Delayed Presentation and Treatment of Popliteal Artery Embolism
RICHARD P. CAMBRIA, M.D., BRIAN A. RIDGE, M.D., DAVID C. BREWSTER, M.D., ASHBY C. MONCURE, M.D., R. CLEMENT DARLING, M.D., and WILLIAM M. ABBOTT, M.D.
In the course of reviewing a 10-year experience with popliteal artery embolism (PAE), two distinct patterns of clinical presentation were identified. In addition to those patients presenting with typical acute (symptom duration less than 7 days) arterial ischemia, a second group was identified who presented with more chronic symptoms. The present study was conducted to contrast the clinical factors and treatment of these two temporal patterns of presentation with PAE. Sixty PAEs in 58 patients were documented by the combination of angiography and/or exploration of the popliteal artery. Acute presentation (AP) was seen in 41 (68%) of these and delayed presentation (DP) was noted in 19 (32%) patients. Delayed presentation patients typically presented with a history of sudden onset of claudication or rest pain and a median symptom duration of 30 days. Eighty per cent of AP patients presented with immediately threatened limbs. Angiography was generally diagnostic of chronic popliteal embolism. In the acute group, 90% were treated with embolectomy alone, while 20% of the DP group required bypass grafting. However in two thirds of the DP group, embolectomy alone performed through a direct popliteal approach was possible. Current results with overall limb salvage (92%) and mortality (7%) represents a substantial improvement compared to the authors' previous experience with PAE. The current study suggests that as many as one third of patients with popliteal artery embolism may present in delayed fashion with chronic symptoms. Furthermore most of these patients can be treated with direct popliteal embolectomy alone with favorable results.
From the Surgical Service of the Massachusetts General Hospital, and the Department of Surgery, Harvard Medical School, Boston, Massachusetts
treated popliteal artery embolism, which was distinctly inferior to the results seen with more proximal iliofemoral emboli."6 Furthermore inadequate or incomplete surgical embolectomy frequently was responsible for the inferior results seen with popliteal embolectomy when compared to femoral embolism. That experience prompted a recommendation for the liberal use of a direct popliteal artery approach and has been accompanied by the recognition of two distinct patterns ofclinical presentation in patients with popliteal embolism. To define the incidence and management of these varied clinical presentations, we reviewed a 10-year experience with PAE, encompassing the period since our last review of this topic. Methods All hospital and office records of the authors' patients with a proved diagnosis of popliteal artery embolism treated between January 1978 and December 1988 were reviewed with an emphasis on the temporal pattern of presentation. The diagnosis was confirmed by angiography and/or operation in all but three patients (two refused revascularization and one was considered too unstable for angiography or embolectomy). Patients found to have acute or chronic atherosclerotic thrombosis, and those in whom the diagnosis of embolism was equivocal, were excluded. Patients were divided into two groups based on the duration of ischemic symptoms at time of hospital presentation. Acute presentation (AP) was defined as symptoms of arterial ischemia of less than 7 days duration and delayed presentation (DP) as symptom duration more than 7 days. Patient demographic and clinical character-
E_
MBOLISM TO THE popliteal artery traditionally has been associated with an acute presentation and significant risk of limb loss.`17 Corroborative data are available from the early experience with popliteal artery trauma, wherein acute injuries, treated by ligation, resulted in limb loss in 67% of cases.8 In a previous report, we noted a 76% limb salvage rate in patients with surgically Presented at the 16th annual meeting of the New England Society for Vascular Surgery, September 21, 1989, Bretton Woods, New Hampshire. Address reprint requests to Richard P. Cambria, M.D., Massachusetts General Hospital, 15 Parkman St., Suite 458, Boston, MA 02114. Accepted for publication August 8, 1990.
50
VOL. 214.- NO. I
DELAYED POPLITEAL ARTERY EMBOLISM
istics and diagnostic and treatment modalities corded.
51
TABLE 2. Presenting Symptoms
were re-
Results
Symptom
Delayed Presentation n = 19 (%)
Sixty popliteal artery emboli (PAE) were identified in 58 patients. Acute presentation was seen in 41 patients (68%), with a median symptom duration of 12 hours (range, 2 hours to 6 days). Delayed presentation was noted in 19 patients (32%), with a median symptom duration of 30 days (range, 7 to 120 days). The average age was 66 years in the DP group and 62 years in the AP group. No significant differences in cardiovascular risk factors between these two groups (hypertension, smoking history, diabetes, heart disease) were found. Table 1 lists the etiology of emboli in the two groups. Minor gangrene was present in three of the late (DP) group, and the remaining patients had a history of sudden onset of claudication or rest pain, which was presumed to represent the embolic event. Eighty per cent of the AP group were thought to have immediately threatened limbs requiring emergent intervention. Table 2 lists the presenting symptoms and physical findings. In the DP group, the average ankle to brachial index (ABI) was 0.32 (claudicators, 0.44; rest pain, 0.27; and gangrene, 0.13). In the AP group, few patients had ABI determination; most patients presented with acute ischemia, with a clinical diagnosis of popliteal embolism, and did not have noninvasive laboratory studies. Patients who presented with weeks or months of symptoms underwent angiography. Thus angiography was performed in 18 of
Claudication Rest pain Acute severe ischemia* Toe gangrene
9 (47) 7 (37) 0 3 (16)
TABLE 1. Etiology of Popliteal Artery Embolism
Etiology Cardiac Atrial fibrillation Recent MI LV aneurysm Endocarditis Coronary surgery Coronary artery disease Total Noncardiac Proximal atherosclerosis Aortic aneurysm Aortic graft Total
Delayed Presentation n = 19 (%) 6 3
Acute
Presentation n = 41 (%)
4 13 (68)
9 2 I 1 1 8 22 (54)
2 2 2 6 (32)
9 2 1 12 (29)
latrogenic Aortic balloon pump Aortic valvuloplasty Angiography Intra op aortic surg Total MI, myocardial infarction; LV, left ventricular.
