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Spontaneous popliteal artery dissection: A case report and review of the literature
Spontaneous popliteal artery dissection: A case report and review of the literature David G. Rabkin, MD, Daniel J. Goldstein, MD, Raja M. Flores, MD, and Alan I. Benvenisty, MD, New York, NY Spontaneous arterial dissection of a peripheral artery involving an extremity is a rare event. We report a case of atraumatic, nonaneurysmal dissection of the popliteal artery that occurred in a 62-year-old man who was admitted with progressive right lowerextremity claudication. Preoperative arteriography was suggestive of arterial dissection, and surgical treatment was undertaken before irreversible ischemia developed. Intraoperatively, a dissection of the popliteal artery was observed, and the patient underwent femoral-popliteal bypass grafting with the ipsilateral, greater saphenous vein and the popliteal artery was ligated distal to the dissection. Spontaneous dissection limited to the popliteal artery has not previously been reported in the literature. Successful management depends on consideration of the diagnosis, particularly when other, more common diseases have been excluded. (J Vasc Surg 1999;29:737-40.)
Primary dissection of pulmonary and peripheral arteries without involvement of the aorta is exceedingly rare.1 Spontaneous peripheral dissections usually involve the renal, carotid, coronary, or pulmonary arteries.2 Although arterial dissection was first described in the 16th century,1,3 Wychulis4 et al in their literature review of 1969 reported only 110 cases of dissections of the peripheral arteries, and of these, only nine involved arteries of the extremities. Two teams have reported dissections that began in the femoral artery and extended to the popliteal artery, and one team reported a dissecting aneurysm of the popliteal artery.4-6 We report a case of spontaneous nonaneurysmal dissection limited to the popliteal artery, which we believe to be the first of its kind to be reported in the literature. CASE REPORT A 62-year-old man with a history of mild hypertension and smoking, who was not taking any medications and had no other risk factors for lower-extremity ischemia,7 developed a cramp in his right leg while running, which resolved on resting. In the next several weeks, the pain returned intermittently with exertion. The patient developed clinical signs of severe (grade II) claudication, with intermittent rest pain.7 From the Division of Vascular Surgery, Department of Surgery, Columbia University, College of Physicians and Surgeons. Reprint requests: Dr A.I. Benvenisty, Department of Surgery, Columbia University, College of Physicians and Surgeons, 161 Fort Washington Ave, Suite 612, New York, NY 10032. Copyright © 1999 by The Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter. 0741-5214/99/$8.00 + 0 24/4/95433
One month after the onset of symptoms, the patient had numbness, paresthesias, and coolness in the right foot when he was retiring to bed, and his wife observed that the foot was cold and white. Both the sensation and pallor resolved on dependency. The patient was seen at another center, where he was examined by a vascular surgeon. Pulses were noted to be present, and the findings of noninvasive flow studies were normal. The patient was referred to a neurologist, who found no abnormalities, but the symptoms, variable in intensity, persisted. Because the calf pain began to limit his activities, was reproducible on exertion, and began to occur nightly, forcing him to sleep with his foot hanging over the edge of the bed, the patient sought further consultation. Two months after the onset of symptoms, a physical examination was notable for a blood pressure of 150/90 mm Hg, a heart rate of 80 beats per minute, normal lowerextremity motor and sensory function, and normal capillary refill. Both feet appeared well perfused, without cutaneous stigmata of arterial insufficiency, although the right foot was noted to be cooler than the left. No pulses were palpable below the right femoral artery. Dampened pressure tracings distal to the thigh, with a right ankle-brachial index of 0.40, were demonstrated by means of noninvasive flow studies. Findings of segmental studies on the left lower extremity were completely normal (Fig 1). In light of these findings and despite the absence of atrial fibrillation, myocardial infarction, or overt valvular disease, an embolic episode was suspected. Wall motion abnormalities, intracardiac thrombus, or significant valvular dysfunction were not revealed by means of a transesophageal echocardiogram. No evidence of aortic arch atheroma was noted. The patient then underwent angiography. Minimal aortoiliac atherosclerotic changes were noted. The vascular anatomy on the left side was unremarkable. On the right, the superficial femoral artery was patent; however, at the level of the adductor canal, a long segment lesion of 737
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Fig 1. Dampened pressure tracing distal to the thigh on the right with an ankle-brachial index of 0.40 was demonstrated by means of preoperative noninvasive flow studies. Segmental pressures were normal in the left lower extremity.
