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Occlusive Arterial Emergencies
Occlusive Arterial Emergencies CARL C. BARTELS, M.D.
Sudden loss of arterial blood supply to part of the body may not only jeopardize the function of that part, but can result in tissue necrosis and the ultimate death of the patient. The patient in whom acute arterial occlusion has occurred is frequently a poor risk because of cardiac or generalized vascular disease. He may be unable to tolerate surgery, whether this be surgical removal of the occlusion or the necrotic part.
ETIOLOGY The most common causes of sudden arterial occlusion are clot embolism and arterial thrombosis. Clot emboli may be multiple. Edema and hemorrhage, together with too tight a cast or bandage, can cause arterial occlusion. Edema in a confined area, as that seen in the anterior tibial compartment syndrome, can result in local loss of blood supply. Dissecting aneurysm of the aorta, aortic and popli teal aneurysm, and false aneurysms may contribute to sudden loss of arterial blood supply peripherally. Peripheral arterial occlusion has been reported in patients with congenital heart disease in whom a venous clot or air embolus has passed through the foramen ovale into the peripheral circulation (paradoxical embolism).5. H. 11 Diseases responsible for clot embolism are primarily those of the heart. Mitral stenosis with atrial fibrillation in earlier studies had been the most common cause, but embolism may also occur in fibrillation without valvular disease. In recent studies, the incidence of embolism has been reported as being higher in patients having myocardial infarction with mural thrombosis. Darling et al.,4 in an analysis of 260 patients treated for arterial emboli, found that in 1948, 64.5 per cent of arterial embolisms resulted from rheumatic heart disease with atrial fibrillation, whereas in the past 10 years this figure was reduced to 35 per cent, arteriosclerotic heart disease being responsible for 51.1 per cent. Hardin and Hendren,lO in their study of 50 patients with arterial emboli, found that arteriosclerotic heart disease was the causative factor in 62 per cent, whereas rheumatic heart disease with atrial fibrillation was responsible in 32 per cent. Clot embolism may also occur in cardiac decompensation, mitral and aortic valvulitis, and subacute bacterial endocarditis. Medical Clinics of North
Ameri.ca~
Vo!. 53, No. 2, March, 1969
335
336
CARL C. BARTELS
Edwards et alY reported a patient in whom a part of an atrial myxoma caused a peripheral embolism. We have had two patients with Teflon aortic grafts in whom emboli of intima from the Teflon have occurred below the graft and in whom replacement had to be made with Dacron grafts. A thrombus, developing from an arteriosclerotic plaque of an artery or from an aneurysm, may break off, :resulting in distal occlusion of the artery or its branches. AlIen et al. l stated that in at least 10 per cent of patients with arteriosclerosis obliterans there is sudden occlusion. It is frequently difficult to determine the cause of an occlusion of an artery. When the cause is not known, serial electrocardiograms and blood enzyme studies may uncover an unsuspected coronary thrombosis that could be responsible for a mural thrombus and embolus. A nonspecific inflammatory process of the arterial wall caused by injury of the intima from an atheromatous plaque may cause edema and clot formation with occlusion of the artery. Acute inflammatory diseases such as thromboangiitis obliterans, polyarteritis, and lupus erythematosus can result in major artery occlusion. Surgical procedures on the heart or on an artery can result in peripheral emboli or thrombosis of arteries. Other factors may be responsible for arterial thrombosis or plugging, such as polycythemia, cryoglobulinemia, or macroglobulinemia, but these usually affect only the smaller end-arteries and do not result in extensive ischemia or loss of a limb. Trauma from the use of intra-arterial injections or catheters has resulted in sudden arterial occlusion. Ischemia can occur without acute arterial occlusion. In venous thrombosis there occasionally can be acute arterial spasm resulting from one of two conditions described as phlegmasia cerulea dolens or venous gangrene. 9
SYMPTOMS Symptoms vary greatly from sudden acute pain to mild numbness, coldness, or paresthesias. In a patient with no previous arterial disease, such as arteriosclerotic occlusive disease, if the occlusion is abrupt and complete, the symptoms are usually pain, paresthesias, coldness, tingling, muscular weakness, and paralysis. When complete occlusion occurs in a patient who has a slowly developing arterial occlusive process, the collateral circulation may have been sufficiently developed so that only mild discomfort, coldness, and paresthesias may be present. The location of the occlusion is also a factor in development of the symptoms. Acute occlusion of the smaller distal arteries is frequently better tolerated with only mild symptoms than acute occlusion of large, more proximal arteries. In the experience of AlIen et aLI the upper extremity has a better ability than the lower extremity to survive acute arterial occlusion. A renal artery occluded by embolism or other causes may be accompanied by flank pain and hematuria. If it is unrecognized, acute hypertension may result.