4 1 1 1 7 (17)
*
Acute Presentation n = 41 (%) 0 8 (20) 33 (80) 0
Loss of sensory or motor function, or evidence of muscle compro-
mise.
19 patients (one refused) with DP and provided the correct diagnosis in 15 of 18 patients. Arteriograms of the other three patients were interpreted as atherosclerotic popliteal occlusions subsequently disproved at surgery. Two of the three had emboli from atherosclerotic disease in the proximal femoral artery. This proximal disease in association with popliteal occlusion led to the incorrect diagnosis of atherosclerotic occlusion. The technical aspects of surgical treatment are detailed in Table 3. Ninety per cent of the AP group were treated with embolectomy alone, while 4 of 19 patients in the DP group required femoral-popliteal or femoral-tibial bypass grafting. Bypass grafts were used either because proximal superficial femoral artery lesions were treated concurrent with the popliteal embolism or because of inability to remove the organized thrombus in the popliteal artery. However two thirds of the DP group were treated with embolectomy alone performed via a direct popliteal approach. While popliteal artery exploration was indicated to remedy the situation, the operative findings were critical to establishing the correct pathologic diagnosis in all but 3 of 19 DP patients. These three patients presented with claudication and arteriograms revealed normal proximal and distal vasculature in association with a known cardiac source for embolism. In the remaining DP patients, operative exploration revealed a densely adherent thrombus in the popliteal artery lumen, but the vessel wall itself was either free of or afflicted with only minor atherosclerosis. Treatment results in the present series are shown in Table 4. One amputation was required in a DP patient TABLE 3. Treatment
Treatment
Delayed Presentation (n = 19)
Presentation (n = 41)
Embolectomy Femoral approach Popliteal approach Embolectomy and bypass Anticoagulation only Amputation only
1 11 4 3 0
8 30 0 2 1
Acute
52
Ann. Surg . JUlY 1991
CAMBRIA AND OTHERS
TABLE 4. Results
Result
Delayed Presentation (n = 19)
Acute Presentation (n = 41)
Limb salvage Death
95% 0%
90% 10%
who had a 6-week history of rest pain that became worse 1 day before admission (diagnosis of popliteal embolus was confirmed at operation and a femoral embolus occurred on the opposite side during the same hospital stay). The three patients in the DP group who presented with minor gangrene healed after successful revascularization. Four amputations were required in AP patients, one in a patient who refused embolectomy and three in patients treated with popliteal embolectomy after prolonged periods of preoperative ischemia. There were no deaths in the DP group and four deaths in the AP group, all secondary to coexisting coronary artery disease. Data from our previous reports" 6 is compared to the overall results of the present series in Table 5. While statistical comparisons are not valid due to some overlap of the review periods, the increased use of a direct approach to the popliteal artery appears to be associated with a trend toward improved limb salvage and declining mortality rates.
