Lower Extremity Atheromatous Embolization John T. Mehigan,
MD,
San Francisco, California
Ronald J. Stoney, MD, San Francisco, California
Acute focal ischemia of the lower extremities secondary to embolization from nonocclusive, atherosclerotic lesions in the aorta and its terminal branches is rare and frequently overlooked. The following report is based upon clinical observations of eleven patients with this syndrome studied and treated on the Vascular Surgery Service of the University of California, San Francisco, and is submitted to further elucidate the distinctive features of this disorder. Table I indicates the location of the ischemic zone, the source of emboli, surgical treatment, and clinical result of the patients in this series. Case histories of four selected patients are detailed to emphasize the clinical features of this syndrome that present to a greater or lesser degree in all the patients. Case Reports Case 1. A thirty-six year old white female had acute painful discoloration of the right great toe. During the next two weeks, similar episodes occurred affecting, successively, the remaining toes and a portion of the heel of the right foot. Examination showed multiple, discrete, cyanotic, tender areas on the tips of all toes of the right foot. A small painful ulceration was present on the lateral aspect of the heel. The pulses in the legs were present but slightly reduced in strength. No bruits were heard. Aortography
(Figure 1A) showed an irregular atherosclerotic lesion of the infrarenal aorta. Right lumbar sympathectomy and aortoiliac resection with prosthetic graft replacement was performed. The resected aorta contained a discrete atheroma with superficial ulceration and adherent thrombotic debris. (Figure 1B.) Postoperatively, the ischemic lesions of the right foot resolved and she has remained asymptomatic. Case 3. A sixty-two year old white female underwent endarterectomy of the terminal aorta and common iliac arteries seven years ago. Spontaneous occlusion of the right iliac artery three years later caused mild right leg claudication. One month prior to her recent admission an acute, focal, painful lesion appeared on the sole of the left foot. This violaceous zone was sharply demarcated from the remainder of the foot, which appeared well perfused. All
Fromthe Departmentof Surgery,University of California
medical Center.
San Francisco. California.
ReprintWp?StS md of SUgW. 94143.
Volume 132, Aqwl
be addressed to Ronald J. Stoney. MD, Lkp#University of Califcmla. San Francisco. Callfomia
should
1076
pulses were present in the affected left leg but were absent in the right leg. Aortography disclosed an irregular atheroma of the proximal infrarenal aorta above the previous endarterectomy. The right common iliac artery was occluded. The aorta was resected and a prosthetic graft was inserted between the aorta and the external iliac artery, restoring blood flow to the legs. Left lumbar sympathectomy was also performed. The resected proximal aorta contained a friable, ulcerative atheroma with adherent thrombus. Postoperatively, the ischemic lesion on the sole of the foot cleared rapidly. Cases 5 and 6. A forty-two year old white male was in excellent health until six months prior to his first admission when he noted the abrupt onset of the first of multiple episodes of aching pain in the arch of the right foot. The first episode persisted for several days and then subsided completely. The subsequent episodes were identical in abrupt onset, but each was more severe and prolonged than the previous one. When admitted to the hospital, he complained of continuous rest pain on the plantar aspect of his foot at the base of the first and second toes. Walking caused a cramping pain in the right heel and plantar arch. Examination showed localized, grey, cyanotic discoloration of the first and second toes of the right foot. (Figure 2B.) Sensation was present but reduced. The remainder of the foot was well perfused, although the ankle pulses were absent. The remaining pulses in the legs were normal. No bruits were heard. Translumhar and femoral arteriography demonstrated a localized filling defect in the right common iliac artery. (Figure “A.) The right posterior tibial and peroneal arteries were occluded in the distal calf and their configuration was consistent with embolic occlusion. The right common iliac artery was resected and replaced with a synthetic graft and right lumbar sympathectomy was performed. The resected specimen contained a fungating, friable, and ulcerated atheroma projecting into the arterial lumen. (Figure 2C.) Postoperatively, the rest pain in the foot disappeared and the perfusion of the ischemic toes returned to normal. The patient was asymptomatic for four years until he had repeated episodes of digital ischemia of the left foot. Examination showed coldness and cyanosis of the forefoot and the previously present posterior tibia1 and dorsalis pedis pulses were absent. An irregular defect in the common femoral artery was the only lesion demonstrable by arteriography in the proximal arterial tree. Left common femoral endarterectomy and left lumbar sympathectomy were performed. The removed lesion was grossly ulcerated