OCCLUSIVE ARTERIAL EMERGENCIES
337
An acute abdominal condition may result from mesenteric artery embolism or thrombosis. Symptoms from cerebral embolism depend on the location and the size of the artery occluded.
PHYSICAL EXAMINATION In the extremities, the absence of pulses helps to confirm the diagnosis of arterial occlusion. Anatomical variation in the position of arteries and the presence of previous occlusive arterial disease and edema may make it impossible to determine the presence or absence of pulsations and to arrive at any final conclusion concerning the cause or location of the arterial block. In the involved extremity, pallor of the skin usually appears early and cyanosis later. There may be grooving of the superficial veins resulting from lack of blood. There may be decrease in skin temperature, loss of sensation, diminution or loss of reflexes, rigidity, and loss of muscle function. Loss of sensation, of reflexes, and of muscle function with muscle rigidity are indicative of severe ischemia, and if some degree of circulation is not re-established, gangrene and loss of the extremity will usually result.
TREATMENT Maintenance of life must be the first consideration. The general state of health with specific reference to cardiac and generalized vascular disease must be considered in deciding the extent and degree of treatment of the patient with an acute arterial occlusion. If acute clot embolism occurs, embolectomy is usually indicated, unless the general state of health of the patient would be jeopardized by surgery. Failure to remove the clot may result in impaired function of the extremity and tissue necrosis, which in itself could be a serious threat to the patient. The clot embolus will lodge at points of bifurcation or anatomical or atheromatous narrowing of an artery. Darling et al.,4 in a review of 260 patients, noted that 68.1 per cent of emboli involved the bifurcation of the aorta or major peripheral· arteries, 22.6 per cent involved cerebral arteries, and 11.3 per cent involved visceral arteries. It is generally agreed that patients with arterial emboli should receive heparin as soon as the diagnosis is considered. This gives protection from propagation of the embolism by thrombosis both proximal and distal to the site of the embolism. It also provides time to evaluate the patient's condition with specific reference to the cardiac status and to the possible source of the embolism. It also provides time to institute appropriate therapy in an attempt to improve the patient's general state of health before any surgical procedure is attempted. Because of the high mortality rate, especially in patients with arteriosclerotic heart disease, careful evaluation is mandatory. The mortality rates for those with rheumatic heart disease vary from 20.4 to 26.6 per cent and for arteriosclerotic heart disease from 34.0 to 74.2 per cent. 4. 6
338
CARL C. BARTELS
In patients with clot embolism, early operation usually off~rs the best results. The best limb survival rate is obtained by surgery performed within 12 hours of the occlusion. 4,1O The results of embolectomy are poorer the longer the embolism remains in an artery, but this does not indicate that embolectomy should not be attempted. In a series of 11 patients who underwent embolectomy 4 days to a month after embolism, only one failure was experienced. Cranley et al,3 reported reviving a limb in the presence of rigor mortis of the muscles. Billig et al,2 reported the case of one patient in whom the extremity was improved after a bypass procedure that was performed for a saddle embolism of the aortic bifurcation 5 months after embolization. The use of the Fogarty7 catheter for removing emboli has been primarily responsible for the improvement in the results of embolectomy in recent years. By this technique, making a relatively simple surgical incision in both inguinal regions and opening the femoral arteries, it is possible to remove emboli from the bifurcation of the aorta down to and including the common femoral artery. In some cases it is possible to remove emboli from the superficial femoral artery. Once the embolus is removed, the possibility of the existence of a more distal thrombosis or embolism must be considered and can best be determined by arteriography or by the extent of the retrograde blood flow from the distal part of the artery. A small suction catheter passed down the femoral artery may pick up a distal clot. It may be necessary to expose the popliteal artery to attempt retrograde flushing. If the embolism is located at the bifurcation of the popliteal artery, exposure of that artery and removal of the embolism may be all that is necessary. Exposure of the posterior tibial artery and retrograde flushing with heparin solution will help to confirm the patency