the popliteal artery extending to the knee joint was appreciated. Below the knee, the popliteal artery was relatively normal, although of small caliber, presumably because of low flow (Fig 2A and B). The possibility of intraluminal thrombus formation was raised, and intra-arterial urokinase (250,000 units) was pulse administered into the lesion for 3.5 hours. Despite further administration of urokinase, no angiographic change was demonstrated (Fig 3). Then a 5-mm angioplasty balloon was introduced, and dilation was performed throughout the diseased segment. The balloon expanded easily, but after the balloon was removed, the appearance was unchanged. The diagnostic impression at this time was that a dissection of the popliteal artery in the vicinity of the occlusion was the basis for the patient’s symptoms and paroxysmal intensity. The patient was taken to the intensive care unit, where his postarteriography course was unremarkable. He was given oral anticoagulation with Coumadin (Du Pont Pharma, Wilmington, Del). Improved claudication symptoms, with an ankle-brachial index of 0.55, were shown by means of a second noninvasive flow study during exercise, and on physical examination, the patient had palpable right pedal pulses. The patient had no more episodes of claudication and was discharged on Coumadin. Nine days after being discharged, however, his ischemic symptoms reappeared. An ankle-brachial index of 0.27 was demonstrated by means of a noninvasive flow study, and
surgical exploration was undertaken. The patient was taken to the operating room and was prepared and draped in the usual supine position. A popliteal incision was made. Above and below the knee, the popliteal artery was dissected free. Then a dissection, which was estimated to be 5 cm long with both a false and true lumen, was observed. It originated proximally and extended down to the level of the knee. An intense inflammatory reaction was found, and there was evidence of bluish discoloration in the wall, which is consistent with dissection. There was minimal atherosclerotic change. No evidence of entrapment of the popliteal artery was observed. A ligation of the below-knee popliteal artery was performed. A reverse saphenous vein graft was used from the superficial femoral artery to the below-knee popliteal artery. The superficial femoral artery was identified and dissected free. Fogarty clamps were used to obtain hemostasis. The below-knee popliteal artery was identified, and care was taken to avoid injury to the nerve or the vein. Then Yasargil clips were used to obtain hemostasis. After the administration of heparin, the vein was anastomosed with 6-0 Prolene in a continuous fashion. After both anastomoses were performed, all clamps were removed, with adequate hemostasis. Immediately after the operation, the patient’s dorsalis pedis and posterior tibial pulses became palpable, and the patient’s symptoms completely resolved. One year after the operation, the patient remained symptom-free.
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Fig 3. Posturokinase, preangioplasty magnetic resonance angiography of the right lower extremity. The popliteal artery lesion is demonstrated.
Fig 2. Preoperative angiography of both lower extremities. A, A long segmental lesion of the popliteal artery extending to the knee joint is demonstrated on the right side, whereas the left lower extremity is unremarkable. B, A close-up of the segmental lesion on the right.
DISCUSSION The case presented has features that are atypical of arterial dissections in other anatomic locations. Dissection is often heralded by severe pain of acute onset localized to the area of disturbed vasculature.
Patients often have signs or symptoms of watershed ischemia distal to the affected vessel or hemodynamic compromise related to rupture and hypovolemia. Spontaneous arterial dissections of peripheral arteries previously reported in the literature are more common in patients younger than 50 years, and the ratio of male-to-female preponderance is 2 to 1.5 The most common clinical association is hypertension, which is present in 90% or more of affected patients,1,2 but it was present in only a mild form in our patient. Pregnancy, Marfan’s syndrome, and fibromuscular dysplasia have also been associated with spontaneous dissection.8 Cystic medial degeneration, a
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degenerative process of unknown etiology correlated with long-standing hypertension, is present in as many as 83% of patients with arterial dissections,9 although it is unclear whether it is an independent risk factor for dissection or a result of hypertension.10 Atherosclerosis, trauma, coarctation, epinephrine-induced dissection, and endocrine factors may also cause medial necrosis and predispose patients to dissection. Because no significant atheromatous changes were found either during the operation or by means of preoperative imaging, it is likely that the dissection was a result of a pre-existing defect in the media of the arterial wall. It is significant that the symptoms were first appreciated while the patient was running. It is possible that the dissection occurred during this activity, perhaps when a transient