Basic data related to clinical decisionmaking in vascular surgery Section EditormJohn M. Porter, MD (Portland, Oregon)
Buerger's Disease (Thromboangiitis Obliterans) Joseph L. Mills, MD,* John M. Porter, MD, Lackland AFB, Texas, and Portland, Oregon
Buerger's disease defines a clinical syndrome characterized by the occurrence of segmental thrombotic occlusions of small and medium-sized arteries in the lower and upper extremities. Affected patients are predominantly young male smokers who present with distal ischemia and, frequently, localized digital gangrene [1,2]. Although previously thought to occur almost exclusively in men, Buerger's disease definitely develops in women, in whom it seems to be increasing in frequency. For reasons that are not clear, the incidence of Buerger's disease in North America has declined precipitously in the last 30 years, although large numbers of patients continue to be reported from the Mediterranean countries, eastern Europe, and the Orient (Table I). This peculiar geographic distribution of the disease has never been explained. Although some have questioned the existence of Buerger's disease [3,4], there now appears little doubt that a clearly definable disease process does exist with a distinct clinical presentation, pathological picture, and natural history, quite distinct from atherosclerosis and the various forms of necrotizing arteritis. Welldefined diagnostic criteria for Buerger's disease have recently been described (Table II), The active phase of Buerger's disease is characterized by an intensely cellular, inflammatory, segmental thrombotic occlusion of distal extremity From the Vascular Surgery Service, Wilford Hall USAF Medical Center, Lackland AFB, Texas*, and the Division of Vascular Surget'y, Oregon Health Sciences University, Portland, Oregon*. Reprint requests: Joseph L. Mills, MD, Chief, Vascular Surgery Services/SGHSG, Wilford Hall USAF Medical Center, Lackland AFB, Texas 78236-5300. The opinions expressed herein are those of the author and do not necessarily reflect the opinions of the United States Air Force or the Department of Defense.
arteries. In contradistinction to necrotizing arteritis, vascular wall architecture is well-preserved, The etiology of Buerger's disease remains as unclear today as it was over 80 years ago when Leo Buerger TABLE I.--Incidence and demographics Incidence of Buerger's disease In the general population (North America) In patients with peripheral vascular disease North America (United States) Italy Eastern Europe (Poland) Orient (Japan) Median age at onset Male:Female ratio
Incidence References 8-11.6/100,000 [21,22]
0.75%
[23]
0.46% 3.3%
[24] [25]
16.6% 34.5 years 7.5:1
[26] [11,25, 27-38] [11,27-29, 31,36]
TABLE II,--Diagnostic criteria A.
Onset distal extremity ischemic symptoms before 45 years of age B. Normal arteries proximal to the popliteal or distal brachial level C. Distal occlusive disease documented by distinctive plethysmographic, arteriographic, or pathologic findings D. Absence of any of the following conditions: 1. proximal embolic source 2. trauma 3. autoimmune disease 4. diabetes 5. hyperlipidemia References [11,26,27,31,39]
570
VOLUME5 NO 6 - 1991
571
BUERGER'S DISEASE