of the tibial artery. The restoration of the pedal pulses is a reassuring sign that circulation has been re-established. Pedal pulses may be absent immediately after operation, but may appear within an hour or two. Emboli in the upper limbs are more likely to lodge in the subclavian, axillary, or brachial arteries. The upper extremity seems to tolerate embolic occlusion better than the legs. Darling et al.,4 in a series of 59 patients treated conservatively for embolic occlusion involving the upper extremity, had two patients who required amputation. Mesenteric and cerebral emboli accounted for one third of the deaths from embolism in their series. Results of both surgery and conservative management in patients with these two problems have been poor. In the postoperative period, the patients who have had embolectomy must be given anticoagulation therapy. Previously the use of heparin after abdominal operation to remove a saddle embolus or an embolus from an iliac artery was somewhat hazardous, because hemorrhage could occur and remain undetected. Incisions required to use the Fogarty catheter are usually superficial, and should hemorrhage occur, it can usually be detected. Anticoagulation therapy should be started with heparin, and as soon as the patient is able to take oral medication, prothrombin depressant agents should be used. Once the therapeutic prothrombin level has been
OCCLUSIVE ARTERIAL EMERGENCIES
339
obtained, administration of heparin can be discontinued but oral anticoagulant should be continued. If the embolism has resulted from a myocardial infarction, anticoagulation should be maintained for a period of 3 to 6 months, and then it can gradually be terminated. If embolism has resulted from auricular fibrillation and fibrillation persists, anticoagulation therapy should be continued indefinitely. Recurrent embolism is common; Darling et al. 4 reported a rate of 45.5 per cent. Adequate anticoagulation must be maintained if there is to be any hope of reducing this. Acute occlusion, whether thrombotic or embolic, in an artery in which there has been slowly progressive arteriosclerotic occlusive disease is less likely to result in severe ischemic changes than acute occlusion of a normal vessel. Because of the gradual narrowing from arteriosclerotic occlusive disease, collateral circulation usually has developed. An arteriogram is of value in determining the degree of arteriosclerotic disease and determining whether a good vessel exists below the block. It also helps to indicate the extent of the block. If a good runoff exists below and the block is of short length, endarterectomy with removal of the clot and the arteriosclerotic process may produce a good result with the return of peripheral pulses. If the disease process in the artery is extensive, a vein bypass graft may be necessary. If an acute occlusion occurs in a patient with extensive arteriosclerotic occlusive disease and the extremity is not in jeopardy, it is frequently better to follow a conservative course of treatment. Anticoagulation therapy may be of value in preventing further thrombosis. Adequate medication should be given for relief of pain. Heat should never be applied to an ischemic part. The involved extremity should never be elevated. The extremity should be in a slightly dependent position; this will help to increase the amount of arterial blood in the extremity. Frequently the patient will have already found that by sitting on the side of the bed and hanging his legs over the edge he will have some diminution in the pain, but this may cause edema of the legs. If the patient is given adequate medication for pain so that he can tolerate having the leg in only a slightly dependent position, the edema will usually subside in 24 to 48 hours. Vasodilators such as tolazoline hydrochloride (Priscoline, 25 mg.) or papaverine hydrochloride, 100 mg., given intra-arterially above the block, may be of value in relieving spasm and symptoms of ischemia. If effective, medication can be repeated as indicated. The patient should be kept warm. He should be advised never to smoke. Buerger's exercises may give some relief of pain and should be used if the patient is physically able to accomplish them. As the patient improves, exercise of the legs with the use of a stationary bicycle and walking will help to improve collateral circulation. Lumbar sympathectomy is of value in a patient who has extensive arteriosclerotic occlusive disease and ischemic pain and in whom arterial surgery is not possible. It will frequently relieve ischemic pain but is of little help in relieving claudication. Limb survival rates vary. Darling et al. l reported a 91.4 per cent limb survival regardless of treatment. Edwards et al. 6 reported an 18.4 per cent limb loss in their series of patients.
