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Diagnosis in Arterial Disease
Diagnosis in Arterial Disease ORMAND C. JULIAN,
M.~.,
PH.D.*
THE diagnosis of arterial disease depends upon pursuit and analysis of aspects of the history of the illness which are suggestive of these conditions, the appreciation of specific findings during the course of a complete general physical examination, and finally upon the application of a rather limited number of special techniques of examination. HISTORY CHARACTERISTICS
The element of the history which comes first in the patient's mind, and which usually is the greatest help to the examining physician, has to do with pain. The earliest symptom produced by any chronic, slowly progressing occlusive disease of the peripheral arteries is often intermittent pain. The pain of intermittent claudication type is seldom produced by any other condition than a chronic arterial occlusion. Intermittent claudication displays distinctive characteristics. It is consistently produced in a patient by a certain amount of exercise and relieved by a rest period of constant duration. It is the hall mark of chronic occlusive disease. Constant pain in peripheral arterial disease may be that of ischemic neuritis, the pain of ulceration, or the pain which is produced by an inflammatory disease of an artery adjacent to a nerve which is thereby irritated. Chronic ischemia of peripheral nerves produces a pain which is usually burning in character. In its severe form it is controlled with difficulty even with narcotics. Differentiation between pain of ischemic neuritis and other forms of constant pain may be made with infrequent error on the basis of the effect of position of the extremity on the symptom. In ischemic neuritis the patient has least discomfort when his legs are dependent, and suffers an increase in pain when they are placed in the horizontal position or elevated. He avoids lying down for any significant period with his legs on a level, and will often present himself with edema of the ankles and feet because of his need for sitting up for long periods. From the University of Illinois College of Medicine and the Cardiovascular Surgical Service, St. Luke's Hospital, Chicago. * Associate Professor of Surgery, University of Illinois College of Medicine; Attending Surgeon, St. Luke's Hospital, Chicago.
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The pain of ulceration, which also is constant, is more severe in ulcers produced by ischemia than it is in traumatic ulcers or in ulcers due to stasis disease. This is probably because there is not only an exposure of sensory nerves and inflammatory irritation of the nerves in the bed of the infected ulcer, but also because there is some element of ischemic neuritis. Absence of pain in an ulcer of the foot or hand may raise serious doubt as to the circulatory origin of the ulcer. An outstanding exception to this meaning of the absence of pain occurs in patients who have diabetes in addition to the arterial insufficiency which produced the ulcer. Coincident diabetic neuritis renders the ulcerated area insensitive. Another exception might be the coincidence of an unrelated neurological lesion with a severe arterial insufficiency. Other painless ulcers would be purely those of a neurological lesion without any particular degree of arterial insufficiency. Subjective coldness is an early symptom in arterial insufficiency, but it is a tremendously variable symptom. It may be absent in cases in which the skin of the involved extremity is objectively very cold, or it may be exaggerated in patients whose skin temperature actually is not as yet very much changed. Inasmuch as subjective coldness is a not uncommon complaint of minor nature in patients who have a completely normal arterial system, its meaning is not very great and its cause is not understood. Sensitivity to temperature of the environment is, on the other hand, a very distinctive factor in arterial disease. Sensitivity to cold is most strikingly met with in the vasospastic conditions in which the Raynaud's phenomenon of severe vasoconstriction is present. The history of a frequent exaggerated response to exposure to cold of the hands or feet manifested by color changes which consist of unmistakable blanching of the skin to be followed by stages of cyanosis and rubor before the color returns to normal, is highly suggestive of an organic or a functional arterial disease. When such a reaction is reported in the history given by the patient, it should be substantiated under observation by exposing the part involved to the stimulus which ordinarily produces this change. The differentiation between the functional arterial condition known as Raynaud's disease in which there is no intrinsic arterial involvement in the early stages at least, and those cases of Raynaud's phenomenon in which the underlying disease is arterial or is secondary to a neurological or some related disorder, is of tremendous importance. It almost always can be made on a basis of combination of differences in the history and examination, and will be discussed later. In peripheral arterial disease, then, the elements of the history which are of greatest importance are the pain, subjective coldness, temperature sensitivity, and color change. Of these, the history of pain, in one form or another, alone is really universal.
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GENERAL PHYSICAL EXAMINATION IN RELATION TO ARTERIAL DISEASE
An immediate impression may be gained concerning the arterial system, particularly in respect to its involvement with degenerative disease, by the general inspection of the patient. The apparent age in relation to stated age, the presence of arcus senilis in the corneal edge, and loss of elasticity of the skin are important observations. The absence of all of these in a patient generally alert and youthful in appearance cannot safely be taken to mean freedom from degenerative disease because symptomatic arteriosclerosis of a segmental nature may notoriously occur at an early age or in a patient who otherwise shows little of the changes of age. Examination of the eyegrounds should come early in the routine examination to form an impression of the state of vessels of arteriolar size. The observation is carried more specifically to the skin, studying the skin temperature by the comparison of its temperature with the contralateral side. Diminished temperature in the proximal part of an extremity, as compared to the other side, is essentially always an indication of arterial insufficiency. Diminished skin temperature in the peripheral part of an extremity may occur more frequently as a result of arterial spasm with no underlying intrinsic vascular disease. The skin color of the part involved is noted initially, but more may be learned by observing the response of skin color to changes in position of the limb from elevation to dependency. The response to elevation in normal subjects is a blanching of the color. This normal response is simply added to and prolonged in patients with arterial insufficiency. Comparison of the color of the simultaneously elevated hands or feet is, therefore, of importance. When a normal extremity is brought into a dependent position after a period of elevation, the skin color passes through a brief stage of intensification in returning to normal. This phase of reactive hyperemia is markedly increased in arterial disease. Therefore when the previously elevated limb is depressed the period of pallor is prolonged as compared to the well, or less involved, other side. During the hyperemic reaction the color change is more deeply pink and longer lasting than it is in the normal. It is considered that this is because a more intense anoxemia of the arteriolar and capillary walls occurred in the diseased extremity than in the normal, and the consefluent period of vascular inactivity is greater in degree and extent. Of two limbs unequally involved with arterial insufficiency, the amount of reactive hyperemia will 4e greater in the more severely diseased. It will also be more delayed in this limb. The skin is further examined for evidences of atrophy and thinning. Chronic arterial insufficiency brings about a distinct cutaneous atrophy. Dryness of the skin is an accompaniment of longstanding ischemic neuritis
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which has produced in effect a peripheral sympathectomy. This very frequently also accompanies the diabetic neuritis which is of importance because of the frequent association of diabetes in arteriosclerosis. When gangrene is present its extent and distribution has meaning. The gangrene of arterial insufficiency diminishes in incidence from the most peripheral part of the toes and fingers unless a mechanical or thermal tra.uma has been applied at some proximal point. The extent of the gangrene may vary from the small pinhead size points of gangrene in Raynaud's disease to ischemic necrosis of an entire foot or hand as is seen in occlusive arterial disease. Diminished nutrition of the peripheral parts of the extremity progressively produces atrophy of the small muscles, particularly the intrinsic muscles of the hand and foot. Palpation of the pulses in all their normal locations constitutes the most important phase of the physical examination in relation to arterial lesions. A part of the record of all general physical examinations should include both the positive and negative findings as to the presence of pulses, and also a comparison between the two sides. In an uncounted number of patients full advantage cannot be taken of a prior examination when an arterial disease is suspected as a new condition because of the incompleteness of physical examination records in regard to pulses. Since arterial disease is an extremely common condition, the need for completeness in every record is evident. SPECIAL EXAMINATIONS
Oscillollletry
Special means of examination pertaining to the arterial system are limited in number. Examination of the extremities with an oscillometer provides an important method of recording degree of circulation for comparing the two sides and for determining at exactly what level the arterial occlusion is functionally important. The oscillometer may provide information as to the presence of normal circulation in patients having so much edema that the pulses are obscured by the swelling. The blood pressure type of oscillometers which are currently in use are so designed as to give readings of the oscillometric index at various inflation pressures of the cuff. Comparative readings made at different times with the same oscillometer will provide a rather crude method of following the course of improvement or deterioration of the circulation in the extremity. Changes within a narrow range are not reliable because differences in wrapping of the cuff alone I\lay vary the readings. Oscillometric indices taken with different instruments cannot be compared at all because of the variation in reading from one to another. Finally, it should be remembered that the oscillometer is only an aid to supplement the observations made by palpation and inspection, and is not a substitute for a good examination.