163
Mehigan
and Stoney
TABLE
I Summary
Case
Patient Age (vr)
lschemic Zone
1 2 3 4 5 6 7 8 9 10 11 12
36 58 62 63 42 46 56 38 75 61 68 60
All toes and heel 2nd, 3rd toes Sole of foot All toes left foot Right lst, 2nd toes Left lst, 2nd toes 2nd, 3rd toes lst, 2nd toes 1st toe lst, 2nd, 3rd toes lst, 2nd toes 2nd toe
of 12 Embolic
Events in 11 Patients Location of Proximal Atheroma Aorta Aorta Aorta Aorta CIA CFA CFA CFA SFA SFA SFA Popliteal artery
Treatment
Result
Resection, graft TEA Resection, graft Resection, graft Resection, graft TEA TEA TEA TEA TEA TEA Bypass with exclusion
Note: TEA = thromboendarterectomy; CIA = common iliac artery; CFA = common femoral artery. All patients underwent lumbar sympathectomy.
Healed Healed Healed Healed Healed Healed Healed Healed Healed Healed Healed Amputation 2nd toe SFA
= superior
F/gure 1A. Preoperative aortogram indicatln~ focal ulcerated atheroma (arrow).
Fitjure 1B. Resected lnfrarenal aorta showinfl atheroma with adherent thrombus (arrow).
ulcerated
with superimposed thrombus. The peripheral ischemic manifestations rapidly resolved and he remains asymptomatic.
Examination of the right foot showed violaceous color changes confined to the second and third toes. (Figure 3A.) The other toes and the remainder of the foot were normal in color and temperature. All pulses in the leg were normal, but a soft bruit was present over the right common femoral artery. Electrocardiogram showed evidence of old myocardial infarction. Translumbar aortography showed a discrete, irregular, nonocclusive lesion on the medial wall of the right common femoral artery. (Figure 4.) The remaining arteries of the legs to the level of the midcalves were normal. Visualization was not obtained beyond these levels.
Case 7. A fifty-six year old white male was in good health until one week prior to admission when he experienced the sudden onset of severe pain in his right second and third toes. The pain persisted and was accompanied by violaceous color changes in those toes. He had had myocardial infarctions one and three years prior to admission with no sequelae. He had no history of claudication, hypertension, or cerebrovascular insufficiency.
164
femoral
artery;
The AmericanJournalof Surgery
Lower Extremity Emboli
comnnm lllac arhwy (arrow).
B, photograph of foot show&g heal cyawtk dbscohwatbn of flmt and second tom C, msecfed common iliac artery showleg fun-prolectlng mml-~~ Into hmhm.
Right common femoral endarterectomy and right lumbar sympathectomy were performed. The atheroma (Figure 5) contained a distinct ulcer crater with adherent thrombus. Postoperatively the right foot became hyperemit. The second and third toes became pain-free within a few days and the abnormal color changes subsided. (Figure 3B.) He has been asymptomatic for the past four years. Comments
Gangrene of a toe secondary to small arterial emboli from a proximal atherosclerotic lesion was predicted by Flory [I] in 1945 to be a logical result of the known behavior of the atherosclerotic plaque. This Volume 132, August 1976
concept was confirmed clinically by Hoye et al [Z] in 1959 in a description of a patient with gangrenous toes, intact pulses, and small vessel atheroemboli from diffuse aortofemoropopliteal disease. Wagner and Martin [3], in their comprehensive summary of the English literature on atheroemboli, found four cases of documented nonaneurysmal aortic atheroemboli and added a case of their own involving a common femoral embolus from a diffusely diseased infrarenal aorta. The patients reported on in our series exhibited similar clinical features. The appearance of ischemia in focal areas of the lower leg or foot was abrupt and often repetitive. A sharp demarcation was present
165
Mehigan and Stoney
Figure 5. Operative dew of open common femoral arterrlotomy showing localized athsroma w/th ulcer and adhemnt thrombus (arrow).