340
CARL C. BARTELS
CONCLUSIONS Sudden arterial occlusion must be considered an emergency problem. The underlying disease responsible for the occlusion is frequently of sufficient seriousness to jeopardize the life of the patient. If clot embolism occurs, embolectomy is indicated in most instances, unless the general state of the patient would be jeopardized by surgery. The patient with generalized arteriosclerotic occlusive disease in whom acute occlusion develops frequently has good collateral circulation, so that the occlusion is often accompanied by only mild symptoms of vascular insufficiency. Furthermore, because extensive arteriosclerotic disease already is present in the extremity, vascular surgery of any type is less successful than in an extremity in which arteriosclerosis is not present. The use of the Fogarty catheter has helped to reduce the operative mortality and morbidity associated with clot embolism. Most arterial emboli are intracardiac in origin. Recurrent embolism is a serious hazard and is best avoided by adequate anticoagulation therapy. Prevention of recurrent embolism, more adequate treatment of heart disease responsible for clot embolism, and prompt recognition and treatment of the initial embolism will help to reduce the morbidity and mortality resulting from clot embolism.
REFERENCES 1. Allen, E. V., Barker, N. W., and Hines, E. A., Jr.: Peripheral Vacular Diseases. Philadel-
phia, W. B. Saunders Co., 1966, pp. 386-402. 2. Billig, D. M., Hallman, G. L., and Cooley, D. A.: Arterial embolism. Surgical treatment and results. Arch. Surg., 95:1-6 (July), 1967. 3. Cranley, J. J., Krause, R. J., Strasser, E. S., et al.: Peripheral arterial embolism: Changing concepts. Surgery, 55:57-63 (Jan.), 1964. 4. Darling, R. C., Austen, W. G., and Linton, R. R.: Arterial embolism. Surg. Gynec. Obstet., 124:106-114 (Jan.), 1967. 5. Durant, T. M., Oppenheimer, M. J., Webster, M. R., et al.: Arterial air embolism. Amer. Heart J., 38:481-500 (Oct.), 1949. 6. Edwards, E. A., Tilney, N., and Lindquist, R. R.: Causes of peripheral embolism and their significance. J.A.M.A., 196: 133-138 (April 11), 1966. 7. Fogarty, T. J., Cranley, J. J., Krause, R. J., et al.: A method for extraction of arterial emboli and thrombi. Surg. Gynec. Obstet., 116:241-244 (Feb.), 1963. 8. Gill, T. J., Ill, and Dammin, G. J.: Paradoxical embolism with renal failure caused by occlusion of the renal arteries. Amer. J. Med., 25 :780-787 (Nov.), 1958. 9. Haimovici, H.: The ischemic forms of venous thrombosis. 1. Phlegmasia cerulea dolens. 2. Venous gangrene. J. Cardiovasc. Surg., Suppl., 164-173 (Sept. 5-18), 1965. 10. Hardin, C. A., and Hendren, T. H.: Arterial embolism. Vase. Dis., 2:11-13 (Jan.), 1965. 11. Ingham, D. W.: Paradoxical embolism. Amer. J. Med. Sci., 196:201-207 (Aug.), 1938.