Comment
It is generally accepted that early intervention is warranted in patients with popliteal embolism and a threatened limb. Elliot9 documented the increase in ischemic complications in patients with arterial emboli in whom preoperative delay exceeded 8 hours. He also noted a decrease in complication rate in those in whom preoperative delay was longer than 7 days. He attributed this to a 'harvesting effect.' (Those with severe ischemia will have died or lost their limb by this time.) Despite several reports in the literature, it is less well appreciated that some patients with arterial embolism who present late can be treated successfully with embolectomy.9'6 Olwin in 1953 reported successful embolectomy in four of six patients who presented 22 hours to 3.5 months after embolism.'0 In 1959 Haimovici reported 10 cases of late embolectomy (13 hours to 20 days), including four popliteal emboli, two of which were treated successfully with delayed embolectomy." However the earlier literature' 14 generally considered 'delayed' embolectomy to be that carried out 8 to 12 hours or more after the presumed onset of symptoms. In fact these reports antedated introduction of the Fogarty embolectomy catheter. Two more recent reports
emphasized that successful delayed embolectomy is sometimes feasible even weeks to months after the onset of embolism, 1516 yet even when considered together they contain only a few patients with popliteal embolism. The etiology of PAE was similar in the two groups of patients. Cardiac sources continue to be the most common etiology of PAE. In an earlier series from our institution,'7 atrial fibrillation alone accounted for 70% of all peripheral emboli while in this series only 25% of patients had atrial fibrillation alone without evidence of ischemic heart disease. This reflects, in part, the decreased incidence of rheumatic heart disease but also the nature of the authors' practice, which includes many patients with both proximal atherosclerotic disease, and previously placed grafts as sources of emboli. Iatrogenic emboli occurred in patients under observation and therefore are all identified early. If this group is eliminated, the incidence of delayed presentation would be even higher. When examined from the perspective of documented popliteal embolism, we found that as many as one of three patients with PAE will present in delayed fashion, several days to weeks after the event. It is our suspicion that such cases frequently are not recognized as being embolic in origin, but rather are treated under the assumption that they represent the sequelae of atherosclerotic occlusive disease. The diagnosis is suggested by the abrupt onset of claudication or rest pain. Differences in collateral circulation, and/or the extent of propagating thrombus, must explain the variation in ischemia experienced by those who present acutely and those with delayed presentation. However no difference in the incidence of clinically evident atherosclerotic vascular disease was found between the two groups, and we intentionally excluded patients with documented or suspected (after treatment) atherosclerotic thrombosis. As we have noted previously, the distinction between embolic and thrombotic occlusion can be problematic,'8 particularly in an era when the demographic and clinical characteristics of patients so affected are quite similar.6 Yet, as we and others have emphasized, such distinction is important because the management and anticipated treatment results vary significantly between embolic and thrombotic occlusion producing acute lower extremity ischemia.'8 9 The diagnosis often depends on complete TABLE 5. Surgical Treatment ofPopliteal Embolism
Treatment/Result
MGH, 1964-19806 (n = 67)
Present Series (n = 60)
Initial embolectomy via direct popliteal approach (%) Limb salvage Death
31% 76% 22%
83% 92% 7%
Vol. 214 No. I
53
DELAYED POPLITEAL ARTERY EMBOLISM
or. -0 $ Oil
FIG. 1. Direct exposure of popliteal artery allowing longitudinal arteriotomy, embolectomy assisted by endarterectomy spatula, and direct visualization of orifice of anterior tibial artery.
*as
.... ... u.li...: :..
.:A. .
jC..
FIG. 2. Closure of arteriotomy with saphenous vein patch using interrupted mattress technique at distal end of arterotomy.
54
CAMBRIA AND OTHERS
angiography, and in accordance with their chronic symptom development, patients presenting in delayed fashion
underwent arteriography. Patients in whom a clinical diagnosis of acute PAE is made routinely are treated with prompt embolectomy. In this series most diagnoses were proved by operative exploration, the ultimate diagnostic test, but angiography generally was diagnostic in the DP group. The angiographic findings supportive of the diagnosis of embolism are (1) convex filling defect in the vessel lumen with abrupt occlusion, (2) poorly developed collateral vessels, (3) lack of associated atherosclerotic disease in adjacent segments of artery, and (4) often found at bifurcations.20 2' A high index of suspicion in patients with the history of acute onset of symptoms (regardless of duration) coexisting with the above angiographic findings should increase diagnostic accuracy and prompt the surgeon to consider direct popliteal artery exploration rather than proceeding initially with distal bypass grafting. Our approach to patients with PAE has been described previously.22 We prefer direct exploration of the popliteal artery if a pulse is present in the popliteal fossa. This is particularly helpful in cases in which the embolism has been present for a prolonged period. Brock, in his 1962 review oflate arterial embolectomy, thought the procedure might be more correctly described as 'thromboendarterectomy.'12 Indeed the technical aspects of such delayed embolectomy are worthy of comment. Catheter embolectomy from a remote site (femoral artery) seldom will be feasible because the organizing embolism has engendered an adherent inflammatory response in the vessel wall. Removal of such chronic emboli requires direct exposure and a sharp dissection off