described an extensive clinical series of patients with this condition [5]. Reports of cutaneous hypersensitivity to tobacco extracts in patients with Buerger's disease are unconfirmed [6]. Numerous, inconsistent, abnormal coagulation parameters have been described, probably due more to the underlying thrombotic process than the actual disease itself [7]. Considerable investigation is currently underway into possible autoimmune factors associated with Buerger's disease [8,9]. Indeed, some investigators have identified significantly elevated levels of anticollagen antibody in patients with Buerger's disease, as well as apparent cellular sensitivity to collagen abstracts [10]. Presently, neither the specificity nor reproducibility of these findings are known. An association of Buerger's disease with specific HLA subtypes A9 and B5 has been reported, but this has not been confirmed by others [11]. Patients with Buerger's disease usually present with distal extremity ischemia. Raynaud's phenomenon and superficial thrombophlebitis are frequently associated conditions (Table III). Upper extremity involvement is strikingly frequent (Tables III and IV). While Buerger's disease is generally confined to distal extremity vessels, well-documented cases have been reported occasionally in unusual anatomic sites (Table IV). The cornerstone of any treatment plan for a patient with Buerger's disease is total abstinence from tobacco. Over the past 80 years, abundant evidence clearly indicates an indisputable relationship between continued smoking and disease progression. Patients rarely, if ever, develop persistent, ongoing, ischemic lesions when tobacco abstinence is complete [11,12]. Numerous investigators have reported a variety of medical therapies including corticosteroids [ 12,13], vasodilators [14,15], anticoagulants and hemorrhealogic agents [11], antiplatelet drugs [16], antibiotics [17], and antimalarials [12], without clear-cut benefit. There has been some anecdotal success in recent reports with prostaglandin E1 infusion [18,19,20], however this therapy is unproven. Lumbar sympathectomy has been used frequently in Buerger's disease patients with persistent pain at rest or nonhealing lesions despite conservative management. There is, however, no prospective randomized trial of lumbar sympathectomy in such patients, and all reports of efficacy are anecdotal (Table V).
TABLE IIl.~Associated conditions Incidence
Superficial thrombophlebitis
37%
Raynaud's phenomenon
34%
Upper extremity involvement
34%
References [11,24-27,31, 32,38,39] [11,24,27,29, 32,39] [11,25,27,34, 35,37,39]
Since Buerger's disease affects predominately the infrapopliteal and pedal arteries, arterial bypass is rarely possible. Only a small percentage of patients have bypassable disease, and bypass patency rates clearly are inferior to those obtained in atherosclerotic or diabetic patients (Table V). The tables which follow outline the available data with regard to natural history and outcome of Buerger's disease. It is interesting to note that, while Buerger's disease presents a significant risk to the patient of major lower extremity amputation, because of the relative sparing of cerebral, visceral, and coronary circulations, life expectancy of patients with Buerger's disease approaches that of the normal population (Table VI).
TABLE IV.--Anatomic distribution of disease Incidence References
Lower extremity only
68%
[11,25,27,33, 34,37]
Upper extremity only 14% Both upper and lower extremity 18% Unusual sites of involvement (histologically documented cases, compatible clinical histories): femoral artery [34] lilac artery [40] visceral arteries [41-44] spermatic artery [37,45,46] Disputable cases (lack complete histologic or arteriographic confirmation): cerebral arteries [47,48] TABLE V.mSurgical treatment of Buerger's disease Percent
Patients undergoing lower extremity sympathectomy for nonhealing foot lesions Patients with surgicallyreconstructable, lower extremity arterial disease Initial success rates of arterial reconstruction
18%
6.4% 29%
References [11,25-27,29, 31,35,36]
[11,26,28,30, 34] [11,26,28,34]