management of occlusive vascular lesions, would allow further embolization and therefore is contraindicated for this entity. Summary
Figure 4. Preoperative right common femoral arterlogram showing a discrete frregufar athetvma on medial wall
between the cutaneous ischemic area and the normally perfused adjacent skin. Pallor was usually followed by violaceous discoloration and often petecchial hemorrhage. Severe pain or impaired sensation were present in the ischemic zone. The major arteries of the affected limb were patent and the distal pulses were usually present. Diagnosis was confirmed by arteriographic demonstration of discrete ulcerative atheroma involving a portion of a proximal major artery or the aorta. When extended to include the vessels of the lower leg and foot, arteriography showed one or more sites of embolic obstruction. No other vascular disease produces this group of clinical features and therefore this syndrome is characteristic among ischemic disorders. Various operative technics were used in this series. All patients underwent lumbar sympathectomy to relieve the cutaneous ischemia. The proximal atheroma, the source of the microemboli, was removed in all patients, and bypass, a common technic for
166
Eleven patients with lower extremity atheromatous microembolization are described. The diagnostic feature of sudden, often repetitive, episodes of focal ischemia, patent major arteries of the legs, and arteriographic demonstration of nonocclusive atheromas of the proxima1 arterial tree are characteristic. Successful removal of the causative lesion in these patients has prbvented further ischemic episodes. References 1. Flory CM: Arterial occlusion produced by emboli from eroded aottic atheromatous plaques. Am J Pathol21: 549, 1945. 2. Hoye SJ, Teitelbaum S, Gore D. Warren R: Atheromatous embolization: a factor in peripheral gangrene. N Eng/ J W 261: 126.1969. 3. Wagner RB, Martin AS: Peripheral atheroembolism: confimvnion of a clinical concept, with a case report and review of the literature. Surgery 73: 353, 1973.
John E. Connolly (Irvine, CA): Emboli to the cerebral circulation from ulcerated plaques at the origin of the internal carotid artery are well known causes of transient ischemic attacks or visual symptoms, and the diagnosis is now commonly sought by carotid arteriogram followed by endarterectomy when the offending site of disease is identified. On the other hand, embolic occlusion of arteries to the visceral organs and the lower extremities is almost always attributed to fibrillation or myocardial infarction. Over the past few years, we also have come to realize that atheromata in major arteries proximal to the embolically
The American Journal of Surgery
Lower Extremity Emboli occluded vessel may be an even more common etiologic source than the heart. Last year we reported our first three documented cases in Surgery 78: 583,1975. Two of these patients had two episodes of common femoral artery occlusion occurring within weeks of each other, treated by routine embolectomy before we -actually identified the artheromatous disease in the clot specimen and performed an aortogram that identified the site of embolization to be the terminal aorta. (Slide) This shows such a specimen. The clot is visible as well as atheromatius material. We believe it is important for the surgeon to carefully examine the specimen before he puts it in formalin. It is often easier to identify it grossly than microscopically. Also, the average pathologist spends very little time or attention in examining a clot. (Slide) This slide demonstrates the microscopic appearance of embolic atheromatous material. (Slide) Here is the aortogram in one of the two patients who had embolization of his common femoral artery on two repeated occasions, before we suspected the diagnosis and obtained an aortogram. You can see the definite disease in the terminal aorta. (Slide) Here is another patient in whom we could not see the offending disease on the frontal projection, but laterally we can see it clearly. This again brings up the recommendation that when you are performing aortography for any reason, it must be accompanied by a lateral view. This patient underwent endarterectomy of this diseased segment without further embolic phenomena to the leg in a follow-up period of eighteen months. (Slide) This is what the aorta looks like in this type of patient. You can readily see why embolic material may break off from this ragged atherosclerotic disease. (Slide) Here is a patient who had the