VASCULAR SURGERY Published six times

a

year under the

THE ANGIOLOGY RESEARCH

auspices of

FOUNDATION, INC.

DIAGNOSTIC CONSIDERATIONS IN OCCLUSIVE ARTERIAL DISEASE D. E. STRANDNESS, JR., M.D., F.A.C.A.

Seattle, Washington

The most

of occlusive arterial disease in the Western world virtue of its involvement of the arterial supply to many By a variety of clinical patterns which a physician must learn to recognize. One of the frequent areas of the circulation which is prone to develop the far-advanced, complicated plaque is the arterial supply to the lower extremities. When the arms are involved, the lesions are most commonly limited to the first portion of the subclavian arteries, with the axillary, brachial, and forearm vessels usually spared. Atherosclerosis is largely a disease of the large and medium-sized arteries which, for the purpose of this discussion, will include the tibial arteries as well, even though some physicians often refer to them as &dquo;small vessels.&dquo; Problems occur only when the cross-sectional area of the artery is reduced to the point at which an abnormal pressure gradient develops, and flow is correspondingly restricted enough to cause symptoms either at rest or with exercise. The key factors in the type of symptoms which result are the location of the obstruction(s) and the functional capabilities of the collateral circulation. The collateral channels can be divided into three major components-the stem vessels, the midzone arteries, and the re-entry arteries.’ The stem and reentry arteries are the first branches of the large and medium-sized arteries. Examples are the profunda femoris artery (a stem vessel) and the geniculate arteries (re-entry channels). The connecting links-the midzone arteriesare the key to limb survival and function. Anatomically, these vessels are much smaller in diameter and thus offer the greatest resistance to flow; therefore the greatest pressure drop occurs across these arteries. The remarkable nature of the collateral channels in terms of limb survival is apparent when it is realized how infrequently a patient with peripheral atherosclerosis comes to amputation. 2, 3 It is now well established that most patients, even with extensive atherosclerosis, will have normal blood flow at rest to the leg, foot, and digits.4 The functional abnormality becomes most common cause

is atherosclerosis. organs, it leads to

From the University of Washington School of Medicine, Seattle, Presented at the 22nd Annual Meeting of the American College of California, January 4-11, 1976.

Washington. Angiology, Palm Springs,

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apparent with the stress of exercise when the amount of blood flow required to prevent muscular ischemia cannot be met by the collateral arteries. ’

CLINICAL PICTURE

From a practical standpoint, it is useful to divide the problems that develop into two categories - symptoms with exercise and symptoms at rest. Although it is clear that patients with occlusive arterial disease can fall into both categories, this distinction has important therapeutic implications.

Symptoms With Exercise The most common complaint of the patient with peripheral atherosclerosis is pain in a muscle or muscles which is brought on by walking and relieved by rest-so-called intermittent claudication. The exact nature, severity, and location of the pain depends entirely upon the level and extent of the occluding process. At this point it is important to call attention to a relatively silent area of the peripheral circulation, the tibial arteries and the peroneal artery. clear that occlusion of one or more of these arteries alone will not intermittent claudication except when the underlying problem is produce When this disease involves these arteries, it is extensive, Buerger’s disease. without and ascending, skip areas, and thus it effectively obstructs potential for the common complaint namely of instep channels. This accounts re-entry claudication and for the very frequent appearance of severe ischemic rest It is

now

pain.&dquo;:; Thus, when atherosclerosis is confined to the tibial and peroneal arteries alone, claudication is not one of the presenting complaints. This pattern of occlusive lesions is most often observed in patients with diabetes mellitus. In an excellent clinical study of 428 patients with diabetes mellitus and atherosclerosis, Wheelock found that 40% of the patients had a palpable popliteal but absent pedal pulses.&dquo; We examined the distribution of lesions as well and were able to show that in amputation material the striking feature of the patient with diabetes mellitus is the very high incidence of involvement of the below-knee arteries.77 When a patient presents with muscular pain brought on by exercise, the lesion responsible must be proximal to the blood supply of the calf muscles the gastrocnemius. It should also be clear that the muscle groups which develop ischemia are dependent upon the most proximal level of the obstruction. At the same time it must be remembered that the more distal muscle groups are the most ischemic with walking. For example, it is not uncommon for the patient with terminal aortic or common iliac occlusion to complain most bitterly of calf claudication with little or no mention of the more proximal muscle groups. Although there are certainly variants in the clinical picture, the important components to be noted are those of the walk-pain-rest cycle. The important features of intermittent claudication are (1) that it is constant from day to day; (2) that it is always worse when walking up stairs or up a hill; and (3) that it is promptly relieved by rest. There is no doubt that the clinical pattern