TABLE VI.mMorbidity and mortality data: amputation and survival rates Amputation
Toe/forefoot Major lower extremity (below or above-knee) Finger amputation Major upper extremity Survival 5 years 10 years
Percentage of patients
19% 19% 6.3% almost never 97% 93.6%
References [11,25,27,38] [11,25,27,31, 35,38] [25,37,38] [11,25,27]
[11,25,38] [38]
572
BUERGER'S DISEASE
REFERENCES 25. 1. ANASARI A. Thromboangiitis obliterans. Current perspectives and future directions. Texas Heart Inst J 1990;17:112-117. 2. MILLS JL, PORTER JM. Buerger's disease. In: CAMERON JL (ed). Current Surgical Therapy--3, Philadelphia: BC Decker, Inc., 1989, pp 575-578. 3. WESSLER S. Buerger's disease revisited. Surg Clin N Am 1969 ;49(3):703-712. 4. WESSLER S, MING SC, GUREWICH V, et al. A critical evaluation of thromboangiitis obliterans. The case against Buerger's disease. N Engl J Med 1960;262(23): 114%1160. 5. BUERGER L. Thromboangiitis obliterans: a study of the vascular lesions leading to presenile spontaneous gangrene. A m J Med Sci 1908;136:567-580. 6. WESTCOTT FN, WRIGHT IS. Tobacco allergy and thromboangiitis obliterans. J Allergy 1938;9:555-564. 7. CRAVEN JL, COTfON RC. Haematological differences between thromboangiitis obliterans and atherosclerosis. Br J Surg 1967;54:862-867. 8. SIMI'C L, PIRNAT L. Immunological aspect of smoking in patients with thromboangiitis obliterans. Vasa 1985;14(4): 34%352. 9. GULATI SM, SINGH KS, THUSOO TK, et al. Immunological studies in thromboangiitis obliterans (Buerger's disease), J Surg Res 1979;27:287-293. 10. ADAR R, PAPA MZ, HALPERN Z, et al. Cellular sensitivity to collagen in thromboangiitis obliterans. N Engl J Med 1983 ;308(19): 1113-1116. 11. MILLS JL, TAYLOR LM Jr, PORTER JM. Buerger's disease in the modern era. Am J Surg 1987;154:123-129. 12. CORELLI F. Buerger's disease: cigarette smoker disease may always be cured by medical therapy alone. Uselessness of operative treatment. J Cardio vasc Surg 1973; 14(I):28-36. 13. CUPPS TR, FAUCI AS. Thromboangiitis obliterans (Buerger's disease, endarteritis obliterans). In: The Vasculitides. Philadelphia: W.B. Saunders & Co, 1981, pp 133-136. 14. MC FADYEN IJ, HOUSLEY E, MAC PHERSON AIS. Intra-arterial reserpine administration in Raynaud's syndrome. Arch lnt Med 1973;132:526-528. 15. PRANDONI AG, MOSER M. Clinical appraisal of intraarterial priscoline therapy in the management of peripheral arterial diseases. Circulation 1954;9:73-81. 16. WILDING RP, FLUTE PK. Dipyridamole in peripheral upper limb ischemia. Lancet 1974;1:999-1000. 17. BARTOLO M, RULLI F, RAFFI S. Buerger's disease: is it a rickettsiosis? Angiology 1980;31(10):660-665. 18, PARDY BJ, LEWIS JD, EASCOTT MS. Preliminary experience with prostaglandins El and I2 in peripheral vascular disease. Surgery 1980;88:826-832. 19, CLIFFORD PC, MARTIN MFR, DIEPPE PA, et al. Prostaglandin E1 infusion for small vessel arterial ischemia. J Cardiovasc Surg 1983;24:503-508. 20, FIESSINGER JN, SCHAEFER M. Trial of iloprost versus aspirin treatment for critical limb ischemia of thromboangiitis obliterans. Lancet 1990;335:555-557. 21. JUERGENS JL. Thromboangiitis obliterans (Buerger's disease). In: FAIRBAIRN JF, JUERGENS JL, SPITTELL JA (eds). Peripheral Vascular Diseases, 4th Ed. Philadelphia: W.B. Saunders & Co., 1972, pp 326-349. 22. DE BAKEY ME, COHEN B. Buerger's disease:follow-up study o f World War 11 army cases. Springfield IL: Charles C, Thomas, 1963, pp 21. 23. DE BAKEY ME, CRAWFORD ES, GARRETT ME, et al. Occlusive disease of the lower extremities in patients 16-37 years of age. Ann Surg 1964;159:873-890. 24. ZANNINI G, COTRULO M. Epidemiological, angio-
26. 27. 28. 29. 30, 31. 32. 33. 34. 35. 36. 37. 38.
39. 40. 41. 42. 43. 44.