same problem, which was not recognized early on, Despite the fact that the patient had an endarterectomy of the abdominal aorta, some of the digits of the feet were lost. (Slide) Note the blocks of the digital arteries in this particular case. (Slide) In conclusion, I would like to emphasize what the authors have brought out so well, namely, that occurrence of atheromatous macro- or microembolism may be more common than represented in the current literature. Second, we believe the key to diagnosis depends upon (1) an awareness of the condition; when you have a patient who clinically has an embolus, you should add proximal atheromatous disease to your thinking, and not just emboli of cardiac origin. (2) When you remove the material, you should carefully examine it grossly, and you should also see that the pathologist examines it carefully. (3) Angiography, of course, is the key to the diagnosis. We think it should be performed by either the translumbar or transaxillary route SO that you do not dislodge atheromatous material. It is very important also to perform digital arterial angiography. If YOU do not find material in the clot, it may well be in the distal circulation. Finally, early establishment of the correct diagnosis will lead to eradication of the embolic source and correction of what we consider a curable condition.
Volume 132, August 1976
John M. Erskine (San Francisco, CA): (Slide) This abdominal aortogram comes from a fifty-seven year old man who had no previous history of cardiac or peripheral vascular disease and was on the golf course when he suddenly noticed the onset of severe pain involving both legs. He had to be carried off the golf course and entered the emergency room with rather extreme manifestations of arterial occlusive disease of an acute nature. Gradually the peripheral pulses returned over a period of several days except for one pedal pulse, and the tenderness and induration in the calf muscles diminished. Ultimately, he underwent an angiocardiogram, which revealed no thrombotic material in the left heart chambers. The catheter was then passed down into the aorta and this film was taken. As you can see, there is not very much abnormal in the anteroposterior aortogram, but (slide) in the lateral view, you can see an ulcerated lesion on the posterior wall of the lower abdominal aorta. He underwent resection of that segment of the aorta, and bifurcation graft was inserted. As you might expect, there was loose amorphous material in arteriosclerotic ulcer of the posterior wall of the aorta. Richard D. Sloop (Salem, OR): (Slide) In this arteriogram is seen a femoral artery at the adductor hiatus in a man whose only symptom was two episodes of pain in two toes, with patchy, digital tip gangrene. This is the only abnormality in the arterial tree. This was narrowed down to a pencil line of lumen. He had pulses distally and no claudication and no skin changes except at the toes. We believe that he was firing emboli down into his digital arteries, and this was managed by local endarterectomy, as described by the authors. Ronald J. Stoney (closing): Doctor Connolly has drawn attention to both micro- and macroembolization. All of our patients had microembolization of atherosclerotic debris to small vessels in the lower extremities. This precludes the recovery of thrombotic microembolic material. In the larger emboli, however, one should look for the identifiable atheromatous material, which will tip you off to a proximal lesion of the aorta or major branches. Both Doctors Connolly and Erskine emphasized lateral aortography. We had no need to use this in the patients presented here, but if you suspect an arterial lesion because of the clinical episodes and focal distal ischemia, and if you do not see it on the normal arteriographic projection, then use the oblique projection. We would emphasize one point Doctor Sloop made, that these patients when they present with this form of atherosclerotic disease-this ischemic syndrome-are usually not claudicators and have never been claudicators; so this event is their first ischemic symptom. The impact of the paper, I think, is that repeated attacks of acute ischemic changes isolated to local areas of the lower leg, foot, or toes should alert one to consider microembolization as a cause. These lesions can be identified by aortography and in this case, and in this syndrome only, the bypass principle of arterial surgery is not indicated. These arterial lesions must be excluded or removed from the arterial tree lest further emboli occur. 167