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Response to Vasodilatation
Observation of the degree to which the blood supply of an affected part may be increased by inducing maximum vasodilatation serves several purposes. The degree of vasodilatation produced by one of several methods may be so great as to indicate that the arteries themselves are normal and that the apparent arterial insufficiency is due to chronic vasoconstriction or abnormally high vasomotor tonus. Lesser amounts of increased circulation can be interpreted in the light of the extent of the arterial disease and give a clue as to the benefits which may be obtained by totally removing the reflex vasomotor tone by doing an appropriate sympathectomy. Such dilatation can be produced by bringing about a reflex vasodilatation. This is most conveniently done by the simple application of heat to the central parts of the body, the abdomen and chest, for sufficient length of time to cause warming and heightening of the color of the skin of the feet. A sympathetic block done in the lumbar region for the leg and in the region of the second and third dorsal ganglia or stellate ganglion for the upper extremity, is another convenient method for making such observation. Peripheral nerve block done at the level of the posterior tibial nerve for the lower extremity and the ulnar for the upper produces sympathetic paralysis in the limited region and may be done as an office procedure. The results from a peripheral nerve block are somewhat handicapped by the fact that cutaneous anesthesia is also produced and the result therefore cannot be interpreted in the light of relief from pain. The reading of the effect of vasodilatation may be made by comparing skin temperature observations, by noting the changes which occur in the palpable pulses or by following the result with an oscillometer or plethysmograph, the oscillometer being, of course, left in place throughout the observation to avoid differences in the wrapping of the cuff. In an extremity having normal blood vessels in an increased state of spasm, the response in skin temperature is as great as 10° to 15° C. In moderate degrees of arterial insufficiency the rise varies between 3° and 8° C. In advanced arterial insufficiency there may be no rise at all, a slight fall, or a meager rise of 1° to U-2°. These methods of observing the changes secondary to vasodilatation are useful only in the absence of an inflammatory process in the areas supplied by the diseased vessels. If inflammation is present it is unlikely that very much further vasodilatation will occur than that which is already present in response to the infection. Biopsy
Biopsy is sometimes a useful method in diagnosis in arterial disease. It is unusual that any opportunity will arise to biopsy the involved vessels themselves. During the course of direct surgical treatment of occlusive arterial disease a portion of artery is often removed and its examination
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Ormand C. Julian 182 provide s a clear patholo gical picture of the change in the vessel. The lesions of superficial phlebit is which occur with Buerge r's disease are frequen tly biopsied. Histological findings charact eristic of Buerge r's lesions as they are seen in the arteries are seldom observed. In an occasional instanc e the inflamm ation of all coats of the vein with prolife ration of giant cells and absorp tion by the develo pment of fibrosis of the media and organiz ation of intralu minal clot may be seen. In most instanc es the superficial phlebit is of Buerge r's disease is morphologically indistin guishable from any segmen tal superficial phlebit is. Muscle biopsy in periart eritis nodosa and, in erythem a nodosum, biopsy of the cutaneo us nodule s may be diagnostic.
Fig. 39. X-ray of both feet on single film to compare bone density in case of posttraumat ic sympath etic dystroph y. Right foot shows distinct osteopor osis.
X-ray Study
The x-ray finding most commo nly associa ted with arterial disease is the disclosure of calcification of the wall of blood vessels involve d in arteriosclerosis oblitera ns or in aneury sm second ary to degene rative arteriosclerosis. Displac ements of surroun ding structu res by aneury smal dilatati on gives a clue to their size and identity . The bone change s seen in x-rays in arterial disease are those of the complications of the disease rather than being charact eristic of the lesions themselves. These consist of finding of osteom yelitis in relation to ischemic necrosis of a part of an
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extremity and the osteoporosis which is observed in patients showing disuse atrophy because of pain of an arterial lesion or the pain of a reflex vasomotor dystrophy. (Fig. 39). Angiography
The most important aid to the diagnosis of arterial disease is found in angiography, particularly in accurately delineating the degree of involvement and its location. This takes the form of angiocardio~raphy and aortography for central lesions and peripheral arteriography for the lesions of the arteries of the extremity. These techniques have recently been described in this publication (February 1955) and will not be repeated here. The various types of angiography enjoy a wide use and the information gained is extremely beneficial. They should not, however, through familiarity become indiscriminately used. Each of the techniques offers certain very distinct, though fortunately infrequent, complications. THE MAJOR DIFFERENTIAL DIAGNOSES
This outline of the general and specific factors in the diagnosis of arterial disease forms a schema upon which these conditions may be at first suspected and then verified. They also form the background for the next, more challenging, step in diagnosis; that is, of making what may be termed the major differential diagnosis in arterial disease. These can be listed as follows: the differentiation of arteriosclerosis from Buerger's disease; Raynaud's disease from Raynaud's phenomenon secondary to something else; acute arterial occlusion due to an embolus from acute arterial occlusion due to thrombosis; acute arterial occlusion from spasm due to trauma or acute thrombophlebitis; abdominal aneurysm from abdominal tumor; and thoracic aneurysm from mediastinal tumor. Arteriosclerosis Obliterans-Buerger's Disease
These are totally different entities. Arteriosclerosis is a degenerative disease in which thickening of the media and intima of the blood vessels leads to narrowing of the lumen which finally becomes obstructed by a thrombus. Buerger's disease is an inflammatory condition which involves all of the coats of the vessel, the adjacent vein and nerve, bringing about occlusion of the arterial lumen and the vein lumen by a thrombus. Arteriosclerosis may involve vessels of all sizes, but in its common form is characteristically a lesion of medium and large size vessels. Itil onset is insidious and in the majority of cases leads to the initial symptom of intermittent claudication before any signs of peripheral ischemia are present. Buerger's disease, on the other hand, is a lesion characteristically of small sized arteries, such as the ulnar, radial, and the lower portions of the anterior and posterior tibial arteries. The early signs of Buerger's disease are often inflammation and ischemia in the peripheral part of the
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extrem ity, and interm ittent claudic ation is a less frequen t initial complaint. Both diseases show a greater occurrence in males than females, but in Buerge r's disease the prepon deranc e is overwhelming. The age of onset of sympto ms separat es the two diseases by 15 to 20 years, that of Buerger's disease being commo n in the second and third decades, while the onset of arteriosclerosis usually occurs over the age of 40. The diagnos is of Buerge r's disease must be questio ned when it is made in the case of a patient who does not use tobacco. A search for evidence of some degree of generalized arteriosclerosis should be made, examin ing the eyegro unds
r Fig. 40. Translumbar aortogram showing complete occlusion of right common iliac artery at aortic bifurcati on. The accurate localizat ion by this techniqu e guided surgical correctio n of the obstruct ion.