the vessel wall in the manner of an endarterectomy (Fig. 1). It has nearly always been possible to establish the appropriate plane of dissection between the thrombus and the vessel wall; dissection in a true endarterectomy plane (within the vessel media) is to be carefully avoided because it may jeopardize the patency of the outflow tract vessels. Complete visualization ofthe embolism and its adherent thrombus mandates a longitudinal arteriotomy, generally carried beyond the origin of the anterior tibial artery and usually closed with a vein patch (Fig. 2). Two thirds of our patients with DP of PAE were treated with a direct popliteal embolectomy, with only 4 of 19 patients requiring a bypass procedure. Those requiring bypass procedures had either some associated atherosclerotic disease of the superficial femoral artery, or the propagating proximal thrombosis was sufficiently organized to preclude easy removal. In these cases short segment vein graft bypasses were used. Adequacy of all reconstructions are assessed by intraoperative pulse volume recording and/or completion angiography. In selected cases intraoperative angioscopy has proved useful in verifying the technical results of reconstruction. It seems
Ann. Surg. * July 1991
likely that this modality will, in time, diminish the use of operative angiography.23 In earlier reports dealing with popliteal emboli, we noted both limb loss and death in 25% of patients. 1"6 We speculated that many treatment failures resulted from incomplete embolectomy of the popliteal and tibial vessels when the procedure was done from a 'remote' arteriotomy in the femoral artery. Our more recent experience with popliteal emboli detailed herein reflects frequent use of a direct popliteal artery approach and has been accompanied by improved results with respect to both limb salvage and overall mortality. Limb salvage was more than 90% in currently treated patients with both acute and delayed presentation of popliteal emboli. While the improvement in limb salvage is attributed to the routine use of a direct popliteal approach for all patients with embolic occlusion at that level, other factors are probably involved in the improved overall survival. Patients with chronic embolism often fit noninvasive lab criteria for rest pain and although the presenting symptom may be claudication alone, we advocate prompt exploration because the reconstruction required is generally quite simple. Furthermore delay in revascularization can result in progressive loss of outflow tract vessels, hemodynamic deterioration, and the subsequent requirement for more distal bypass. If the diagnosis ofchronic PAE is suspected, angiography is indicated to verify the diagnosis. This has obvious implications for patient treatment, regardless ofwhether revascularization is indicated because permanent anticoagulation is indicated in patients with PAE.9 These favorable results suggest that a direct surgical approach should be considered in all patients with acute or chronic popliteal artery embolism. References 1. Abbott WM, McCabe CJ, Maloney RD, Wirthlin LS. Embolism of the popliteal artery. Surg Gynecol Obstet 1984; 159:533-536. 2. Barker CF, Rosato FE, Roberts B. Peripheral arterial embolism. Surg Gynecol Obstet 1966; 123:22-26. 3. Thompson JE, Sigler L, Raut PS, et al. Arterial embolectomy: a 20 year experience with 163 cases. Surgery 1970; 67:212-220. 4. Kendrick J, Thompson BW, Read RC, et al. Arterial embolectomy in the leg: results in a referral hospital. Am J Surg 1981; 142: 739-743. 5. Panetta T, Thompson JE, Talkington CM, et al. Arterial embolectomy: a 34 year experience with 400 cases. Surg Clin North Am 1986; 66:339-353. 6. Abbott WM, Maloney RD, McCabe CJ, et al. Arterial embolism; a forty-four year perspective. Am J Surg 1982; 143:460-462. 7. Brewster DC, Chin AK, Fogarty TJ. Arterial Thromboembolism. In Rutherford RB, ed. Textbook of Vascular Surgery, 3rd Ed. Philadelphia: WB Saunders, 1989, pp 548-564. 8. DeBakey ME, Simeone FA. Battle injuries of the arteries in world war II: an analysis of 2,471 cases. Ann Surg 1946; 123:534-579. 9. Elliot JP, Hageman JH, Szilagyi DC, et al. Arterial embolization: problems of source, multiplicity, recurrence, and delayed treatment. Surgery 1980; 88:833-845.
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DELAYED POPLITEAL ARTERY EMBOLISM
10. Olwin, JH, Dye WS, Julian DC. Late peripheral arterial embolectomy. Arch Surg 1953; 66:480-487. 11. Haimovici H. Late arterial embolectomy. Surgery 1959; 46:775786. 12. Brock R. Late arterial embolectomy. J Cardiovasc Surg 1962; 3:3947. 13. Spencer FC, Eiseman B. Delayed arterial embolectomy-a new concept. Surgery 1964; 55:64-72. 14. Naqui MA, MacKenwie, DH, Allen LS, Gaum D. Delayed arterial embolectomy. Can J Surg 1974; 17:335-339. 15. Jarrett GC, Dacumos GC, Crummy AB, et al. Late appearance of arterial emboli: diagnosis and management. Surgery 1979; 86: 898-905. 16. Levin-BH, Giordano JM. Delayed arterial embolectomy. Surg Gynecol Obstet 1982; 155:549-551. 17. Darling RC, Austen WG, Linton RR. Arterial embolism. Surg Gynecol Obstet 1967; 124:106-114.
55
18. Cambria RP, Abbott WM. Acute arterial thrombosis of the lower extremity: its natural history contrasted with arterial embolism. Arch Surg 1984; 119:784-787. 19. Dale WA. Differential management of acute peripheral arterial ischemia. J Vasc Surg 1984; 1:269-275. 20. Johnsrude IS. Arteriography and therapeutic procedures of the extremities. In Johnsrude IS, Jackson DC, Dunick NR, eds. A Practical Approach to Angiography, 2nd Ed. Boston: Little, Brown and Co., 1987, pp 164-165. 21. Bron KM. Femoral arteriography. In Abrams HL, ed. Angiography, Vol. 11, 2nd Ed. Boston: Little, Brown and Co., 1971, pp 1221 1249. 22. Cambria RP. Acute lower extremity ischemia. In Brewster DC, ed. Common Problems in Vascular Surgery. Chicago: Year Book Medical Publishers, 1989, pp 224-230. 23. White GH, White RA, Kopchok GE, et al. Intraoperative video angioscopy compared with arteriography during peripheral operations. J Vasc Surg 1987; 6:488-495.