MD,
San Francisco, California
Ronald J. Stoney, MD, San Francisco, California
Acute focal ischemia of the lower extremities secondary to embolization from nonocclusive, atherosclerotic lesions in the aorta and its terminal branches is rare and frequently overlooked. The following report is based upon clinical observations of eleven patients with this syndrome studied and treated on the Vascular Surgery Service of the University of California, San Francisco, and is submitted to further elucidate the distinctive features of this disorder. Table I indicates the location of the ischemic zone, the source of emboli, surgical treatment, and clinical result of the patients in this series. Case histories of four selected patients are detailed to emphasize the clinical features of this syndrome that present to a greater or lesser degree in all the patients. Case Reports Case 1. A thirty-six year old white female had acute painful discoloration of the right great toe. During the next two weeks, similar episodes occurred affecting, successively, the remaining toes and a portion of the heel of the right foot. Examination showed multiple, discrete, cyanotic, tender areas on the tips of all toes of the right foot. A small painful ulceration was present on the lateral aspect of the heel. The pulses in the legs were present but slightly reduced in strength. No bruits were heard. Aortography
(Figure 1A) showed an irregular atherosclerotic lesion of the infrarenal aorta. Right lumbar sympathectomy and aortoiliac resection with prosthetic graft replacement was performed. The resected aorta contained a discrete atheroma with superficial ulceration and adherent thrombotic debris. (Figure 1B.) Postoperatively, the ischemic lesions of the right foot resolved and she has remained asymptomatic. Case 3. A sixty-two year old white female underwent endarterectomy of the terminal aorta and common iliac arteries seven years ago. Spontaneous occlusion of the right iliac artery three years later caused mild right leg claudication. One month prior to her recent admission an acute, focal, painful lesion appeared on the sole of the left foot. This violaceous zone was sharply demarcated from the remainder of the foot, which appeared well perfused. All
Fromthe Departmentof Surgery,University of California
medical Center.
San Francisco. California.
ReprintWp?StS md of SUgW. 94143.
Volume 132, Aqwl
be addressed to Ronald J. Stoney. MD, Lkp#University of Califcmla. San Francisco. Callfomia
should
1076
pulses were present in the affected left leg but were absent in the right leg. Aortography disclosed an irregular atheroma of the proximal infrarenal aorta above the previous endarterectomy. The right common iliac artery was occluded. The aorta was resected and a prosthetic graft was inserted between the aorta and the external iliac artery, restoring blood flow to the legs. Left lumbar sympathectomy was also performed. The resected proximal aorta contained a friable, ulcerative atheroma with adherent thrombus. Postoperatively, the ischemic lesion on the sole of the foot cleared rapidly. Cases 5 and 6. A forty-two year old white male was in excellent health until six months prior to his first admission when he noted the abrupt onset of the first of multiple episodes of aching pain in the arch of the right foot. The first episode persisted for several days and then subsided completely. The subsequent episodes were identical in abrupt onset, but each was more severe and prolonged than the previous one. When admitted to the hospital, he complained of continuous rest pain on the plantar aspect of his foot at the base of the first and second toes. Walking caused a cramping pain in the right heel and plantar arch. Examination showed localized, grey, cyanotic discoloration of the first and second toes of the right foot. (Figure 2B.) Sensation was present but reduced. The remainder of the foot was well perfused, although the ankle pulses were absent. The remaining pulses in the legs were normal. No bruits were heard. Translumhar and femoral arteriography demonstrated a localized filling defect in the right common iliac artery. (Figure “A.) The right posterior tibial and peroneal arteries were occluded in the distal calf and their configuration was consistent with embolic occlusion. The right common iliac artery was resected and replaced with a synthetic graft and right lumbar sympathectomy was performed. The resected specimen contained a fungating, friable, and ulcerated atheroma projecting into the arterial lumen. (Figure 2C.) Postoperatively, the rest pain in the foot disappeared and the perfusion of the ischemic toes returned to normal. The patient was asymptomatic for four years until he had repeated episodes of digital ischemia of the left foot. Examination showed coldness and cyanosis of the forefoot and the previously present posterior tibia1 and dorsalis pedis pulses were absent. An irregular defect in the common femoral artery was the only lesion demonstrable by arteriography in the proximal arterial tree. Left common femoral endarterectomy and left lumbar sympathectomy were performed. The removed lesion was grossly ulcerated