for arterio lar changes, and the vessels of the abdom en and lower extremiti es by x-ray for signs of calcification. Arteriosclerosis obliter ans is associa ted with early loss of pulsati ons in the major vessels of the extremity , while in Buerge r's disease it is uncom mon for the poplite al pulse to be absent or the brachia l artery pulse lost before severe change s have appear ed periphe rally. The presenc e or history of the occurrence of superficial phlebit is indicat es Buerge r's disease. Arterio grams in arteriosclerosis routine ly show high arterial occlusi on or narrow ing by the develo pment of filling defects in such major vessels as the superficial femoral, iliac or aortic bifurca tion (Fig. 40). In Buerge r's disease the arteries down to mid-ca lf or nearly to the wrist are usually open, and fill smooth ly with the contras t medium , while the localiza tion
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in the smaller vessels is shown by their failure to fill. A demonstration of segmental occlusion in a large artery is unusual in Buerger's disea.se. Raynaud's Disease--Raynaud's PhenOlnenon
It is well recognized that the initial reports of Raynaud on symmetrical gangrene associated with severe attacks of arterial spasm in the hands and feet contain not only cases which may still be called Raynaud's disease but also instances of arteriosclerosis and Buerger's disease in which vasospastic phenomena were marked. The term "Raynaud's disease" is now confined to those cases demonstrating the typical changes of acute vascular syncope of the extremity in which the initiating lesion is not a morphological change in the vessel. The cause of the attacks is considered to be either an increased local sensitivity to stimuli which normally produce vasoconstriction or a pathological reinforcement of the reflex mechanism which responds to the stimulus. The cause of this heightened functional response remains unknown. Certain arterial disease, principally arteriosclerosis and Buerger's disease, as well as such neurological conditions as a herniated intervertebral disk, scalenus anticus syndrome, or posttraumatic sympathetic dystrophy, may bring about color changes in response to cold or emotional stimuli identical to those of Raynaud's disease. Other conditions which are commonly the cause of attacks similar to those seen in Raynaud's disease are early scleroderma, trauma from continuous use of pneumatic tools, and heavy metal poisoning. The differentiation between Raynaud's disease of idiopathic etiology and Raynaud's phenomenon on the basis of some other condition is important. Raynaud's disease itself is remarkably symmetrical. The course is one in which there is a progressive lessening of the severity of cold application or emotional stimulus needed to cause one of the attacks. For a long time after the onset there is no demonstrable change in the parts involved except during the course of an attack. Late in the disease some atrophy of the skin and loss of substance of the distal part of the digits occurs and very small pinhead-sized areas of gangrene may develop on the tips of the fingers or toes. It is important to note that the palpable pulses in the extremity are not disturbed in Raynaud's disease. Any remarkable deviation from the symmetrical nature of the attacks should immediately arouse the suspicion that there is an underlying disease. The great preponderance of Raynaud's disease in females renders the diagnosis suspect when the attacks occur in a man. Any loss of pulses at the wrist or ankle would be uncharacteristic of Raynaud's disease and indicates that the attacks seen are Raynaud's phenomena on the basis of either Buerger's disease or arteriosclerosis. The presence of gangmne of greater than the minute extent indicated above, indicates an arterial disease. Early thickening of the skin and stiffness of the joints, particu-
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larly of the hands, suggests that the attacks are those of Raynaud's phenomenon on the basis of a scleroderma. Neurological changes of anesthesia, muscle atrophy or weakness indicates a scalenus anticus syndrome or a herniated intervertebral disk. An outstanding characteristic of Raynaud's disease is that there is no pain. During the course of the attack there will be discomfort and some numbness if the attack is lasting, but the presence of pain, either during or between attacks, is a strong indication contrary to Raynaud's disease. ElDbolislD-Arterial ThrolDbosis
An acute arterial occlusion, whether it is due to embolism or to thrombosis of an arteriosclerotic segment of the artery, represents a surgical emergency requiring operative relief of the obstruction. Success in removal of an embolus far outstrips the success in relieving obstruction when it is due to thrombosis and arteriosclerosis. Preparations needed for maximum hope of success in removing a thrombotic occlusion include having in readiness a suitable vascular segment for use as a graft, if it should be needed, and in general the preparations in this instance are far greater than those required for removal of an embolus. The differentiation of the cause of an acute arterial occlusion is, therefore, important and although it is not always possible, should be sought in every case. In a high proportion of cases in which the causation is an embolus, a cardiac lesion will be demonstrable to explain the source of the embolus. The common ones are auricular fibrillation on the basis of mitral stenosis, arteriosclerotic heart disease, or a metabolic disease, such as hyperthyroidism. The mural thrombi which form over a myocardial infarct after a coronary occlusion provide another frequent source of peripheral arterial emboli. Spontaneous intracardiac mural thrombi undoubtedly explain a number of peripheral emboli, but this possibility does not aid in the differentiation between the two diseases. The final source of emboli is the formation of an intraluminal clot along the wall of the aorta in the presence of ulcerative arteriosclerosis. This similarly does not help in the differential diagnosis because it cannot be diagnosed accurately in the living patient. In the absence of a cardiac lesion which may be suspected as the source of an embolus a differentiation may be suggested by the acuteness of the onset and the severity of the ischemic symptoms in relation to the size of the vessel obstructed. The lodgment of the embolus causes an acute and severe reflex vasoconstriction which accentuates the degree of occlusion produced by the arterial block. The symptoms are rapid in onset and, since the spasm to a large extent inactivates the collateral bed, they are entirely in keeping with the level of occlusion or may extend higher than the level of occlusien would. indicate. On the other hand, a thrombosis of
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an arteriosclerotic segment usually occurs after a long period of gradual narrowing at the site of the obstruction. The thrombosis then may be of a lumen which is already considerably narrowed. There is no sudden expansile irritation to the artery and the degree of reflex vasoconstriction is minimal as compared to embolism. This comparative lack of reflex arterial spasm and the prior development of the collateral arterial bed, because of the gradual occlusion, makes the onset of symptoms more benign and the severity of the ischemia may fail to correspond to the size of the vessel involved. Another factor which intensifies the reaction to occlusion in embolism is that an embolus usually lodges at a major bifurcation. Therefore, it often occludes a large artery such as the superficial femoral artery, while at the same time it mechanically blocks the major collateral vessel for this channel, namely the profunda femoris. On the other hand, an arterial thrombosis of the superficial femoral artery usually occurs at such a level as to spare the major collateral. In the superficial femoral artery, as an example, the occlusion is most common at the adductor hiatus or immediately below the profunda femoris branch of the common femoral. These differences allow a fairly meager basis for differentiation and thrombosis and embolus will be finally diagnosed in many cases only when the area is explored as it should be for relief of the obstruction. Acute Arterial Occlusion-Arterial Spaslll Secondary to Traullla, Acute Throlllbophlebitis, Etc.