45. 46. 47. 48. 9
9
ANNALS OF VASCULAR SURGERY
graphic, and clinical aspects of Buerger's disease. J Cardiovasc Surg 1973;14(1):17-20. NIELUBOWICZ J, ROSNOWSKI A, PRUSZYNSKI B, et al. Natural history of Buerger's disease. J Cardiovasc Surg 1980;21:529-540. SHIONOYA S, BAN I, NAKATA Y, et al. Diagnosis, pathology and treatment of Buerger's disease. Surgery 1974; 75(5):695-700. OLIN JW, YOUNG JR, GRAOR RA, et al. The changing clinical spectrum of thromboangiitis obliterans (Buerger's disease). Circulation 1990;82 (Suppl IV):IV-3-IV-8. LARGIADER J, SCHNEIDER E, BRUNNER U, et al. Arterial reconstruction in Buerger's disease (thromboangiitis obliterans). Vasa 1986;15:174--179. SHIONOYA S. What is Buerger's disease? World J Surg 1983;7:544-551. STOJANOVIC VK, MARCOVIC A, ARSOV V, et al. Clinical course and therapy of Buerger's disease. J Cardiovase Surg 1973;14(1):5-8. SZILAGY1 DE, DE RUSSO FJ, ELLIOTT JP. Thromboangiitis obliterans. Clinico-angiographic correlations; Arch Surg 1964;88:824-835. ALLEN EV, BROWN CE. Thrombo-angiitis obliterans: a clinical study of 200 cases. Ann Intern Med 1928;1:535-549, EADIE DGA, MANN CV, SMITH PG. Buerger's disease: a clinical and pathological re-examination. Br J Surg 1968;55:452456. INADA K, 1WASH1MA Y, OKADA A, et al. Nonatherosclerotic segmental arterial occlusion of the extremity. Arch Surg 1974;108:663-667. KINARE SG, KHER YR, RAO G, et al. Pattern of occlusive peripheral vascular disease in India. Angiology 1976;27:165-180. KRADJIAN R, BOWLES LR, EDWARDS WS. Peripheral arterial disease in Ceylon. Surgery 1971 ;69(4):523-525. McKUSICK VA, HARRIS WS, OTTESEN OE, et al. Buerger's disease: a distinct clinical and pathologic entity. JAMA 1962;181(1):93-100. McPHERSON JR, JUERGENS JL, GIFFORD R W . Thromboangiitis obliterans and arteriosclerosis obliterans. Clinical and prognostic differences. Ann lnt Med 1963;59(3): 288-296. MOZES M, CAHANSKY G, DOITSCH V, et al. The association of atherosclerosis and Buerger's disease: a clinical and radiological study. J Cardiovasc Surg 1970;11:52-59. SHIONOYA S, BAN I NAKATA Y, et al. Involvement of the iliac artery in Buerger's disease. J Cardiovasc Surg 1978;19:6%76. DEITCH EA, SIKKEMA WW. Intestinal manifestation of Buerger's disease: case report and literature review. Am Surg 1981 ;47:326-328. HERRINGTON JL, GROSSMAN LA. Surgical lesions of the small and large intestine resulting from Buerger's disease. Ann Surg 1968;168(6):107%1087. ROSEN N, SOMMER I, KNOBEL B. Intestinal Buerger's disease. Arch Pathol Lab Med 1985;109(10):962-963. ROSENBERGER A, M U N K J, SCHRAMEK A, et al. The angiographic appearance of thromboangiitis obliterans (Buerger's disease) in the abdominal visceral vessels. Br J Radiol 1973;46:337-343. BUERGER L. The Circulatory Disturbances o f the Extremities. Philadelphia: W.B. Saunders & Co., 1924. NESBIT RM, HODGSON NB. Thromboangiitis obliterans of the spermatic cord. J Urol 1960;83:445--447. DRAKE ME. Winiwarter-Buerger's disease ("thromboangiitis obliterans") with cerebral involvement. JAMA 1982;248: 1870-1872. ZULCH KJ. Does the cerebral form of Buerger's disease really exist? Angiology 1969;20(2):61-68.