pulse

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of intermittent claudication is one of the most constant pictures encountered in clinical medicine and is one of the easiest to recognize. However it can be and is confused with problems that involve the neuromuscular system, particularly the spine and hips. A variety of lesions, such as degenerative joint disease, herniated nucleus pulposus, spinal stenosis, and tumors, can produce symptoms referable to the legs which have on occasion been confused with true intermittent claudication.~8

From a diagnostic standpoint, it is again necessary to refer to the walkpain-rest cycle because with the pseudoclaudication syndrome, it is no longer constant. The symptoms will vary extensively from day to day and will often be produced by either sitting or standing. Also, if the patient needs to lie down for relief, the physician can almost be assured that he or she is not dealing with vascular insufficiency. It must be mentioned that it is possible for the two problems to coexist. When this occurs, proper interpretation of the symptoms, particularly in terms of which ones are the important elements in the patient’s illness, becomes paramount in importance. From a clinical standpoint, the location of the muscle pain and its severity provides the clinican with important clues to the level and extent of the arterial involvement. In general, patients with aortoiliac disease are the most disabled. This makes good sense physiologically, because with disease at this level the entire limb is dependent upon the collateral circulation. Contrast this with the patient with a superficial femoral occlusion. Here the thigh muscles are normally supplied and the calf muscles are the major group deprived of normal input with walking. It must also be recognized that when the occlusions involve multiple levels, the problems are going to be more severe. Since each new occlusion requires another collateral network, the blood supply to the limb becomes dependent upon more than one series of high-resistance pathways. These are the patients who not only complain of severe claudication but, as will be discussed later, also present with rest pain, tissue necrosis, and gangrene. It should be apparent by this point that a well-taken history will usually be sufficient to establish the basis for the patient’s complaints. The physical examination is simply confirmatory, providing information relative to the most proximal level of the arterial involvement. The attention is directed to the level of the palpable pulses and the presence of bruits. In general, pulses are not felt distal to sites of complete occlusion unless the collateral arteries are nearly the same size as the parent vessel. When pulses are palpable distal to the site of an arterial plaque, it means that there is not a large pressure gradient at rest. This has led to the description of a small subset of patients with the phenomenon of disappearing pulses with exercise.99 These disappearing pulses are most characteristically found in patients with stenoses in the common iliac arteries. With exercise and the resulting increase in flow, the velocity through the stenosis also increases and leads to a fall in the pressure distally. This fall is responsible for the disappearance of the peripheral pulses. Bruits should be listened for from the level of the abdominal aorta to both

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popliteal arteries. Their presence simply signifies turbulence produced by the eddies that develop distal to the narrowed area. These eddies in turn impact with the arterial wall, setting it into vibration and thus making the presence of the narrowing detectable.’° However, if the stenosis becomes very high grade (greater than 80% reduction in cross-sectional area), the bruit may disappear entirely because of the marked reduction in flow through the involved area. Obviously, with total occlusion, no bruit will be detected. Symptoms at Rest When the patient develops pain at rest, it is clear evidence that blood How to the involved area is below resting levels. This leads to the three major methods of presentation-ischemic rest pain, tissue necrosis, and gangrene. One or more may be present, nearly always involving the distal foot and digits. The pain is as typical as that which is observed with claudication in that it is always aggravated when the foot is either level or elevated and in its early stages is partially or completely relieved by dependency. It must be appreciated that the pain pattern may be modified considerably in the patient with diabetes mellitus who also has a peripheral neuropathy. The patient may have extensive ischemia, tissue necrosis, and gangrene and have no pain at all. The clinical significance of the symptoms at rest are that they generally represent terminal, far-advanced, multilevel disease which must be, in part, corrected by operative therapy if amputation is to be avoided. These are the patients who most desperately need more blood flow to their feet. ’