Loss of peripheral pulses, pallor of the skin, some degree of sensory change and paralysis of the muscles of the foot or arm may be present to simulate an anatomical acute occlusion of an artery in a variety of conditions in which acute occlusion is not actually present. Accurate diagnosis in these cases is sometimes difficult, but is particularly important in order that the patient will be spared a useless exploration of a supposedly occluded artery. Three conditions are most troublesome because of their frequency and their ability to simulate occlusion. Included in these three is the arterial spasm which accompanies trauma. The problem here is to determine whether vasospasm or an arterial lesion such as an intramural thrombosis has been caused by trauma. The second common condition is seen in the early stages of many caseE of acute deep thrombophlebitis of the lower extremity in which the vascular spasm is intense and accounts for much of the pain of the phlebitis at this stage. The third situation is seen in patients who have recently suffered a myocardial infarction. If such a patient has also a degree of arteriosclerosis of an extremity, the reduction in cardiac output and fall in arterial blood pressure may bring about such a depression of circulation in the extremity through its diseased arteries that an acute occlusion is very strongly suggested.
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The differential diagnosis in the case of trauma is satisfactorily made by studying the response of skin temperature and the return of pulses when a sympathetic block is done. Occasionally it will be desirable to obtain an . arteriogram of the part to make the differential diagnosis (Fig. 41). The differentiation in acute thrombophlebitis will be made very quickly on the basis of a sympathetic block which will usually bring about a warming of the extremity to a point in excess of the temperature of the opposite leg and will, in addition, have the virtue of relieving most of the patient's pain. The pulses incidentally should return after a sympathetic block in the early so-called white stage of thrombophlebitis.
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Fig. 41. A, Traumatic intramural hematoma of popliteal artery diagnosed by arteriogram. B, Arteriogram made 1 month after repair.
The problem in judgment in the case of a patient whose extremity simulates an acute occlusion during the depression of blood pressure following a Iryocardial infarct is very difficult. If the supposed occlusion is observed early after its onset, a tendency to fluctuate in severity may be watched for as the patient's blood pressure improves. It is also important to note that most peripheral emboli in cases of coronary occlusion occur during the fifth to eighth day after the heart attack, when the mural thrombus has had an opportunity to form in the heart. An apparent arterial embolism within the first 24 hours after a coronary occlusion is less apt to be real than one that occurs at the end of a week. The signs of arterial occlusion, if they are due to the depression in circulation, are
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unlikely to be progressive. A fundamental difficulty in this situation is that, if the blood pressure continues to be depressed in the presence of peripheral arteriosclerosis, the simulated occlusion may become real because of intra-arterial thrombosis. It has been amply demonstrated that in such cases the removal of the occluding clot is infrequently successful because, after removal, the same mechanism of depressed blood pressure is in effect and the clot reforms. Ahdolllinal AneUrYSlll-Ahdolllinal TUlllor
Errors in differentiating midline tumors of the abdomen and arteriosclerotic aneurysms of the abdominal aorta have occurred three times in
B A Fig. 42. A, Translumbar aortogram of abdominal aortic aneurysm. B, Postoperative aortogram in same case after resection and homologous artery graft.
our series of 40 cases of aneurysms considered for resection. Two of these occurred in relation to congenital deformities of the kidney. One horseshoe kidney and one pelvic disk-shaped kidney were found at operation, both in relation to a mild aneurysmal dilatation of the aorta. In neither case was the underlying aneurysm resectable because the blood supply for the kidney arose from multiple arteries coming from the portion of the aorta which would have had to be resected. The obvious aid in diagnosis indicated here is an intravenous pyelogram. This had been done in the case of the horseshoe kidney and the true nature of the renal deformity was not diagnosed on the film. In the case of the pelvic kidney pyelography had not been done. The third error in diagnosis proved to be a large m(;)tastatic nodule arising from a primary tumor in the testicle of the patient. The testicular tumor was very small and was found only after the microscopic diagnosis had been made on the metastatic lesion.
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Fig. 43. Chest x-ray of mediastinal mass proved at operation to be arteriosclerotic aneurysm. No distinct expansile pulse was seen on .fluoroscopy.
Fig. 44. A, Dr.1wing of aneurysm shown in Figure 43. Direct observation showed only slight expansile pUlsation until compressed by palpating hand. B, C, Schema of successful resection and graft.
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It is evident that our diagnostic acumen in distinguishing abdominal aneurysm -from tumor is not infallible. The aids in diagnosis include demonstration of the calcified wall of an aneurysm and displacement of the viscera as shown by x-rays of the abdomen taken both in the anteroposterior and lateral directions. Intravenous urography aids not only in ruling out the unusual finding of a deformed kidney, but also in visualizing the ureters which are characteristically displaced by an aneurysm. Aortography does not need routinely to be done, but provides a typical picture of an aortic aneurysm when it is used. In interpreting the findings in an aortogram of an abdominal aneurysm the Diodrast-filled portion of the aneurysm will be found to be quite small in relation to theactual size of the lesion because of the filling-in of much of the expanded vessel with blood clot, leaving a smaller passage for the flow of blood through the aneurysm. Aortography also provides a means of visualizing the graft used in replacing the aortic bifurcation after removal of the aneurysm (Fig. 42, A, B). Thoracic AneuryslIl-Mediastinal TUlllor
The ability of an aneurysm to fill either the anterior or posterior mediastinum superiorly, or any portion of the mediastinum inferiorly, produces instances in which it is difficult to distinguish between aneurysm a.nd a solitary mediastinal tumor which has a smooth contour. On fluoroscopy expansile pulsations are most difficult to see and distinguish from simple motion transmitted from the heart action. Because of their contained pressure and the inelasticity of the vessel wall which is actually the cause of an aneurysm, expansile pulsations are not remarkable even at the time of operation when the aneurysm is palpated by the surgeon. Unless the wall to the lesion is compressed by the palpating hand the pulsations are not great. At fluoroscopy, therefore, not too much can be expected from this observation (Fig. 43). Good differentiation in difficult cases depends upon angiocardiography done either by the intravenous injection of Diodrast in the brachial vein of one of the arms, or more directly, by its injection through a catheter which has been introduced intra-arterially into the region of the lesion. The history of syphilis or the presence of a positive blood or spinal fluid serology is helpful except in the few cases of arteriosclerotic thoracic aneurysm. In arteriosclerotic aneurysm there is usually on x-ray a visible elongation and, therefore, widening of the loop of the arch of the aorta. The final diagnosis of aneurysm or tumor may sometimes only be made at the time of surgical exploration for resection of the lesion (Fig. 44). 25 E. Washington Street Chicago 2, Illinois.