RICHARD P. CAMBRIA, M.D., BRIAN A. RIDGE, M.D., DAVID C. BREWSTER, M.D., ASHBY C. MONCURE, M.D., R. CLEMENT DARLING, M.D., and WILLIAM M. ABBOTT, M.D.
In the course of reviewing a 10-year experience with popliteal artery embolism (PAE), two distinct patterns of clinical presentation were identified. In addition to those patients presenting with typical acute (symptom duration less than 7 days) arterial ischemia, a second group was identified who presented with more chronic symptoms. The present study was conducted to contrast the clinical factors and treatment of these two temporal patterns of presentation with PAE. Sixty PAEs in 58 patients were documented by the combination of angiography and/or exploration of the popliteal artery. Acute presentation (AP) was seen in 41 (68%) of these and delayed presentation (DP) was noted in 19 (32%) patients. Delayed presentation patients typically presented with a history of sudden onset of claudication or rest pain and a median symptom duration of 30 days. Eighty per cent of AP patients presented with immediately threatened limbs. Angiography was generally diagnostic of chronic popliteal embolism. In the acute group, 90% were treated with embolectomy alone, while 20% of the DP group required bypass grafting. However in two thirds of the DP group, embolectomy alone performed through a direct popliteal approach was possible. Current results with overall limb salvage (92%) and mortality (7%) represents a substantial improvement compared to the authors' previous experience with PAE. The current study suggests that as many as one third of patients with popliteal artery embolism may present in delayed fashion with chronic symptoms. Furthermore most of these patients can be treated with direct popliteal embolectomy alone with favorable results.
From the Surgical Service of the Massachusetts General Hospital, and the Department of Surgery, Harvard Medical School, Boston, Massachusetts
treated popliteal artery embolism, which was distinctly inferior to the results seen with more proximal iliofemoral emboli."6 Furthermore inadequate or incomplete surgical embolectomy frequently was responsible for the inferior results seen with popliteal embolectomy when compared to femoral embolism. That experience prompted a recommendation for the liberal use of a direct popliteal artery approach and has been accompanied by the recognition of two distinct patterns ofclinical presentation in patients with popliteal embolism. To define the incidence and management of these varied clinical presentations, we reviewed a 10-year experience with PAE, encompassing the period since our last review of this topic. Methods All hospital and office records of the authors' patients with a proved diagnosis of popliteal artery embolism treated between January 1978 and December 1988 were reviewed with an emphasis on the temporal pattern of presentation. The diagnosis was confirmed by angiography and/or operation in all but three patients (two refused revascularization and one was considered too unstable for angiography or embolectomy). Patients found to have acute or chronic atherosclerotic thrombosis, and those in whom the diagnosis of embolism was equivocal, were excluded. Patients were divided into two groups based on the duration of ischemic symptoms at time of hospital presentation. Acute presentation (AP) was defined as symptoms of arterial ischemia of less than 7 days duration and delayed presentation (DP) as symptom duration more than 7 days. Patient demographic and clinical character-
E_
MBOLISM TO THE popliteal artery traditionally has been associated with an acute presentation and significant risk of limb loss.`17 Corroborative data are available from the early experience with popliteal artery trauma, wherein acute injuries, treated by ligation, resulted in limb loss in 67% of cases.8 In a previous report, we noted a 76% limb salvage rate in patients with surgically Presented at the 16th annual meeting of the New England Society for Vascular Surgery, September 21, 1989, Bretton Woods, New Hampshire. Address reprint requests to Richard P. Cambria, M.D., Massachusetts General Hospital, 15 Parkman St., Suite 458, Boston, MA 02114. Accepted for publication August 8, 1990.
50
VOL. 214.- NO. I
DELAYED POPLITEAL ARTERY EMBOLISM
istics and diagnostic and treatment modalities corded.
51
TABLE 2. Presenting Symptoms
were re-
Results
Symptom
Delayed Presentation n = 19 (%)
Sixty popliteal artery emboli (PAE) were identified in 58 patients. Acute presentation was seen in 41 patients (68%), with a median symptom duration of 12 hours (range, 2 hours to 6 days). Delayed presentation was noted in 19 patients (32%), with a median symptom duration of 30 days (range, 7 to 120 days). The average age was 66 years in the DP group and 62 years in the AP group. No significant differences in cardiovascular risk factors between these two groups (hypertension, smoking history, diabetes, heart disease) were found. Table 1 lists the etiology of emboli in the two groups. Minor gangrene was present in three of the late (DP) group, and the remaining patients had a history of sudden onset of claudication or rest pain, which was presumed to represent the embolic event. Eighty per cent of the AP group were thought to have immediately threatened limbs requiring emergent intervention. Table 2 lists the presenting symptoms and physical findings. In the DP group, the average ankle to brachial index (ABI) was 0.32 (claudicators, 0.44; rest pain, 0.27; and gangrene, 0.13). In the AP group, few patients had ABI determination; most patients presented with acute ischemia, with a clinical diagnosis of popliteal embolism, and did not have noninvasive laboratory studies. Patients who presented with weeks or months of symptoms underwent angiography. Thus angiography was performed in 18 of
Claudication Rest pain Acute severe ischemia* Toe gangrene
9 (47) 7 (37) 0 3 (16)
TABLE 1. Etiology of Popliteal Artery Embolism
Etiology Cardiac Atrial fibrillation Recent MI LV aneurysm Endocarditis Coronary surgery Coronary artery disease Total Noncardiac Proximal atherosclerosis Aortic aneurysm Aortic graft Total
Delayed Presentation n = 19 (%) 6 3
Acute
Presentation n = 41 (%)
4 13 (68)
9 2 I 1 1 8 22 (54)
2 2 2 6 (32)
9 2 1 12 (29)
latrogenic Aortic balloon pump Aortic valvuloplasty Angiography Intra op aortic surg Total MI, myocardial infarction; LV, left ventricular.