increase in blood pressure caused elevation of the intima and a reduction in the diameter of the true lumen, providing the mechanism for ischemic pain on exertion. Because the patient had a patent deep femoral artery, collateral circulation allowed for viability of the lower extremity. Although the possibility of iatrogenic dissection during preoperative angioplasty cannot be excluded, we believe that it is unlikely because clinical and radiographic evidence of dissection (Figs 2A and B, and 3) and symptoms existed before angioplasty. Furthermore, we believe that angioplasty was justified in these circumstances because of the uncertainty of the diagnosis of dissection and the possibility of atherosclerotic disease, despite the mild changes seen by means of angiography (Fig 2). Evidence for the dissection is supported by the intraoperative findings and the evanescent nature of the patient’s symptoms. This case demonstrates that arterial dissection needs to be included in the differential diagnosis of
new onset claudication, particularly in patients with normal contralateral flow. The diagnosis may be difficult to make preoperatively and requires a high index of suspicion once other, more common etiologies have been excluded. Vascular reconstruction of the diseased vessel appears warranted; therapeutic options include resection of the diseased segment. In this case, ligation and bypass grafting were performed and seemed most appropriate. REFERENCES 1. DeBakey ME, McCollum CH, Crawford ES, Morris GC. Dissection and dissecting aneurysms of the aorta: twenty-year follow-up of five hundred twenty-seven patients treated surgically. Surgery 1982;92:1118. 2. Guthrie W, MacLean H. Dissecting aneurysms of arteries other than the aorta. J Pathol 1972;108:219-35. 3. Scarpa A. A treatise on the anatomy, pathology and surgical treatment of aneurysm. Wishart J, translation. Edinburgh: Mundell, Duig, and Stevenson; 1808. p.82. 4. Wychulis AR, Kincaid OW, Wallace RB. Primary dissecting aneurysms of peripheral arteries. Mayo Clin Proc 1969; 44:804-10. 5. Page MH, Leslie GJ, Thorburn C. Dissecting aneurysm of the femoral and popliteal arteries. Med J Aust 1984;140:24-5. 6. Movitz D. Dissecting aneurysm of the femoral and popliteal artery. Surgery 45;1959:834-9. 7. Rutherford RB, Flanigan DP, Gupta SK, Johnston KW, et al. Suggested standards for reports dealing with lower extremity ischemia. J Vasc Surg 1986;4:80-94. 8. Lie JT, Juergens JL. Degenerative arterial diseases other than atherosclerosis. In: Juergens JL, Spittel JA, Fairbairn JF II, editors. Peripheral vascular diseases. 5th ed. Philadelphia: WB Saunders; 1980. p. 237-51. 9. Edwards BS, Stanson AW, Holley KE, Sheps SG. Isolated renal artery dissection. Presentation, evaluation, management, and pathology. Mayo Clin Proc 1982;57:564-71. 10. Bogousslavsky J, Despland P, Regli F. Spontaneous carotid dissection with acute stroke. Arch Neurol 1987;44:137-40.
Submitted Mar 23, 1998; accepted Oct 23, 1998.
Primary dissection of pulmonary and peripheral arteries without involvement of the aorta is exceedingly rare.1 Spontaneous peripheral dissections usually involve the renal, carotid, coronary, or pulmonary arteries.2 Although arterial dissection was first described in the 16th century,1,3 Wychulis4 et al in their literature review of 1969 reported only 110 cases of dissections of the peripheral arteries, and of these, only nine involved arteries of the extremities. Two teams have reported dissections that began in the femoral artery and extended to the popliteal artery, and one team reported a dissecting aneurysm of the popliteal artery.4-6 We report a case of spontaneous nonaneurysmal dissection limited to the popliteal artery, which we believe to be the first of its kind to be reported in the literature. CASE REPORT A 62-year-old man with a history of mild hypertension and smoking, who was not taking any medications and had no other risk factors for lower-extremity ischemia,7 developed a cramp in his right leg while running, which resolved on resting. In the next several weeks, the pain returned intermittently with exertion. The patient developed clinical signs of severe (grade II) claudication, with intermittent rest pain.7 From the Division of Vascular Surgery, Department of Surgery, Columbia University, College of Physicians and Surgeons. Reprint requests: Dr A.I. Benvenisty, Department of Surgery, Columbia University, College of Physicians and Surgeons, 161 Fort Washington Ave, Suite 612, New York, NY 10032. Copyright © 1999 by The Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter. 0741-5214/99/$8.00 + 0 24/4/95433