Buerger's Disease (Thromboangiitis Obliterans) Joseph L. Mills, MD,* John M. Porter, MD, Lackland AFB, Texas, and Portland, Oregon
Buerger's disease defines a clinical syndrome characterized by the occurrence of segmental thrombotic occlusions of small and medium-sized arteries in the lower and upper extremities. Affected patients are predominantly young male smokers who present with distal ischemia and, frequently, localized digital gangrene [1,2]. Although previously thought to occur almost exclusively in men, Buerger's disease definitely develops in women, in whom it seems to be increasing in frequency. For reasons that are not clear, the incidence of Buerger's disease in North America has declined precipitously in the last 30 years, although large numbers of patients continue to be reported from the Mediterranean countries, eastern Europe, and the Orient (Table I). This peculiar geographic distribution of the disease has never been explained. Although some have questioned the existence of Buerger's disease [3,4], there now appears little doubt that a clearly definable disease process does exist with a distinct clinical presentation, pathological picture, and natural history, quite distinct from atherosclerosis and the various forms of necrotizing arteritis. Welldefined diagnostic criteria for Buerger's disease have recently been described (Table II), The active phase of Buerger's disease is characterized by an intensely cellular, inflammatory, segmental thrombotic occlusion of distal extremity From the Vascular Surgery Service, Wilford Hall USAF Medical Center, Lackland AFB, Texas*, and the Division of Vascular Surget'y, Oregon Health Sciences University, Portland, Oregon*. Reprint requests: Joseph L. Mills, MD, Chief, Vascular Surgery Services/SGHSG, Wilford Hall USAF Medical Center, Lackland AFB, Texas 78236-5300. The opinions expressed herein are those of the author and do not necessarily reflect the opinions of the United States Air Force or the Department of Defense.
arteries. In contradistinction to necrotizing arteritis, vascular wall architecture is well-preserved, The etiology of Buerger's disease remains as unclear today as it was over 80 years ago when Leo Buerger TABLE I.--Incidence and demographics Incidence of Buerger's disease In the general population (North America) In patients with peripheral vascular disease North America (United States) Italy Eastern Europe (Poland) Orient (Japan) Median age at onset Male:Female ratio
Incidence References 8-11.6/100,000 [21,22]
0.75%
[23]
0.46% 3.3%
[24] [25]
16.6% 34.5 years 7.5:1
[26] [11,25, 27-38] [11,27-29, 31,36]
TABLE II,--Diagnostic criteria A.
Onset distal extremity ischemic symptoms before 45 years of age B. Normal arteries proximal to the popliteal or distal brachial level C. Distal occlusive disease documented by distinctive plethysmographic, arteriographic, or pathologic findings D. Absence of any of the following conditions: 1. proximal embolic source 2. trauma 3. autoimmune disease 4. diabetes 5. hyperlipidemia References [11,26,27,31,39]
570
VOLUME5 NO 6 - 1991
571
BUERGER'S DISEASE
described an extensive clinical series of patients with this condition [5]. Reports of cutaneous hypersensitivity to tobacco extracts in patients with Buerger's disease are unconfirmed [6]. Numerous, inconsistent, abnormal coagulation parameters have been described, probably due more to the underlying thrombotic process than the actual disease itself [7]. Considerable investigation is currently underway into possible autoimmune factors associated with Buerger's disease [8,9]. Indeed, some investigators have identified significantly elevated levels of anticollagen antibody in patients with Buerger's disease, as well as apparent cellular sensitivity to collagen abstracts [10]. Presently, neither the specificity nor reproducibility of these findings are known. An association of Buerger's disease with specific HLA subtypes A9 and B5 has been reported, but this has not been confirmed by others [11]. Patients with Buerger's disease usually present with distal extremity ischemia. Raynaud's phenomenon and superficial thrombophlebitis are frequently associated conditions (Table III). Upper extremity involvement is strikingly frequent (Tables III and IV). While Buerger's disease is generally confined to distal extremity vessels, well-documented cases have been reported occasionally in unusual anatomic sites (Table IV). The cornerstone of any treatment plan for a patient with Buerger's disease is total abstinence from tobacco. Over the past 80 years, abundant evidence clearly indicates an indisputable relationship between continued smoking and disease progression. Patients rarely, if ever, develop persistent, ongoing, ischemic lesions when tobacco abstinence is complete [11,12]. Numerous investigators have reported a variety of medical therapies including corticosteroids [ 12,13], vasodilators [14,15], anticoagulants and hemorrhealogic agents [11], antiplatelet drugs [16], antibiotics [17], and antimalarials [12], without clear-cut benefit. There has been some anecdotal success in recent reports with prostaglandin E1 infusion [18,19,20], however this therapy is unproven. Lumbar sympathectomy has been used frequently in Buerger's disease patients with persistent pain at rest or nonhealing lesions despite conservative management. There is, however, no prospective randomized trial of lumbar sympathectomy in such patients, and all reports of efficacy are anecdotal (Table V).
