 2.0 miles hour for 5 min. He noted aching in the calves during the latter part of the exercise protocol and
during the recovery period. Following exercise, there was maintenance of normal ABIs with simultaneous rise in ankle and
brachial pressures. Plethysmographic tracings obtained at the ankle demonstrated a normal increase in perfusion following
exercise with continued normal waveform morphology. There was no evidence of exercise induced ischemia; the symptoms were
therefore not secondary to arterial insufficiency. PT-posterior tibia; DP-dorsal pedis BP-blood pressure.
B
D
Peripheral Vascular Disease
https://t.me/med1917
A
63
B
FIGURE 6-5. Physiologic nonivasive testing in an obese 48-year-old woman complaining of cramping pain in the left calf when
walking more than 100 yards. She also noted occasional buttock discomfort when climbing stairs. The examination indicates the
pressure of severe obstruction in the left iliac arterial system. A. Resting segmented limb pressures demonstrate a significant
decrease in the left high thigh pressure when compared to the right. No additional significant gradients are present on the left.
Examination on the right is normal with an ABI greater than 1.0. B: Doppler waveforms analysis is markedly abnormal throughout
the left lower extremity. The left common femoral artery waveform is broad and monophasic. Note that further degradation below
the common femoral artery may be difficult to detect. On the right there is degradation of the posterior tibial artery waveform
which may indicate disease in this vessel. The remaining waveforms show no significant abnormality. C: Resting volume
plethysmography recordings are dramatically degraded in the left thigh indicative of significant inflow obstruction. Distal to this
there remains a normal progression in amplitude to the calf suggesting that the femoral popliteal system is intact. Note the
diminutive amplitude of the thigh waveforms on the right. This is frequently seen in obese patients with a relatively low muscle
mass. PT-posterior tibia; DP-dorsal pedis.
mination of SLPs remains a simple, reproducible means
of quantifying PVD and its effects on the perfusion status
of the extremities (Figs. 6-4A and 6-5A).
regarding the location and severity of PVD. Although
directional Doppler waveform information is part of
more sophisticated duplex Doppler techniques, the information can be obtained with simpler, less expensive
Doppler waveform analysis
Frequently performed in conjunction with SLPs, Doppler waveform analysis (DWA) represents another of the
traditional techniques for the evaluation of vascular disease. Assessing the changes that occur in the directional
Doppler waveform can provide additional information
continuous wave (CW) Doppler instrumentation. Using
a CW Doppler probe aligned longitudinally with the long
axis and at about 45 degrees to the transverse axis, directional Doppler waveforms are obtained at multiple levels
where the arteries are superficial, typically including the
common femoral, popliteal, posterior tibial, and dorsalis
pedis arteries. Waveforms also can be obtained from the
C
Соседние файлы в папке Библиотека им академика М.И. Перельмана