163
Mehigan
and Stoney
TABLE
I Summary
Case
Patient Age (vr)
lschemic Zone
1 2 3 4 5 6 7 8 9 10 11 12
36 58 62 63 42 46 56 38 75 61 68 60
All toes and heel 2nd, 3rd toes Sole of foot All toes left foot Right lst, 2nd toes Left lst, 2nd toes 2nd, 3rd toes lst, 2nd toes 1st toe lst, 2nd, 3rd toes lst, 2nd toes 2nd toe
of 12 Embolic
Events in 11 Patients Location of Proximal Atheroma Aorta Aorta Aorta Aorta CIA CFA CFA CFA SFA SFA SFA Popliteal artery
Treatment
Result
Resection, graft TEA Resection, graft Resection, graft Resection, graft TEA TEA TEA TEA TEA TEA Bypass with exclusion
Note: TEA = thromboendarterectomy; CIA = common iliac artery; CFA = common femoral artery. All patients underwent lumbar sympathectomy.
Healed Healed Healed Healed Healed Healed Healed Healed Healed Healed Healed Amputation 2nd toe SFA
= superior
F/gure 1A. Preoperative aortogram indicatln~ focal ulcerated atheroma (arrow).
Fitjure 1B. Resected lnfrarenal aorta showinfl atheroma with adherent thrombus (arrow).
ulcerated
with superimposed thrombus. The peripheral ischemic manifestations rapidly resolved and he remains asymptomatic.
Examination of the right foot showed violaceous color changes confined to the second and third toes. (Figure 3A.) The other toes and the remainder of the foot were normal in color and temperature. All pulses in the leg were normal, but a soft bruit was present over the right common femoral artery. Electrocardiogram showed evidence of old myocardial infarction. Translumbar aortography showed a discrete, irregular, nonocclusive lesion on the medial wall of the right common femoral artery. (Figure 4.) The remaining arteries of the legs to the level of the midcalves were normal. Visualization was not obtained beyond these levels.
Case 7. A fifty-six year old white male was in good health until one week prior to admission when he experienced the sudden onset of severe pain in his right second and third toes. The pain persisted and was accompanied by violaceous color changes in those toes. He had had myocardial infarctions one and three years prior to admission with no sequelae. He had no history of claudication, hypertension, or cerebrovascular insufficiency.
164
femoral
artery;
The AmericanJournalof Surgery
Lower Extremity Emboli
comnnm lllac arhwy (arrow).
B, photograph of foot show&g heal cyawtk dbscohwatbn of flmt and second tom C, msecfed common iliac artery showleg fun-prolectlng mml-~~ Into hmhm.
Right common femoral endarterectomy and right lumbar sympathectomy were performed. The atheroma (Figure 5) contained a distinct ulcer crater with adherent thrombus. Postoperatively the right foot became hyperemit. The second and third toes became pain-free within a few days and the abnormal color changes subsided. (Figure 3B.) He has been asymptomatic for the past four years. Comments
Gangrene of a toe secondary to small arterial emboli from a proximal atherosclerotic lesion was predicted by Flory [I] in 1945 to be a logical result of the known behavior of the atherosclerotic plaque. This Volume 132, August 1976
concept was confirmed clinically by Hoye et al [Z] in 1959 in a description of a patient with gangrenous toes, intact pulses, and small vessel atheroemboli from diffuse aortofemoropopliteal disease. Wagner and Martin [3], in their comprehensive summary of the English literature on atheroemboli, found four cases of documented nonaneurysmal aortic atheroemboli and added a case of their own involving a common femoral embolus from a diffusely diseased infrarenal aorta. The patients reported on in our series exhibited similar clinical features. The appearance of ischemia in focal areas of the lower leg or foot was abrupt and often repetitive. A sharp demarcation was present
165
Mehigan and Stoney
Figure 5. Operative dew of open common femoral arterrlotomy showing localized athsroma w/th ulcer and adhemnt thrombus (arrow).