TABLE IIl.~Associated conditions Incidence
Superficial thrombophlebitis
37%
Raynaud's phenomenon
34%
Upper extremity involvement
34%
References [11,24-27,31, 32,38,39] [11,24,27,29, 32,39] [11,25,27,34, 35,37,39]
Since Buerger's disease affects predominately the infrapopliteal and pedal arteries, arterial bypass is rarely possible. Only a small percentage of patients have bypassable disease, and bypass patency rates clearly are inferior to those obtained in atherosclerotic or diabetic patients (Table V). The tables which follow outline the available data with regard to natural history and outcome of Buerger's disease. It is interesting to note that, while Buerger's disease presents a significant risk to the patient of major lower extremity amputation, because of the relative sparing of cerebral, visceral, and coronary circulations, life expectancy of patients with Buerger's disease approaches that of the normal population (Table VI).
TABLE IV.--Anatomic distribution of disease Incidence References
Lower extremity only
68%
[11,25,27,33, 34,37]
Upper extremity only 14% Both upper and lower extremity 18% Unusual sites of involvement (histologically documented cases, compatible clinical histories): femoral artery [34] lilac artery [40] visceral arteries [41-44] spermatic artery [37,45,46] Disputable cases (lack complete histologic or arteriographic confirmation): cerebral arteries [47,48] TABLE V.mSurgical treatment of Buerger's disease Percent
Patients undergoing lower extremity sympathectomy for nonhealing foot lesions Patients with surgicallyreconstructable, lower extremity arterial disease Initial success rates of arterial reconstruction
18%
6.4% 29%
References [11,25-27,29, 31,35,36]
[11,26,28,30, 34] [11,26,28,34]
TABLE VI.mMorbidity and mortality data: amputation and survival rates Amputation
Toe/forefoot Major lower extremity (below or above-knee) Finger amputation Major upper extremity Survival 5 years 10 years
Percentage of patients
19% 19% 6.3% almost never 97% 93.6%
References [11,25,27,38] [11,25,27,31, 35,38] [25,37,38] [11,25,27]
[11,25,38] [38]
572
BUERGER'S DISEASE
REFERENCES 25. 1. ANASARI A. Thromboangiitis obliterans. Current perspectives and future directions. Texas Heart Inst J 1990;17:112-117. 2. MILLS JL, PORTER JM. Buerger's disease. In: CAMERON JL (ed). Current Surgical Therapy--3, Philadelphia: BC Decker, Inc., 1989, pp 575-578. 3. WESSLER S. Buerger's disease revisited. Surg Clin N Am 1969 ;49(3):703-712. 4. WESSLER S, MING SC, GUREWICH V, et al. A critical evaluation of thromboangiitis obliterans. The case against Buerger's disease. N Engl J Med 1960;262(23): 114%1160. 5. BUERGER L. Thromboangiitis obliterans: a study of the vascular lesions leading to presenile spontaneous gangrene. A m J Med Sci 1908;136:567-580. 