4 1 1 1 7 (17)
*
Acute Presentation n = 41 (%) 0 8 (20) 33 (80) 0
Loss of sensory or motor function, or evidence of muscle compro-
mise.
19 patients (one refused) with DP and provided the correct diagnosis in 15 of 18 patients. Arteriograms of the other three patients were interpreted as atherosclerotic popliteal occlusions subsequently disproved at surgery. Two of the three had emboli from atherosclerotic disease in the proximal femoral artery. This proximal disease in association with popliteal occlusion led to the incorrect diagnosis of atherosclerotic occlusion. The technical aspects of surgical treatment are detailed in Table 3. Ninety per cent of the AP group were treated with embolectomy alone, while 4 of 19 patients in the DP group required femoral-popliteal or femoral-tibial bypass grafting. Bypass grafts were used either because proximal superficial femoral artery lesions were treated concurrent with the popliteal embolism or because of inability to remove the organized thrombus in the popliteal artery. However two thirds of the DP group were treated with embolectomy alone performed via a direct popliteal approach. While popliteal artery exploration was indicated to remedy the situation, the operative findings were critical to establishing the correct pathologic diagnosis in all but 3 of 19 DP patients. These three patients presented with claudication and arteriograms revealed normal proximal and distal vasculature in association with a known cardiac source for embolism. In the remaining DP patients, operative exploration revealed a densely adherent thrombus in the popliteal artery lumen, but the vessel wall itself was either free of or afflicted with only minor atherosclerosis. Treatment results in the present series are shown in Table 4. One amputation was required in a DP patient TABLE 3. Treatment
Treatment
Delayed Presentation (n = 19)
Presentation (n = 41)
Embolectomy Femoral approach Popliteal approach Embolectomy and bypass Anticoagulation only Amputation only
1 11 4 3 0
8 30 0 2 1
Acute
52
Ann. Surg . JUlY 1991
CAMBRIA AND OTHERS
TABLE 4. Results
Result
Delayed Presentation (n = 19)
Acute Presentation (n = 41)
Limb salvage Death
95% 0%
90% 10%
who had a 6-week history of rest pain that became worse 1 day before admission (diagnosis of popliteal embolus was confirmed at operation and a femoral embolus occurred on the opposite side during the same hospital stay). The three patients in the DP group who presented with minor gangrene healed after successful revascularization. Four amputations were required in AP patients, one in a patient who refused embolectomy and three in patients treated with popliteal embolectomy after prolonged periods of preoperative ischemia. There were no deaths in the DP group and four deaths in the AP group, all secondary to coexisting coronary artery disease. Data from our previous reports" 6 is compared to the overall results of the present series in Table 5. While statistical comparisons are not valid due to some overlap of the review periods, the increased use of a direct approach to the popliteal artery appears to be associated with a trend toward improved limb salvage and declining mortality rates.