M.~.,
PH.D.*
THE diagnosis of arterial disease depends upon pursuit and analysis of aspects of the history of the illness which are suggestive of these conditions, the appreciation of specific findings during the course of a complete general physical examination, and finally upon the application of a rather limited number of special techniques of examination. HISTORY CHARACTERISTICS
The element of the history which comes first in the patient's mind, and which usually is the greatest help to the examining physician, has to do with pain. The earliest symptom produced by any chronic, slowly progressing occlusive disease of the peripheral arteries is often intermittent pain. The pain of intermittent claudication type is seldom produced by any other condition than a chronic arterial occlusion. Intermittent claudication displays distinctive characteristics. It is consistently produced in a patient by a certain amount of exercise and relieved by a rest period of constant duration. It is the hall mark of chronic occlusive disease. Constant pain in peripheral arterial disease may be that of ischemic neuritis, the pain of ulceration, or the pain which is produced by an inflammatory disease of an artery adjacent to a nerve which is thereby irritated. Chronic ischemia of peripheral nerves produces a pain which is usually burning in character. In its severe form it is controlled with difficulty even with narcotics. Differentiation between pain of ischemic neuritis and other forms of constant pain may be made with infrequent error on the basis of the effect of position of the extremity on the symptom. In ischemic neuritis the patient has least discomfort when his legs are dependent, and suffers an increase in pain when they are placed in the horizontal position or elevated. He avoids lying down for any significant period with his legs on a level, and will often present himself with edema of the ankles and feet because of his need for sitting up for long periods. From the University of Illinois College of Medicine and the Cardiovascular Surgical Service, St. Luke's Hospital, Chicago. * Associate Professor of Surgery, University of Illinois College of Medicine; Attending Surgeon, St. Luke's Hospital, Chicago.
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The pain of ulceration, which also is constant, is more severe in ulcers produced by ischemia than it is in traumatic ulcers or in ulcers due to stasis disease. This is probably because there is not only an exposure of sensory nerves and inflammatory irritation of the nerves in the bed of the infected ulcer, but also because there is some element of ischemic neuritis. Absence of pain in an ulcer of the foot or hand may raise serious doubt as to the circulatory origin of the ulcer. An outstanding exception to this meaning of the absence of pain occurs in patients who have diabetes in addition to the arterial insufficiency which produced the ulcer. Coincident diabetic neuritis renders the ulcerated area insensitive. Another exception might be the coincidence of an unrelated neurological lesion with a severe arterial insufficiency. Other painless ulcers would be purely those of a neurological lesion without any particular degree of arterial insufficiency. Subjective coldness is an early symptom in arterial insufficiency, but it is a tremendously variable symptom. It may be absent in cases in which the skin of the involved extremity is objectively very cold, or it may be exaggerated in patients whose skin temperature actually is not as yet very much changed. Inasmuch as subjective coldness is a not uncommon complaint of minor nature in patients who have a completely normal arterial system, its meaning is not very great and its cause is not understood. Sensitivity to temperature of the environment is, on the other hand, a very distinctive factor in arterial disease. Sensitivity to cold is most strikingly met with in the vasospastic conditions in which the Raynaud's phenomenon of severe vasoconstriction is present. The history of a frequent exaggerated response to exposure to cold of the hands or feet manifested by color changes which consist of unmistakable blanching of the skin to be followed by stages of cyanosis and rubor before the color returns to normal, is highly suggestive of an organic or a functional arterial disease. When such a reaction is reported in the history given by the patient, it should be substantiated under observation by exposing the part involved to the stimulus which ordinarily produces this change. The differentiation between the functional arterial condition known as Raynaud's disease in which there is no intrinsic arterial involvement in the early stages at least, and those cases of Raynaud's phenomenon in which the underlying disease is arterial or is secondary to a neurological or some related disorder, is of tremendous importance. It almost always can be made on a basis of combination of differences in the history and examination, and will be discussed later. In peripheral arterial disease, then, the elements of the history which are of greatest importance are the pain, subjective coldness, temperature sensitivity, and color change. Of these, the history of pain, in one form or another, alone is really universal.
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GENERAL PHYSICAL EXAMINATION IN RELATION TO ARTERIAL DISEASE
An immediate impression may be gained concerning the arterial system, particularly in respect to its involvement with degenerative disease, by the general inspection of the patient. The apparent age in relation to stated age, the presence of arcus senilis in the corneal edge, and loss of elasticity of the skin are important observations. The absence of all of these in a patient generally alert and youthful in appearance cannot safely be taken to mean freedom from degenerative disease because symptomatic arteriosclerosis of a segmental nature may notoriously occur at an early age or in a patient who otherwise shows little of the changes of age. Examination of the eyegrounds should come early in the routine examination to form an impression of the state of vessels of arteriolar size. The observation is carried more specifically to the skin, studying the skin temperature by the comparison of its temperature with the contralateral side. Diminished temperature in the proximal part of an extremity, as compared to the other side, is essentially always an indication of arterial insufficiency. Diminished skin temperature in the peripheral part of an extremity may occur more frequently as a result of arterial spasm with no underlying intrinsic vascular disease. The skin color of the part involved is noted initially, but more may be learned by observing the response of skin color to changes in position of the limb from elevation to dependency. The response to elevation in normal subjects is a blanching of the color. This normal response is simply added to and prolonged in patients with arterial insufficiency. Comparison of the color of the simultaneously elevated hands or feet is, therefore, of importance. When a normal extremity is brought into a dependent position after a period of elevation, the skin color passes through a brief stage of intensification in returning to normal. This phase of reactive hyperemia is markedly increased in arterial disease. Therefore when the previously elevated limb is depressed the period of pallor is prolonged as compared to the well, or less involved, other side. During the hyperemic reaction the color change is more deeply pink and longer lasting than it is in the normal. It is considered that this is because a more intense anoxemia of the arteriolar and capillary walls occurred in the diseased extremity than in the normal, and the consefluent period of vascular inactivity is greater in degree and extent. Of two limbs unequally involved with arterial insufficiency, the amount of reactive hyperemia will 4e greater in the more severely diseased. It will also be more delayed in this limb. The skin is further examined for evidences of atrophy and thinning. Chronic arterial insufficiency brings about a distinct cutaneous atrophy. Dryness of the skin is an accompaniment of longstanding ischemic neuritis
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which has produced in effect a peripheral sympathectomy. This very frequently also accompanies the diabetic neuritis which is of importance because of the frequent association of diabetes in arteriosclerosis. When gangrene is present its extent and distribution has meaning. The gangrene of arterial insufficiency diminishes in incidence from the most peripheral part of the toes and fingers unless a mechanical or thermal tra.uma has been applied at some proximal point. The extent of the gangrene may vary from the small pinhead size points of gangrene in Raynaud's disease to ischemic necrosis of an entire foot or hand as is seen in occlusive arterial disease. Diminished nutrition of the peripheral parts of the extremity progressively produces atrophy of the small muscles, particularly the intrinsic muscles of the hand and foot. Palpation of the pulses in all their normal locations constitutes the most important phase of the physical examination in relation to arterial lesions. A part of the record of all general physical examinations should include both the positive and negative findings as to the presence of pulses, and also a comparison between the two sides. In an uncounted number of patients full advantage cannot be taken of a prior examination when an arterial disease is suspected as a new condition because of the incompleteness of physical examination records in regard to pulses. Since arterial disease is an extremely common condition, the need for completeness in every record is evident. SPECIAL EXAMINATIONS
Oscillollletry
Special means of examination pertaining to the arterial system are limited in number. Examination of the extremities with an oscillometer provides an important method of recording degree of circulation for comparing the two sides and for determining at exactly what level the arterial occlusion is functionally important. The oscillometer may provide information as to the presence of normal circulation in patients having so much edema that the pulses are obscured by the swelling. The blood pressure type of oscillometers which are currently in use are so designed as to give readings of the oscillometric index at various inflation pressures of the cuff. Comparative readings made at different times with the same oscillometer will provide a rather crude method of following the course of improvement or deterioration of the circulation in the extremity. Changes within a narrow range are not reliable because differences in wrapping of the cuff alone I\lay vary the readings. Oscillometric indices taken with different instruments cannot be compared at all because of the variation in reading from one to another. Finally, it should be remembered that the oscillometer is only an aid to supplement the observations made by palpation and inspection, and is not a substitute for a good examination.