One month after the onset of symptoms, the patient had numbness, paresthesias, and coolness in the right foot when he was retiring to bed, and his wife observed that the foot was cold and white. Both the sensation and pallor resolved on dependency. The patient was seen at another center, where he was examined by a vascular surgeon. Pulses were noted to be present, and the findings of noninvasive flow studies were normal. The patient was referred to a neurologist, who found no abnormalities, but the symptoms, variable in intensity, persisted. Because the calf pain began to limit his activities, was reproducible on exertion, and began to occur nightly, forcing him to sleep with his foot hanging over the edge of the bed, the patient sought further consultation. Two months after the onset of symptoms, a physical examination was notable for a blood pressure of 150/90 mm Hg, a heart rate of 80 beats per minute, normal lowerextremity motor and sensory function, and normal capillary refill. Both feet appeared well perfused, without cutaneous stigmata of arterial insufficiency, although the right foot was noted to be cooler than the left. No pulses were palpable below the right femoral artery. Dampened pressure tracings distal to the thigh, with a right ankle-brachial index of 0.40, were demonstrated by means of noninvasive flow studies. Findings of segmental studies on the left lower extremity were completely normal (Fig 1). In light of these findings and despite the absence of atrial fibrillation, myocardial infarction, or overt valvular disease, an embolic episode was suspected. Wall motion abnormalities, intracardiac thrombus, or significant valvular dysfunction were not revealed by means of a transesophageal echocardiogram. No evidence of aortic arch atheroma was noted. The patient then underwent angiography. Minimal aortoiliac atherosclerotic changes were noted. The vascular anatomy on the left side was unremarkable. On the right, the superficial femoral artery was patent; however, at the level of the adductor canal, a long segment lesion of 737
738 Rabkin et al
JOURNAL OF VASCULAR SURGERY April 1999
Fig 1. Dampened pressure tracing distal to the thigh on the right with an ankle-brachial index of 0.40 was demonstrated by means of preoperative noninvasive flow studies. Segmental pressures were normal in the left lower extremity.
the popliteal artery extending to the knee joint was appreciated. Below the knee, the popliteal artery was relatively normal, although of small caliber, presumably because of low flow (Fig 2A and B). The possibility of intraluminal thrombus formation was raised, and intra-arterial urokinase (250,000 units) was pulse administered into the lesion for 3.5 hours. Despite further administration of urokinase, no angiographic change was demonstrated (Fig 3). Then a 5-mm angioplasty balloon was introduced, and dilation was performed throughout the diseased segment. The balloon expanded easily, but after the balloon was removed, the appearance was unchanged. The diagnostic impression at this time was that a dissection of the popliteal artery in the vicinity of the occlusion was the basis for the patient’s symptoms and paroxysmal intensity. The patient was taken to the intensive care unit, where his postarteriography course was unremarkable. He was given oral anticoagulation with Coumadin (Du Pont Pharma, Wilmington, Del). Improved claudication symptoms, with an ankle-brachial index of 0.55, were shown by means of a second noninvasive flow study during exercise, and on physical examination, the patient had palpable right pedal pulses. The patient had no more episodes of claudication and was discharged on Coumadin. Nine days after being discharged, however, his ischemic symptoms reappeared. An ankle-brachial index of 0.27 was demonstrated by means of a noninvasive flow study, and
surgical exploration was undertaken. The patient was taken to the operating room and was prepared and draped in the usual supine position. A popliteal incision was made. Above and below the knee, the popliteal artery was dissected free. Then a dissection, which was estimated to be 5 cm long with both a false and true lumen, was observed. It originated proximally and extended down to the level of the knee. An intense inflammatory reaction was found, and there was evidence of bluish discoloration in the wall, which is consistent with dissection. There was minimal atherosclerotic change. No evidence of entrapment of the popliteal artery was observed. A ligation of the below-knee popliteal artery was performed. A reverse saphenous vein graft was used from the superficial femoral artery to the below-knee popliteal artery. The superficial femoral artery was identified and dissected free. Fogarty clamps were used to obtain hemostasis. The below-knee popliteal artery was identified, and care was taken to avoid injury to the nerve or the vein. Then Yasargil clips were used to obtain hemostasis. After the administration of heparin, the vein was anastomosed with 6-0 Prolene in a continuous fashion. After both anastomoses were performed, all clamps were removed, with adequate hemostasis. Immediately after the operation, the patient’s dorsalis pedis and posterior tibial pulses became palpable, and the patient’s symptoms completely resolved. One year after the operation, the patient remained symptom-free.
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Fig 3. Posturokinase, preangioplasty magnetic resonance angiography of the right lower extremity. The popliteal artery lesion is demonstrated.
Fig 2. Preoperative angiography of both lower extremities. A, A long segmental lesion of the popliteal artery extending to the knee joint is demonstrated on the right side, whereas the left lower extremity is unremarkable. B, A close-up of the segmental lesion on the right.