ANCILLARY DIAGNOSTIC PROCEDURES

By the time a thorough history and physical examination has been completed, the diagnosis is accurately made with few exceptions. It is at this point that the physician has to decide what further tests are necessary and why. The most common practice today is to proceed directly to arteriography, but this need not be done unless direct arterial surgery is contemplated to correct the underlying obstruction to blood flow. In recent years there has been increasing interest in setting up a peripheral vascular laboratory which in many respects functions similarly to cardiac units and pulmonary function stations. Before considering the type of information which can be obtained, it is necessary to justify the need for acquiring additional diagnostic data. Patients with occlusive arterial disease can obviously span the entire spectrum of the disorder, ranging from minimal to no disability to the case with threatened or actual tissue loss. These extremes really need no further clarification at that point, because the disease has already defined itself in no uncertain terms. However it is very useful to obtain further quantitative information concerning the functional consequences of the disease in order to provide (1) certain unbiased data on the stage and location of the disease; (2) a baseline from which changes in the disease can be assessed independently of patient and physician bias; (3) reliable indices from which the results of therapy can

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judged; (4) a data base on the patient, the interpretation of which is not dependent upon change in physician or housestaff; and (5) intelligible information which has a singular interpretation to all physicians who understand the disease and the testing procedures. As in many areas in clinical medicine, there has been a proliferation of diagnostic tests which are often a source of confusion to the inexperienced physician. Regardless of the approach used, the basic physiology of the arterial circulation can best and most simply be understood in terms of pressure, flow, and peripheral resistance. Ideally, we would like to know pressure (pulsatile and mean), flow (pulsatile and mean), and the resistance to flow at all levels of the arterial circulation, down to and including the arterioles. Since this information in toto is clearly not available, a comprobe

mise is in order. The compromises which must be made are not unreasonable if the physician accepts the following information as correct: 1. In the normal arterial circulation, the pressure pulse is amplified as it traverses the peripheral arteries. This means that the systolic pressure at the ankle will exceed that of the central aorta.&dquo; 2. The normal arteries are a low-resistance system down to the level of the arterioles. This is reflected in the less than 10 mmHg drop in mean pressure between the central aorta and small peripheral arteries.&dquo; 3. There is a gradual reduction in the peak velocity of flow toward the

periphery.&dquo; 4. Under

flow in the peripheral arteries normally goes very transient reversal of flow in early to mid-diastole.’2 5. With exercise, flow (volume and velocity) goes up and systolic and mean pressures are maintained, but flow reversal disappears and the flow itself 12, 13 may become quasi-steady during the hyperemic phase.

resting conditions,

to zero, with

a

Arterial narrowing and occlusion affect the above parameters as follows. 1. Proximal to the point of arterial narrowing and occlusion, pulse, and mean blood pressure remain unchanged. However systolic pressure decreases across the involved area as the earliest manifestation of the added resistance caused by the diseased segment and midzone collateral arteries.’4 As the resistance to flow increases as more collateral beds are added in series, the mean pressure falls as well, and indeed the pulsatile pressure component may be lost entirely. 2. The drops in systolic and mean blood pressure are accurate reflections of the conversion of the peripheral arteries into a high-resistance system. 15 3. Peak velocity flow is reduced even further than usual.’2 4. Flow distal to the stenosis or below the collateral re-entry channels no longer returns to zero, and there is no flow reversal. Thus flow tends to become quasi-steady.166 5. With exercise, pressures distal to the involved areas fall to very low levels and require prolonged periods (up to 30 minutes in some instances) to return to baseline. 15 .

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Given these assumptions, what variables can be measured to evaluate the observed changes? 1. Central aortic pressure cannot be measured but it can be reasonably estimated from indirect arm blood pressures by using either the Korotkoff sounds or the ultrasonic technique. 2. The degree of the potential energy losses can be estimated by measuring the ankle systolic pressure by either a Doppler or plethysmographic method. If the ankle systolic pressure is less than arm systolic, arterial narrowing or obstruction is a certainty.&dquo; Experience has shown that if the ankle pressure is ~ 50% of arm pressure, occlusion of a single segment is likely. Below this pressure, multiple levels of disease are found. 3. The phasic changes in flow velocity can be estimated with a directionsensing continuous wave velocity detector. Absence of reverse flow with quasi-steady flow is certain evidence of arterial narrowing and occlusion. 12 4. The pressure changes at the ankle after exercise can be reliably measured by the Doppler technique. These in turn reflect the degree of muscular ischemia, the extent of the reduction in peripheral resistance, and the magnitude of the relatively fixed collateral artery resistance The final fact that must be accepted is that any change in the disease which is reflected by a change in the resistance to flow will be accurately reflected by the pressures recorded at the level of the arm and ankle and expressed as the ankle-to-arm pressure ratio (normal -1).18 The basic equipment required to gather these data includes a directional velocity detector, a suitable D-C recorder, blood pressure cuffs, and a treadmill. It is of course possible to add other diagnostic methods, such as a pulse volume recorder, a variety of plethysmographs, isotope clearance methods, and thermography, but in general they add little to the desired information and add greatly not only to the cost of the tests but to the complexity of the