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Response to Vasodilatation
Observation of the degree to which the blood supply of an affected part may be increased by inducing maximum vasodilatation serves several purposes. The degree of vasodilatation produced by one of several methods may be so great as to indicate that the arteries themselves are normal and that the apparent arterial insufficiency is due to chronic vasoconstriction or abnormally high vasomotor tonus. Lesser amounts of increased circulation can be interpreted in the light of the extent of the arterial disease and give a clue as to the benefits which may be obtained by totally removing the reflex vasomotor tone by doing an appropriate sympathectomy. Such dilatation can be produced by bringing about a reflex vasodilatation. This is most conveniently done by the simple application of heat to the central parts of the body, the abdomen and chest, for sufficient length of time to cause warming and heightening of the color of the skin of the feet. A sympathetic block done in the lumbar region for the leg and in the region of the second and third dorsal ganglia or stellate ganglion for the upper extremity, is another convenient method for making such observation. Peripheral nerve block done at the level of the posterior tibial nerve for the lower extremity and the ulnar for the upper produces sympathetic paralysis in the limited region and may be done as an office procedure. The results from a peripheral nerve block are somewhat handicapped by the fact that cutaneous anesthesia is also produced and the result therefore cannot be interpreted in the light of relief from pain. The reading of the effect of vasodilatation may be made by comparing skin temperature observations, by noting the changes which occur in the palpable pulses or by following the result with an oscillometer or plethysmograph, the oscillometer being, of course, left in place throughout the observation to avoid differences in the wrapping of the cuff. In an extremity having normal blood vessels in an increased state of spasm, the response in skin temperature is as great as 10° to 15° C. In moderate degrees of arterial insufficiency the rise varies between 3° and 8° C. In advanced arterial insufficiency there may be no rise at all, a slight fall, or a meager rise of 1° to U-2°. These methods of observing the changes secondary to vasodilatation are useful only in the absence of an inflammatory process in the areas supplied by the diseased vessels. If inflammation is present it is unlikely that very much further vasodilatation will occur than that which is already present in response to the infection. Biopsy
Biopsy is sometimes a useful method in diagnosis in arterial disease. It is unusual that any opportunity will arise to biopsy the involved vessels themselves. During the course of direct surgical treatment of occlusive arterial disease a portion of artery is often removed and its examination
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Ormand C. Julian 182 provide s a clear patholo gical picture of the change in the vessel. The lesions of superficial phlebit is which occur with Buerge r's disease are frequen tly biopsied. Histological findings charact eristic of Buerge r's lesions as they are seen in the arteries are seldom observed. In an occasional instanc e the inflamm ation of all coats of the vein with prolife ration of giant cells and absorp tion by the develo pment of fibrosis of the media and organiz ation of intralu minal clot may be seen. In most instanc es the superficial phlebit is of Buerge r's disease is morphologically indistin guishable from any segmen tal superficial phlebit is. Muscle biopsy in periart eritis nodosa and, in erythem a nodosum, biopsy of the cutaneo us nodule s may be diagnostic.
Fig. 39. X-ray of both feet on single film to compare bone density in case of posttraumat ic sympath etic dystroph y. Right foot shows distinct osteopor osis.
X-ray Study
The x-ray finding most commo nly associa ted with arterial disease is the disclosure of calcification of the wall of blood vessels involve d in arteriosclerosis oblitera ns or in aneury sm second ary to degene rative arteriosclerosis. Displac ements of surroun ding structu res by aneury smal dilatati on gives a clue to their size and identity . The bone change s seen in x-rays in arterial disease are those of the complications of the disease rather than being charact eristic of the lesions themselves. These consist of finding of osteom yelitis in relation to ischemic necrosis of a part of an
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extremity and the osteoporosis which is observed in patients showing disuse atrophy because of pain of an arterial lesion or the pain of a reflex vasomotor dystrophy. (Fig. 39). Angiography
The most important aid to the diagnosis of arterial disease is found in angiography, particularly in accurately delineating the degree of involvement and its location. This takes the form of angiocardio~raphy and aortography for central lesions and peripheral arteriography for the lesions of the arteries of the extremity. These techniques have recently been described in this publication (February 1955) and will not be repeated here. The various types of angiography enjoy a wide use and the information gained is extremely beneficial. They should not, however, through familiarity become indiscriminately used. Each of the techniques offers certain very distinct, though fortunately infrequent, complications. THE MAJOR DIFFERENTIAL DIAGNOSES
This outline of the general and specific factors in the diagnosis of arterial disease forms a schema upon which these conditions may be at first suspected and then verified. They also form the background for the next, more challenging, step in diagnosis; that is, of making what may be termed the major differential diagnosis in arterial disease. These can be listed as follows: the differentiation of arteriosclerosis from Buerger's disease; Raynaud's disease from Raynaud's phenomenon secondary to something else; acute arterial occlusion due to an embolus from acute arterial occlusion due to thrombosis; acute arterial occlusion from spasm due to trauma or acute thrombophlebitis; abdominal aneurysm from abdominal tumor; and thoracic aneurysm from mediastinal tumor. Arteriosclerosis Obliterans-Buerger's Disease
These are totally different entities. Arteriosclerosis is a degenerative disease in which thickening of the media and intima of the blood vessels leads to narrowing of the lumen which finally becomes obstructed by a thrombus. Buerger's disease is an inflammatory condition which involves all of the coats of the vessel, the adjacent vein and nerve, bringing about occlusion of the arterial lumen and the vein lumen by a thrombus. Arteriosclerosis may involve vessels of all sizes, but in its common form is characteristically a lesion of medium and large size vessels. Itil onset is insidious and in the majority of cases leads to the initial symptom of intermittent claudication before any signs of peripheral ischemia are present. Buerger's disease, on the other hand, is a lesion characteristically of small sized arteries, such as the ulnar, radial, and the lower portions of the anterior and posterior tibial arteries. The early signs of Buerger's disease are often inflammation and ischemia in the peripheral part of the
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extrem ity, and interm ittent claudic ation is a less frequen t initial complaint. Both diseases show a greater occurrence in males than females, but in Buerge r's disease the prepon deranc e is overwhelming. The age of onset of sympto ms separat es the two diseases by 15 to 20 years, that of Buerger's disease being commo n in the second and third decades, while the onset of arteriosclerosis usually occurs over the age of 40. The diagnos is of Buerge r's disease must be questio ned when it is made in the case of a patient who does not use tobacco. A search for evidence of some degree of generalized arteriosclerosis should be made, examin ing the eyegro unds
r Fig. 40. Translumbar aortogram showing complete occlusion of right common iliac artery at aortic bifurcati on. The accurate localizat ion by this techniqu e guided surgical correctio n of the obstruct ion.