Comment
It is generally accepted that early intervention is warranted in patients with popliteal embolism and a threatened limb. Elliot9 documented the increase in ischemic complications in patients with arterial emboli in whom preoperative delay exceeded 8 hours. He also noted a decrease in complication rate in those in whom preoperative delay was longer than 7 days. He attributed this to a 'harvesting effect.' (Those with severe ischemia will have died or lost their limb by this time.) Despite several reports in the literature, it is less well appreciated that some patients with arterial embolism who present late can be treated successfully with embolectomy.9'6 Olwin in 1953 reported successful embolectomy in four of six patients who presented 22 hours to 3.5 months after embolism.'0 In 1959 Haimovici reported 10 cases of late embolectomy (13 hours to 20 days), including four popliteal emboli, two of which were treated successfully with delayed embolectomy." However the earlier literature' 14 generally considered 'delayed' embolectomy to be that carried out 8 to 12 hours or more after the presumed onset of symptoms. In fact these reports antedated introduction of the Fogarty embolectomy catheter. Two more recent reports
emphasized that successful delayed embolectomy is sometimes feasible even weeks to months after the onset of embolism, 1516 yet even when considered together they contain only a few patients with popliteal embolism. The etiology of PAE was similar in the two groups of patients. Cardiac sources continue to be the most common etiology of PAE. In an earlier series from our institution,'7 atrial fibrillation alone accounted for 70% of all peripheral emboli while in this series only 25% of patients had atrial fibrillation alone without evidence of ischemic heart disease. This reflects, in part, the decreased incidence of rheumatic heart disease but also the nature of the authors' practice, which includes many patients with both proximal atherosclerotic disease, and previously placed grafts as sources of emboli. Iatrogenic emboli occurred in patients under observation and therefore are all identified early. If this group is eliminated, the incidence of delayed presentation would be even higher. When examined from the perspective of documented popliteal embolism, we found that as many as one of three patients with PAE will present in delayed fashion, several days to weeks after the event. It is our suspicion that such cases frequently are not recognized as being embolic in origin, but rather are treated under the assumption that they represent the sequelae of atherosclerotic occlusive disease. The diagnosis is suggested by the abrupt onset of claudication or rest pain. Differences in collateral circulation, and/or the extent of propagating thrombus, must explain the variation in ischemia experienced by those who present acutely and those with delayed presentation. However no difference in the incidence of clinically evident atherosclerotic vascular disease was found between the two groups, and we intentionally excluded patients with documented or suspected (after treatment) atherosclerotic thrombosis. As we have noted previously, the distinction between embolic and thrombotic occlusion can be problematic,'8 particularly in an era when the demographic and clinical characteristics of patients so affected are quite similar.6 Yet, as we and others have emphasized, such distinction is important because the management and anticipated treatment results vary significantly between embolic and thrombotic occlusion producing acute lower extremity ischemia.'8 9 The diagnosis often depends on complete TABLE 5. Surgical Treatment ofPopliteal Embolism
Treatment/Result
MGH, 1964-19806 (n = 67)
Present Series (n = 60)
Initial embolectomy via direct popliteal approach (%) Limb salvage Death
31% 76% 22%
83% 92% 7%
Vol. 214 No. I
53
DELAYED POPLITEAL ARTERY EMBOLISM
or. -0 $ Oil
FIG. 1. Direct exposure of popliteal artery allowing longitudinal arteriotomy, embolectomy assisted by endarterectomy spatula, and direct visualization of orifice of anterior tibial artery.
*as
.... ... u.li...: :..
.:A. .
jC..
FIG. 2. Closure of arteriotomy with saphenous vein patch using interrupted mattress technique at distal end of arterotomy.
54
CAMBRIA AND OTHERS
angiography, and in accordance with their chronic symptom development, patients presenting in delayed fashion
underwent arteriography. Patients in whom a clinical diagnosis of acute PAE is made routinely are treated with prompt embolectomy. In this series most diagnoses were proved by operative exploration, the ultimate diagnostic test, but angiography generally was diagnostic in the DP group. The angiographic findings supportive of the diagnosis of embolism are (1) convex filling defect in the vessel lumen with abrupt occlusion, (2) poorly developed collateral vessels, (3) lack of associated atherosclerotic disease in adjacent segments of artery, and (4) often found at bifurcations.20 2' A high index of suspicion in patients with the history of acute onset of symptoms (regardless of duration) coexisting with the above angiographic findings should increase diagnostic accuracy and prompt the surgeon to consider direct popliteal artery exploration rather than proceeding initially with distal bypass grafting. Our approach to patients with PAE has been described previously.22 We prefer direct exploration of the popliteal artery if a pulse is present in the popliteal fossa. This is particularly helpful in cases in which the embolism has been present for a prolonged period. Brock, in his 1962 review oflate arterial embolectomy, thought the procedure might be more correctly described as 'thromboendarterectomy.'12 Indeed the technical aspects of such delayed embolectomy are worthy of comment. Catheter embolectomy from a remote site (femoral artery) seldom will be feasible because the organizing embolism has engendered an adherent inflammatory response in the vessel wall. Removal of such chronic emboli requires direct exposure and a sharp dissection off the vessel wall in the