DISCUSSION The case presented has features that are atypical of arterial dissections in other anatomic locations. Dissection is often heralded by severe pain of acute onset localized to the area of disturbed vasculature.
Patients often have signs or symptoms of watershed ischemia distal to the affected vessel or hemodynamic compromise related to rupture and hypovolemia. Spontaneous arterial dissections of peripheral arteries previously reported in the literature are more common in patients younger than 50 years, and the ratio of male-to-female preponderance is 2 to 1.5 The most common clinical association is hypertension, which is present in 90% or more of affected patients,1,2 but it was present in only a mild form in our patient. Pregnancy, Marfan’s syndrome, and fibromuscular dysplasia have also been associated with spontaneous dissection.8 Cystic medial degeneration, a
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degenerative process of unknown etiology correlated with long-standing hypertension, is present in as many as 83% of patients with arterial dissections,9 although it is unclear whether it is an independent risk factor for dissection or a result of hypertension.10 Atherosclerosis, trauma, coarctation, epinephrine-induced dissection, and endocrine factors may also cause medial necrosis and predispose patients to dissection. Because no significant atheromatous changes were found either during the operation or by means of preoperative imaging, it is likely that the dissection was a result of a pre-existing defect in the media of the arterial wall. It is significant that the symptoms were first appreciated while the patient was running. It is possible that the dissection occurred during this activity, perhaps when a transient increase in blood pressure caused elevation of the intima and a reduction in the diameter of the true lumen, providing the mechanism for ischemic pain on exertion. Because the patient had a patent deep femoral artery, collateral circulation allowed for viability of the lower extremity. Although the possibility of iatrogenic dissection during preoperative angioplasty cannot be excluded, we believe that it is unlikely because clinical and radiographic evidence of dissection (Figs 2A and B, and 3) and symptoms existed before angioplasty. Furthermore, we believe that angioplasty was justified in these circumstances because of the uncertainty of the diagnosis of dissection and the possibility of atherosclerotic disease, despite the mild changes seen by means of angiography (Fig 2). Evidence for the dissection is supported by the intraoperative findings and the evanescent nature of the patient’s symptoms. This case demonstrates that arterial dissection needs to be included in the differential diagnosis of
new onset claudication, particularly in patients with normal contralateral flow. The diagnosis may be difficult to make preoperatively and requires a high index of suspicion once other, more common etiologies have been excluded. Vascular reconstruction of the diseased vessel appears warranted; therapeutic options include resection of the diseased segment. In this case, ligation and bypass grafting were performed and seemed most appropriate. REFERENCES 1. DeBakey ME, McCollum CH, Crawford ES, Morris GC. Dissection and dissecting aneurysms of the aorta: twenty-year follow-up of five hundred twenty-seven patients treated surgically. Surgery 1982;92:1118. 2. Guthrie W, MacLean H. Dissecting aneurysms of arteries other than the aorta. J Pathol 1972;108:219-35. 3. Scarpa A. A treatise on the anatomy, pathology and surgical treatment of aneurysm. Wishart J, translation. Edinburgh: Mundell, Duig, and Stevenson; 1808. p.82. 4. Wychulis AR, Kincaid OW, Wallace RB. Primary dissecting aneurysms of peripheral arteries. Mayo Clin Proc 1969; 44:804-10. 5. Page MH, Leslie GJ, Thorburn C. Dissecting aneurysm of the femoral and popliteal arteries. Med J Aust 1984;140:24-5. 6. Movitz D. Dissecting aneurysm of the femoral and popliteal artery. Surgery 45;1959:834-9. 7. Rutherford RB, Flanigan DP, Gupta SK, Johnston KW, et al. Suggested standards for reports dealing with lower extremity ischemia. J Vasc Surg 1986;4:80-94. 8. Lie JT, Juergens JL. Degenerative arterial diseases other than atherosclerosis. In: Juergens JL, Spittel JA, Fairbairn JF II, editors. Peripheral vascular diseases. 5th ed. Philadelphia: WB Saunders; 1980. p. 237-51. 9. Edwards BS, Stanson AW, Holley KE, Sheps SG. Isolated renal artery dissection. Presentation, evaluation, management, and pathology. Mayo Clin Proc 1982;57:564-71. 10. Bogousslavsky J, Despland P, Regli F. Spontaneous carotid dissection with acute stroke. Arch Neurol 1987;44:137-40.
Submitted Mar 23, 1998; accepted Oct 23, 1998.