6. WESTCOTT FN, WRIGHT IS. Tobacco allergy and thromboangiitis obliterans. J Allergy 1938;9:555-564. 7. CRAVEN JL, COTfON RC. Haematological differences between thromboangiitis obliterans and atherosclerosis. Br J Surg 1967;54:862-867. 8. SIMI'C L, PIRNAT L. Immunological aspect of smoking in patients with thromboangiitis obliterans. Vasa 1985;14(4): 34%352. 9. GULATI SM, SINGH KS, THUSOO TK, et al. Immunological studies in thromboangiitis obliterans (Buerger's disease), J Surg Res 1979;27:287-293. 10. ADAR R, PAPA MZ, HALPERN Z, et al. Cellular sensitivity to collagen in thromboangiitis obliterans. N Engl J Med 1983 ;308(19): 1113-1116. 11. MILLS JL, TAYLOR LM Jr, PORTER JM. Buerger's disease in the modern era. Am J Surg 1987;154:123-129. 12. CORELLI F. Buerger's disease: cigarette smoker disease may always be cured by medical therapy alone. Uselessness of operative treatment. J Cardio vasc Surg 1973; 14(I):28-36. 13. CUPPS TR, FAUCI AS. Thromboangiitis obliterans (Buerger's disease, endarteritis obliterans). In: The Vasculitides. Philadelphia: W.B. Saunders & Co, 1981, pp 133-136. 14. MC FADYEN IJ, HOUSLEY E, MAC PHERSON AIS. Intra-arterial reserpine administration in Raynaud's syndrome. Arch lnt Med 1973;132:526-528. 15. PRANDONI AG, MOSER M. Clinical appraisal of intraarterial priscoline therapy in the management of peripheral arterial diseases. Circulation 1954;9:73-81. 16. WILDING RP, FLUTE PK. Dipyridamole in peripheral upper limb ischemia. Lancet 1974;1:999-1000. 17. BARTOLO M, RULLI F, RAFFI S. Buerger's disease: is it a rickettsiosis? Angiology 1980;31(10):660-665. 18, PARDY BJ, LEWIS JD, EASCOTT MS. Preliminary experience with prostaglandins El and I2 in peripheral vascular disease. Surgery 1980;88:826-832. 19, CLIFFORD PC, MARTIN MFR, DIEPPE PA, et al. Prostaglandin E1 infusion for small vessel arterial ischemia. J Cardiovasc Surg 1983;24:503-508. 20, FIESSINGER JN, SCHAEFER M. Trial of iloprost versus aspirin treatment for critical limb ischemia of thromboangiitis obliterans. Lancet 1990;335:555-557. 21. JUERGENS JL. Thromboangiitis obliterans (Buerger's disease). In: FAIRBAIRN JF, JUERGENS JL, SPITTELL JA (eds). Peripheral Vascular Diseases, 4th Ed. Philadelphia: W.B. Saunders & Co., 1972, pp 326-349. 22. DE BAKEY ME, COHEN B. Buerger's disease:follow-up study o f World War 11 army cases. Springfield IL: Charles C, Thomas, 1963, pp 21. 23. DE BAKEY ME, CRAWFORD ES, GARRETT ME, et al. Occlusive disease of the lower extremities in patients 16-37 years of age. Ann Surg 1964;159:873-890. 24. ZANNINI G, COTRULO M. Epidemiological, angio-
26. 27. 28. 29. 30, 31. 32. 33. 34. 35. 36. 37. 38.
39. 40. 41. 42. 43. 44.