procedure. SUMMARY

The diagnostic approaches to the problem of occlusive arterial disease have been reviewed. The history and physical examination are most useful in establishing the diagnosis, localizing the most proximal level of the arterial involvement, and categorizing the patient’s stage of disease. Functional evaluation of limb blood pressures and flow velocity at rest and after exercise provide useful data for estimating the degree of the arterial involvement, and this information can be used as the baseline for evaluating the effects of

therapy. D. E.

Strandness, Jr., M.D. Professor of Surgery University of Washington School

of Medicine

Seattle, Washington 98195

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277 REFERENCES 1.

Longland, C. J.: The collateral circulation of the limb.

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Boyd, A.

M.: The natural

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55: 591, 1962. Med., 3. Imparato, A. M., Kim, G., Davidson, T., course. Surgery, 78: 795, 1975. 4.

et al.: Intermittent claudication: Its natural

J. T.: Arterial occlusion and intermittent claudication, in Physiology of the Circulation in Human Limbs in Health and Disease. Philadelphia, W. B. Saunders,

Shepherd, 1963.

McKusick, V. A., Harris, W. S., Ottesen, O. E., et al.: Buerger’s disease: A distinct clinical and pathologic entity. J.A.M.A., 181: 5, 1962. 6. Wheelock, F. C., Jr.: Transmetatarsal amputations and arterial surgery in diabetic patients. N. Engl. J. Med., 264: 316, 1961. 7. Strandness, D. E., Jr., Priest, R. E., Gibbons, G. E.: A combined clinical and pathologic 13: 366, 1964. study of diabetic and nondiabetic peripheral arterial disease. Diabetes, 8. Silver, R. A., Schevle, H. L., Stacks, J. K., et al.: Intermittent claudication of neurospinal origin. Arch. Surg., 98: 523, 1969. 9. DeWeese, J. A.: Pedal pulses disappearing with exercise: A test for intermittent claudication. N. Engl. J. Med., 262: 1214, 1960. 10. Lees, R. S., Dewey, C. F., Jr.: Phonoangiography: A new noninvasive diagnostic method for studying arterial disease. Proc. Natl. Acad. Sci. U.S.A., 67: 935, 1970. 11. McDonald, D. A.: Blood Flow in Arteries. Baltimore, Williams & Wilkins, 1960. 12. Yao, S. T.: Hemodynamic studies in peripheral arterial disease. Br. J. Surg., 57: 761, 1970. 13. Stahler, C., Strandness, D. E., Jr.: Ankle blood pressure response to graded treadmill 5.

exercise.

Angiology,

18: 237, 1967.

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W. E., Fry, W. J., Kraft, R. O., et al.: Hemodynamic mechanism for pulse changes Keitzer, in occlusive vascular disease. 57: 1965.

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Sumner,

Surgery,

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D. S., Strandness, D. E., Jr.: The relationship between calf blood flow and ankle blood pressure in patients with intermittent claudication. Surgery, 65: 673, 1969. 16. Strandness, D. E., Jr., Sumner, D. S.: Hemodynamics for Surgeons. New York, Grune & Stratton, 1975. 17. Carter, S. A.: Clinical measurement of systolic pressures in limbs with arterial disease. 207: 1869, 1969. J.A.M.A., 18. Strandness, D. E., Jr.: Exercise testing in the evaluation of patients undergoing direct arterial surgery. J. Cardiovasc. Surg., 11: 192, 1970.

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Diagnostic considerations in occlusive arterial disease.

VASCULAR SURGERY Published six times a year under the THE ANGIOLOGY RESEARCH auspices of FOUNDATION, INC. DIAGNOSTIC CONSIDERATIONS IN OCCLUSIVE...
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