for arterio lar changes, and the vessels of the abdom en and lower extremiti es by x-ray for signs of calcification. Arteriosclerosis obliter ans is associa ted with early loss of pulsati ons in the major vessels of the extremity , while in Buerge r's disease it is uncom mon for the poplite al pulse to be absent or the brachia l artery pulse lost before severe change s have appear ed periphe rally. The presenc e or history of the occurrence of superficial phlebit is indicat es Buerge r's disease. Arterio grams in arteriosclerosis routine ly show high arterial occlusi on or narrow ing by the develo pment of filling defects in such major vessels as the superficial femoral, iliac or aortic bifurca tion (Fig. 40). In Buerge r's disease the arteries down to mid-ca lf or nearly to the wrist are usually open, and fill smooth ly with the contras t medium , while the localiza tion
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in the smaller vessels is shown by their failure to fill. A demonstration of segmental occlusion in a large artery is unusual in Buerger's disea.se. Raynaud's Disease--Raynaud's PhenOlnenon
It is well recognized that the initial reports of Raynaud on symmetrical gangrene associated with severe attacks of arterial spasm in the hands and feet contain not only cases which may still be called Raynaud's disease but also instances of arteriosclerosis and Buerger's disease in which vasospastic phenomena were marked. The term "Raynaud's disease" is now confined to those cases demonstrating the typical changes of acute vascular syncope of the extremity in which the initiating lesion is not a morphological change in the vessel. The cause of the attacks is considered to be either an increased local sensitivity to stimuli which normally produce vasoconstriction or a pathological reinforcement of the reflex mechanism which responds to the stimulus. The cause of this heightened functional response remains unknown. Certain arterial disease, principally arteriosclerosis and Buerger's disease, as well as such neurological conditions as a herniated intervertebral disk, scalenus anticus syndrome, or posttraumatic sympathetic dystrophy, may bring about color changes in response to cold or emotional stimuli identical to those of Raynaud's disease. Other conditions which are commonly the cause of attacks similar to those seen in Raynaud's disease are early scleroderma, trauma from continuous use of pneumatic tools, and heavy metal poisoning. The differentiation between Raynaud's disease of idiopathic etiology and Raynaud's phenomenon on the basis of some other condition is important. Raynaud's disease itself is remarkably symmetrical. The course is one in which there is a progressive lessening of the severity of cold application or emotional stimulus needed to cause one of the attacks. For a long time after the onset there is no demonstrable change in the parts involved except during the course of an attack. Late in the disease some atrophy of the skin and loss of substance of the distal part of the digits occurs and very small pinhead-sized areas of gangrene may develop on the tips of the fingers or toes. It is important to note that the palpable pulses in the extremity are not disturbed in Raynaud's disease. Any remarkable deviation from the symmetrical nature of the attacks should immediately arouse the suspicion that there is an underlying disease. The great preponderance of Raynaud's disease in females renders the diagnosis suspect when the attacks occur in a man. Any loss of pulses at the wrist or ankle would be uncharacteristic of Raynaud's disease and indicates that the attacks seen are Raynaud's phenomena on the basis of either Buerger's disease or arteriosclerosis. The presence of gangmne of greater than the minute extent indicated above, indicates an arterial disease. Early thickening of the skin and stiffness of the joints, particu-
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larly of the hands, suggests that the attacks are those of Raynaud's phenomenon on the basis of a scleroderma. Neurological changes of anesthesia, muscle atrophy or weakness indicates a scalenus anticus syndrome or a herniated intervertebral disk. An outstanding characteristic of Raynaud's disease is that there is no pain. During the course of the attack there will be discomfort and some numbness if the attack is lasting, but the presence of pain, either during or between attacks, is a strong indication contrary to Raynaud's disease. ElDbolislD-Arterial ThrolDbosis
An acute arterial occlusion, whether it is due to embolism or to thrombosis of an arteriosclerotic segment of the artery, represents a surgical emergency requiring operative relief of the obstruction. Success in removal of an embolus far outstrips the success in relieving obstruction when it is due to thrombosis and arteriosclerosis. Preparations needed for maximum hope of success in removing a thrombotic occlusion include having in readiness a suitable vascular segment for use as a graft, if it should be needed, and in general the preparations in this instance are far greater than those required for removal of an embolus. The differentiation of the cause of an acute arterial occlusion is, therefore, important and although it is not always possible, should be sought in every case. In a high proportion of cases in which the causation is an embolus, a cardiac lesion will be demonstrable to explain the source of the embolus. The common ones are auricular fibrillation on the basis of mitral stenosis, arteriosclerotic heart disease, or a metabolic disease, such as hyperthyroidism. The mural thrombi which form over a myocardial infarct after a coronary occlusion provide another frequent source of peripheral arterial emboli. Spontaneous intracardiac mural thrombi undoubtedly explain a number of peripheral emboli, but this possibility does not aid in the differentiation between the two diseases. The final source of emboli is the formation of an intraluminal clot along the wall of the aorta in the presence of ulcerative arteriosclerosis. This similarly does not help in the differential diagnosis because it cannot be diagnosed accurately in the living patient. In the absence of a cardiac lesion which may be suspected as the source of an embolus a differentiation may be suggested by the acuteness of the onset and the severity of the ischemic symptoms in relation to the size of the vessel obstructed. The lodgment of the embolus causes an acute and severe reflex vasoconstriction which accentuates the degree of occlusion produced by the arterial block. The symptoms are rapid in onset and, since the spasm to a large extent inactivates the collateral bed, they are entirely in keeping with the level of occlusion or may extend higher than the level of occlusien would. indicate. On the other hand, a thrombosis of
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an arteriosclerotic segment usually occurs after a long period of gradual narrowing at the site of the obstruction. The thrombosis then may be of a lumen which is already considerably narrowed. There is no sudden expansile irritation to the artery and the degree of reflex vasoconstriction is minimal as compared to embolism. This comparative lack of reflex arterial spasm and the prior development of the collateral arterial bed, because of the gradual occlusion, makes the onset of symptoms more benign and the severity of the ischemia may fail to correspond to the size of the vessel involved. Another factor which intensifies the reaction to occlusion in embolism is that an embolus usually lodges at a major bifurcation. Therefore, it often occludes a large artery such as the superficial femoral artery, while at the same time it mechanically blocks the major collateral vessel for this channel, namely the profunda femoris. On the other hand, an arterial thrombosis of the superficial femoral artery usually occurs at such a level as to spare the major collateral. In the superficial femoral artery, as an example, the occlusion is most common at the adductor hiatus or immediately below the profunda femoris branch of the common femoral. These differences allow a fairly meager basis for differentiation and thrombosis and embolus will be finally diagnosed in many cases only when the area is explored as it should be for relief of the obstruction. Acute Arterial Occlusion-Arterial Spaslll Secondary to Traullla, Acute Throlllbophlebitis, Etc.