45. 46. 47. 48. 9
9
ANNALS OF VASCULAR SURGERY
graphic, and clinical aspects of Buerger's disease. J Cardiovasc Surg 1973;14(1):17-20. NIELUBOWICZ J, ROSNOWSKI A, PRUSZYNSKI B, et al. Natural history of Buerger's disease. J Cardiovasc Surg 1980;21:529-540. SHIONOYA S, BAN I, NAKATA Y, et al. Diagnosis, pathology and treatment of Buerger's disease. Surgery 1974; 75(5):695-700. OLIN JW, YOUNG JR, GRAOR RA, et al. The changing clinical spectrum of thromboangiitis obliterans (Buerger's disease). Circulation 1990;82 (Suppl IV):IV-3-IV-8. LARGIADER J, SCHNEIDER E, BRUNNER U, et al. Arterial reconstruction in Buerger's disease (thromboangiitis obliterans). Vasa 1986;15:174--179. SHIONOYA S. What is Buerger's disease? World J Surg 1983;7:544-551. STOJANOVIC VK, MARCOVIC A, ARSOV V, et al. Clinical course and therapy of Buerger's disease. J Cardiovase Surg 1973;14(1):5-8. SZILAGY1 DE, DE RUSSO FJ, ELLIOTT JP. Thromboangiitis obliterans. Clinico-angiographic correlations; Arch Surg 1964;88:824-835. ALLEN EV, BROWN CE. Thrombo-angiitis obliterans: a clinical study of 200 cases. Ann Intern Med 1928;1:535-549, EADIE DGA, MANN CV, SMITH PG. Buerger's disease: a clinical and pathological re-examination. Br J Surg 1968;55:452456. INADA K, 1WASH1MA Y, OKADA A, et al. Nonatherosclerotic segmental arterial occlusion of the extremity. Arch Surg 1974;108:663-667. KINARE SG, KHER YR, RAO G, et al. Pattern of occlusive peripheral vascular disease in India. Angiology 1976;27:165-180. KRADJIAN R, BOWLES LR, EDWARDS WS. Peripheral arterial disease in Ceylon. Surgery 1971 ;69(4):523-525. McKUSICK VA, HARRIS WS, OTTESEN OE, et al. Buerger's disease: a distinct clinical and pathologic entity. JAMA 1962;181(1):93-100. McPHERSON JR, JUERGENS JL, GIFFORD R W . Thromboangiitis obliterans and arteriosclerosis obliterans. Clinical and prognostic differences. Ann lnt Med 1963;59(3): 288-296. MOZES M, CAHANSKY G, DOITSCH V, et al. The association of atherosclerosis and Buerger's disease: a clinical and radiological study. J Cardiovasc Surg 1970;11:52-59. SHIONOYA S, BAN I NAKATA Y, et al. Involvement of the iliac artery in Buerger's disease. J Cardiovasc Surg 1978;19:6%76. DEITCH EA, SIKKEMA WW. Intestinal manifestation of Buerger's disease: case report and literature review. Am Surg 1981 ;47:326-328. HERRINGTON JL, GROSSMAN LA. Surgical lesions of the small and large intestine resulting from Buerger's disease. Ann Surg 1968;168(6):107%1087. ROSEN N, SOMMER I, KNOBEL B. Intestinal Buerger's disease. Arch Pathol Lab Med 1985;109(10):962-963. ROSENBERGER A, M U N K J, SCHRAMEK A, et al. The angiographic appearance of thromboangiitis obliterans (Buerger's disease) in the abdominal visceral vessels. Br J Radiol 1973;46:337-343. BUERGER L. The Circulatory Disturbances o f the Extremities. Philadelphia: W.B. Saunders & Co., 1924. NESBIT RM, HODGSON NB. Thromboangiitis obliterans of the spermatic cord. J Urol 1960;83:445--447. DRAKE ME. Winiwarter-Buerger's disease ("thromboangiitis obliterans") with cerebral involvement. JAMA 1982;248: 1870-1872. ZULCH KJ. Does the cerebral form of Buerger's disease really exist? Angiology 1969;20(2):61-68.