management of occlusive vascular lesions, would allow further embolization and therefore is contraindicated for this entity. Summary
Figure 4. Preoperative right common femoral arterlogram showing a discrete frregufar athetvma on medial wall
between the cutaneous ischemic area and the normally perfused adjacent skin. Pallor was usually followed by violaceous discoloration and often petecchial hemorrhage. Severe pain or impaired sensation were present in the ischemic zone. The major arteries of the affected limb were patent and the distal pulses were usually present. Diagnosis was confirmed by arteriographic demonstration of discrete ulcerative atheroma involving a portion of a proximal major artery or the aorta. When extended to include the vessels of the lower leg and foot, arteriography showed one or more sites of embolic obstruction. No other vascular disease produces this group of clinical features and therefore this syndrome is characteristic among ischemic disorders. Various operative technics were used in this series. All patients underwent lumbar sympathectomy to relieve the cutaneous ischemia. The proximal atheroma, the source of the microemboli, was removed in all patients, and bypass, a common technic for
166
Eleven patients with lower extremity atheromatous microembolization are described. The diagnostic feature of sudden, often repetitive, episodes of focal ischemia, patent major arteries of the legs, and arteriographic demonstration of nonocclusive atheromas of the proxima1 arterial tree are characteristic. Successful removal of the causative lesion in these patients has prbvented further ischemic episodes. References 1. Flory CM: Arterial occlusion produced by emboli from eroded aottic atheromatous plaques. Am J Pathol21: 549, 1945. 2. Hoye SJ, Teitelbaum S, Gore D. Warren R: Atheromatous embolization: a factor in peripheral gangrene. N Eng/ J W 261: 126.1969. 3. Wagner RB, Martin AS: Peripheral atheroembolism: confimvnion of a clinical concept, with a case report and review of the literature. Surgery 73: 353, 1973.
John E. Connolly (Irvine, CA): Emboli to the cerebral circulation from ulcerated plaques at the origin of the internal carotid artery are well known causes of transient ischemic attacks or visual symptoms, and the diagnosis is now commonly sought by carotid arteriogram followed by endarterectomy when the offending site of disease is identified. On the other hand, embolic occlusion of arteries to the visceral organs and the lower extremities is almost always attributed to fibrillation or myocardial infarction. Over the past few years, we also have come to realize that atheromata in major arteries proximal to the embolically
The American Journal of Surgery
Lower Extremity Emboli occluded vessel may be an even more common etiologic source than the heart. Last year we reported our first three documented cases in Surgery 78: 583,1975. Two of these patients had two episodes of common femoral artery occlusion occurring within weeks of each other, treated by routine embolectomy before we -actually identified the artheromatous disease in the clot specimen and performed an aortogram that identified the site of embolization to be the terminal aorta. (Slide) This shows such a specimen. The clot is visible as well as atheromatius material. We believe it is important for the surgeon to carefully examine the specimen before he puts it in formalin. It is often easier to identify it grossly than microscopically. Also, the average pathologist spends very little time or attention in examining a clot. (Slide) This slide demonstrates the microscopic appearance of embolic atheromatous material. (Slide) Here is the aortogram in one of the two patients who had embolization of his common femoral artery on two repeated occasions, before we suspected the diagnosis and obtained an aortogram. You can see the definite disease in the terminal aorta. (Slide) Here is another patient in whom we could not see the offending disease on the frontal projection, but laterally we can see it clearly. This again brings up the recommendation that when you are performing aortography for any reason, it must be accompanied by a lateral view. This patient underwent endarterectomy of this diseased segment without further embolic phenomena to the leg in a follow-up period of eighteen months. (Slide) This is what the aorta looks like in this type of patient. You can readily see why embolic material may break off from this ragged atherosclerotic disease. (Slide) Here is a patient who had the same problem, which