manner of an endarterectomy (Fig. 1). It has nearly always been possible to establish the appropriate plane of dissection between the thrombus and the vessel wall; dissection in a true endarterectomy plane (within the vessel media) is to be carefully avoided because it may jeopardize the patency of the outflow tract vessels. Complete visualization ofthe embolism and its adherent thrombus mandates a longitudinal arteriotomy, generally carried beyond the origin of the anterior tibial artery and usually closed with a vein patch (Fig. 2). Two thirds of our patients with DP of PAE were treated with a direct popliteal embolectomy, with only 4 of 19 patients requiring a bypass procedure. Those requiring bypass procedures had either some associated atherosclerotic disease of the superficial femoral artery, or the propagating proximal thrombosis was sufficiently organized to preclude easy removal. In these cases short segment vein graft bypasses were used. Adequacy of all reconstructions are assessed by intraoperative pulse volume recording and/or completion angiography. In selected cases intraoperative angioscopy has proved useful in verifying the technical results of reconstruction. It seems
Ann. Surg. * July 1991
likely that this modality will, in time, diminish the use of operative angiography.23 In earlier reports dealing with popliteal emboli, we noted both limb loss and death in 25% of patients. 1"6 We speculated that many treatment failures resulted from incomplete embolectomy of the popliteal and tibial vessels when the procedure was done from a 'remote' arteriotomy in the femoral artery. Our more recent experience with popliteal emboli detailed herein reflects frequent use of a direct popliteal artery approach and has been accompanied by improved results with respect to both limb salvage and overall mortality. Limb salvage was more than 90% in currently treated patients with both acute and delayed presentation of popliteal emboli. While the improvement in limb salvage is attributed to the routine use of a direct popliteal approach for all patients with embolic occlusion at that level, other factors are probably involved in the improved overall survival. Patients with chronic embolism often fit noninvasive lab criteria for rest pain and although the presenting symptom may be claudication alone, we advocate prompt exploration because the reconstruction required is generally quite simple. Furthermore delay in revascularization can result in progressive loss of outflow tract vessels, hemodynamic deterioration, and the subsequent requirement for more distal bypass. If the diagnosis ofchronic PAE is suspected, angiography is indicated to verify the diagnosis. This has obvious implications for patient treatment, regardless ofwhether revascularization is indicated because permanent anticoagulation is indicated in patients with PAE.9 These favorable results suggest that a direct surgical approach should be considered in all patients with acute or chronic popliteal artery embolism. References 1. Abbott WM, McCabe CJ, Maloney RD, Wirthlin LS. Embolism of the popliteal artery. Surg Gynecol Obstet 1984; 159:533-536. 2. Barker CF, Rosato FE, Roberts B. Peripheral arterial embolism. Surg Gynecol Obstet 1966; 123:22-26. 3. Thompson JE, Sigler L, Raut PS, et al. Arterial embolectomy: a 20 year experience with 163 cases. Surgery 1970; 67:212-220. 4. Kendrick J, Thompson BW, Read RC, et al. Arterial embolectomy in the leg: results in a referral hospital. Am J Surg 1981; 142: 739-743. 5. Panetta T, Thompson JE, Talkington CM, et al. Arterial embolectomy: a 34 year experience with 400 cases. Surg Clin North Am 1986; 66:339-353. 6. Abbott WM, Maloney RD, McCabe CJ, et al. Arterial embolism; a forty-four year perspective. Am J Surg 1982; 143:460-462. 7. Brewster DC, Chin AK, Fogarty TJ. Arterial Thromboembolism. In Rutherford RB, ed. Textbook of Vascular Surgery, 3rd Ed. Philadelphia: WB Saunders, 1989, pp 548-564. 8. DeBakey ME, Simeone FA. Battle injuries of the arteries in world war II: an analysis of 2,471 cases. Ann Surg 1946; 123:534-579. 9. Elliot JP, Hageman JH, Szilagyi DC, et al. Arterial embolization: problems of source, multiplicity, recurrence, and delayed treatment. Surgery 1980; 88:833-845.
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DELAYED POPLITEAL ARTERY EMBOLISM
10. Olwin, JH, Dye WS, Julian DC. Late peripheral arterial embolectomy. Arch Surg 1953; 66:480-487. 11. Haimovici H. Late arterial embolectomy. Surgery 1959; 46:775786. 12. Brock R. Late arterial embolectomy. J Cardiovasc Surg 1962; 3:3947. 13. Spencer FC, Eiseman B. Delayed arterial embolectomy-a new concept. Surgery 1964; 55:64-72. 14. Naqui MA, MacKenwie, DH, Allen LS, Gaum D. Delayed arterial embolectomy. Can J Surg 1974; 17:335-339. 15. Jarrett GC, Dacumos GC, Crummy AB, et al. Late appearance of arterial emboli: diagnosis and management. Surgery 1979; 86: 898-905. 16. Levin-BH, Giordano JM. Delayed arterial embolectomy. Surg Gynecol Obstet 1982; 155:549-551. 17. Darling RC, Austen WG, Linton RR. Arterial embolism. Surg Gynecol Obstet 1967; 124:106-114.
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18. Cambria RP, Abbott WM. Acute arterial thrombosis of the lower extremity: its natural history contrasted with arterial embolism. Arch Surg 1984; 119:784-787. 19. Dale WA. Differential management of acute peripheral arterial ischemia. J Vasc Surg 1984; 1:269-275. 20. Johnsrude IS. Arteriography and therapeutic procedures of the extremities. In Johnsrude IS, Jackson DC, Dunick NR, eds. A Practical Approach to Angiography, 2nd Ed. Boston: Little, Brown and Co., 1987, pp 164-165. 21. Bron KM. Femoral arteriography. In Abrams HL, ed. Angiography, Vol. 11, 2nd Ed. Boston: Little, Brown and Co., 1971, pp 1221 1249. 22. Cambria RP. Acute lower extremity ischemia. In Brewster DC, ed. Common Problems in Vascular Surgery. Chicago: Year Book Medical Publishers, 1989, pp 224-230. 23. White GH, White RA, Kopchok GE, et al. Intraoperative video angioscopy compared with arteriography during peripheral operations. J Vasc Surg 1987; 6:488-495.