Loss of peripheral pulses, pallor of the skin, some degree of sensory change and paralysis of the muscles of the foot or arm may be present to simulate an anatomical acute occlusion of an artery in a variety of conditions in which acute occlusion is not actually present. Accurate diagnosis in these cases is sometimes difficult, but is particularly important in order that the patient will be spared a useless exploration of a supposedly occluded artery. Three conditions are most troublesome because of their frequency and their ability to simulate occlusion. Included in these three is the arterial spasm which accompanies trauma. The problem here is to determine whether vasospasm or an arterial lesion such as an intramural thrombosis has been caused by trauma. The second common condition is seen in the early stages of many caseE of acute deep thrombophlebitis of the lower extremity in which the vascular spasm is intense and accounts for much of the pain of the phlebitis at this stage. The third situation is seen in patients who have recently suffered a myocardial infarction. If such a patient has also a degree of arteriosclerosis of an extremity, the reduction in cardiac output and fall in arterial blood pressure may bring about such a depression of circulation in the extremity through its diseased arteries that an acute occlusion is very strongly suggested.
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The differential diagnosis in the case of trauma is satisfactorily made by studying the response of skin temperature and the return of pulses when a sympathetic block is done. Occasionally it will be desirable to obtain an . arteriogram of the part to make the differential diagnosis (Fig. 41). The differentiation in acute thrombophlebitis will be made very quickly on the basis of a sympathetic block which will usually bring about a warming of the extremity to a point in excess of the temperature of the opposite leg and will, in addition, have the virtue of relieving most of the patient's pain. The pulses incidentally should return after a sympathetic block in the early so-called white stage of thrombophlebitis.
A
B
Fig. 41. A, Traumatic intramural hematoma of popliteal artery diagnosed by arteriogram. B, Arteriogram made 1 month after repair.
The problem in judgment in the case of a patient whose extremity simulates an acute occlusion during the depression of blood pressure following a Iryocardial infarct is very difficult. If the supposed occlusion is observed early after its onset, a tendency to fluctuate in severity may be watched for as the patient's blood pressure improves. It is also important to note that most peripheral emboli in cases of coronary occlusion occur during the fifth to eighth day after the heart attack, when the mural thrombus has had an opportunity to form in the heart. An apparent arterial embolism within the first 24 hours after a coronary occlusion is less apt to be real than one that occurs at the end of a week. The signs of arterial occlusion, if they are due to the depression in circulation, are
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unlikely to be progressive. A fundamental difficulty in this situation is that, if the blood pressure continues to be depressed in the presence of peripheral arteriosclerosis, the simulated occlusion may become real because of intra-arterial thrombosis. It has been amply demonstrated that in such cases the removal of the occluding clot is infrequently successful because, after removal, the same mechanism of depressed blood pressure is in effect and the clot reforms. Ahdolllinal AneUrYSlll-Ahdolllinal TUlllor
Errors in differentiating midline tumors of the abdomen and arteriosclerotic aneurysms of the abdominal aorta have occurred three times in
B A Fig. 42. A, Translumbar aortogram of abdominal aortic aneurysm. B, Postoperative aortogram in same case after resection and homologous artery graft.
our series of 40 cases of aneurysms considered for resection. Two of these occurred in relation to congenital deformities of the kidney. One horseshoe kidney and one pelvic disk-shaped kidney were found at operation, both in relation to a mild aneurysmal dilatation of the aorta. In neither case was the underlying aneurysm resectable because the blood supply for the kidney arose from multiple arteries coming from the portion of the aorta which would have had to be resected. The obvious aid in diagnosis indicated here is an intravenous pyelogram. This had been done in the case of the horseshoe kidney and the true nature of the renal deformity was not diagnosed on the film. In the case of the pelvic kidney pyelography had not been done. The third error in diagnosis proved to be a large m(;)tastatic nodule arising from a primary tumor in the testicle of the patient. The testicular tumor was very small and was found only after the microscopic diagnosis had been made on the metastatic lesion.
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Fig. 43. Chest x-ray of mediastinal mass proved at operation to be arteriosclerotic aneurysm. No distinct expansile pulse was seen on .fluoroscopy.
Fig. 44. A, Dr.1wing of aneurysm shown in Figure 43. Direct observation showed only slight expansile pUlsation until compressed by palpating hand. B, C, Schema of successful resection and graft.
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It is evident that our diagnostic acumen in distinguishing abdominal aneurysm -from tumor is not infallible. The aids in diagnosis include demonstration of the calcified wall of an aneurysm and displacement of the viscera as shown by x-rays of the abdomen taken both in the anteroposterior and lateral directions. Intravenous urography aids not only in ruling out the unusual finding of a deformed kidney, but also in visualizing the ureters which are characteristically displaced by an aneurysm. Aortography does not need routinely to be done, but provides a typical picture of an aortic aneurysm when it is used. In interpreting the findings in an aortogram of an abdominal aneurysm the Diodrast-filled portion of the aneurysm will be found to be quite small in relation to theactual size of the lesion because of the filling-in of much of the expanded vessel with blood clot, leaving a smaller passage for the flow of blood through the aneurysm. Aortography also provides a means of visualizing the graft used in replacing the aortic bifurcation after removal of the aneurysm (Fig. 42, A, B). Thoracic AneuryslIl-Mediastinal TUlllor
The ability of an aneurysm to fill either the anterior or posterior mediastinum superiorly, or any portion of the mediastinum inferiorly, produces instances in which it is difficult to distinguish between aneurysm a.nd a solitary mediastinal tumor which has a smooth contour. On fluoroscopy expansile pulsations are most difficult to see and distinguish from simple motion transmitted from the heart action. Because of their contained pressure and the inelasticity of the vessel wall which is actually the cause of an aneurysm, expansile pulsations are not remarkable even at the time of operation when the aneurysm is palpated by the surgeon. Unless the wall to the lesion is compressed by the palpating hand the pulsations are not great. At fluoroscopy, therefore, not too much can be expected from this observation (Fig. 43). Good differentiation in difficult cases depends upon angiocardiography done either by the intravenous injection of Diodrast in the brachial vein of one of the arms, or more directly, by its injection through a catheter which has been introduced intra-arterially into the region of the lesion. The history of syphilis or the presence of a positive blood or spinal fluid serology is helpful except in the few cases of arteriosclerotic thoracic aneurysm. In arteriosclerotic aneurysm there is usually on x-ray a visible elongation and, therefore, widening of the loop of the arch of the aorta. The final diagnosis of aneurysm or tumor may sometimes only be made at the time of surgical exploration for resection of the lesion (Fig. 44). 25 E. Washington Street Chicago 2, Illinois.