was not recognized early on, Despite the fact that the patient had an endarterectomy of the abdominal aorta, some of the digits of the feet were lost. (Slide) Note the blocks of the digital arteries in this particular case. (Slide) In conclusion, I would like to emphasize what the authors have brought out so well, namely, that occurrence of atheromatous macro- or microembolism may be more common than represented in the current literature. Second, we believe the key to diagnosis depends upon (1) an awareness of the condition; when you have a patient who clinically has an embolus, you should add proximal atheromatous disease to your thinking, and not just emboli of cardiac origin. (2) When you remove the material, you should carefully examine it grossly, and you should also see that the pathologist examines it carefully. (3) Angiography, of course, is the key to the diagnosis. We think it should be performed by either the translumbar or transaxillary route SO that you do not dislodge atheromatous material. It is very important also to perform digital arterial angiography. If YOU do not find material in the clot, it may well be in the distal circulation. Finally, early establishment of the correct diagnosis will lead to eradication of the embolic source and correction of what we consider a curable condition.
Volume 132, August 1976
John M. Erskine (San Francisco, CA): (Slide) This abdominal aortogram comes from a fifty-seven year old man who had no previous history of cardiac or peripheral vascular disease and was on the golf course when he suddenly noticed the onset of severe pain involving both legs. He had to be carried off the golf course and entered the emergency room with rather extreme manifestations of arterial occlusive disease of an acute nature. Gradually the peripheral pulses returned over a period of several days except for one pedal pulse, and the tenderness and induration in the calf muscles diminished. Ultimately, he underwent an angiocardiogram, which revealed no thrombotic material in the left heart chambers. The catheter was then passed down into the aorta and this film was taken. As you can see, there is not very much abnormal in the anteroposterior aortogram, but (slide) in the lateral view, you can see an ulcerated lesion on the posterior wall of the lower abdominal aorta. He underwent resection of that segment of the aorta, and bifurcation graft was inserted. As you might expect, there was loose amorphous material in arteriosclerotic ulcer of the posterior wall of the aorta. Richard D. Sloop (Salem, OR): (Slide) In this arteriogram is seen a femoral artery at the adductor hiatus in a man whose only symptom was two episodes of pain in two toes, with patchy, digital tip gangrene. This is the only abnormality in the arterial tree. This was narrowed down to a pencil line of lumen. He had pulses distally and no claudication and no skin changes except at the toes. We believe that he was firing emboli down into his digital arteries, and this was managed by local endarterectomy, as described by the authors. Ronald J. Stoney (closing): Doctor Connolly has drawn attention to both micro- and macroembolization. All of our patients had microembolization of atherosclerotic debris to small vessels in the lower extremities. This precludes the recovery of thrombotic microembolic material. In the larger emboli, however, one should look for the identifiable atheromatous material, which will tip you off to a proximal lesion of the aorta or major branches. Both Doctors Connolly and Erskine emphasized lateral aortography. We had no need to use this in the patients presented here, but if you suspect an arterial lesion because of the clinical episodes and focal distal ischemia, and if you do not see it on the normal arteriographic projection, then use the oblique projection. We would emphasize one point Doctor Sloop made, that these patients when they present with this form of atherosclerotic disease-this ischemic syndrome-are usually not claudicators and have never been claudicators; so this event is their first ischemic symptom. The impact of the paper, I think, is that repeated attacks of acute ischemic changes isolated to local areas of the lower leg, foot, or toes should alert one to consider microembolization as a cause. These lesions can be identified by aortography and in this case, and in this syndrome only, the bypass principle of arterial surgery is not indicated. These arterial lesions must be excluded or removed from the arterial tree lest further emboli occur. 167