Sudden loss of arterial blood supply to part of the body may not only jeopardize the function of that part, but can result in tissue necrosis and the ultimate death of the patient. The patient in whom acute arterial occlusion has occurred is frequently a poor risk because of cardiac or generalized vascular disease. He may be unable to tolerate surgery, whether this be surgical removal of the occlusion or the necrotic part.
ETIOLOGY The most common causes of sudden arterial occlusion are clot embolism and arterial thrombosis. Clot emboli may be multiple. Edema and hemorrhage, together with too tight a cast or bandage, can cause arterial occlusion. Edema in a confined area, as that seen in the anterior tibial compartment syndrome, can result in local loss of blood supply. Dissecting aneurysm of the aorta, aortic and popli teal aneurysm, and false aneurysms may contribute to sudden loss of arterial blood supply peripherally. Peripheral arterial occlusion has been reported in patients with congenital heart disease in whom a venous clot or air embolus has passed through the foramen ovale into the peripheral circulation (paradoxical embolism).5. H. 11 Diseases responsible for clot embolism are primarily those of the heart. Mitral stenosis with atrial fibrillation in earlier studies had been the most common cause, but embolism may also occur in fibrillation without valvular disease. In recent studies, the incidence of embolism has been reported as being higher in patients having myocardial infarction with mural thrombosis. Darling et al.,4 in an analysis of 260 patients treated for arterial emboli, found that in 1948, 64.5 per cent of arterial embolisms resulted from rheumatic heart disease with atrial fibrillation, whereas in the past 10 years this figure was reduced to 35 per cent, arteriosclerotic heart disease being responsible for 51.1 per cent. Hardin and Hendren,lO in their study of 50 patients with arterial emboli, found that arteriosclerotic heart disease was the causative factor in 62 per cent, whereas rheumatic heart disease with atrial fibrillation was responsible in 32 per cent. Clot embolism may also occur in cardiac decompensation, mitral and aortic valvulitis, and subacute bacterial endocarditis. Medical Clinics of North
Ameri.ca~
Vo!. 53, No. 2, March, 1969
335
336
CARL C. BARTELS
Edwards et alY reported a patient in whom a part of an atrial myxoma caused a peripheral embolism. We have had two patients with Teflon aortic grafts in whom emboli of intima from the Teflon have occurred below the graft and in whom replacement had to be made with Dacron grafts. A thrombus, developing from an arteriosclerotic plaque of an artery or from an aneurysm, may break off, :resulting in distal occlusion of the artery or its branches. AlIen et al. l stated that in at least 10 per cent of patients with arteriosclerosis obliterans there is sudden occlusion. It is frequently difficult to determine the cause of an occlusion of an artery. When the cause is not known, serial electrocardiograms and blood enzyme studies may uncover an unsuspected coronary thrombosis that could be responsible for a mural thrombus and embolus. A nonspecific inflammatory process of the arterial wall caused by injury of the intima from an atheromatous plaque may cause edema and clot formation with occlusion of the artery. Acute inflammatory diseases such as thromboangiitis obliterans, polyarteritis, and lupus erythematosus can result in major artery occlusion. Surgical procedures on the heart or on an artery can result in peripheral emboli or thrombosis of arteries. Other factors may be responsible for arterial thrombosis or plugging, such as polycythemia, cryoglobulinemia, or macroglobulinemia, but these usually affect only the smaller end-arteries and do not result in extensive ischemia or loss of a limb. Trauma from the use of intra-arterial injections or catheters has resulted in sudden arterial occlusion. Ischemia can occur without acute arterial occlusion. In venous thrombosis there occasionally can be acute arterial spasm resulting from one of two conditions described as phlegmasia cerulea dolens or venous gangrene. 9
SYMPTOMS Symptoms vary greatly from sudden acute pain to mild numbness, coldness, or paresthesias. In a patient with no previous arterial disease, such as arteriosclerotic occlusive disease, if the occlusion is abrupt and complete, the symptoms are usually pain, paresthesias, coldness, tingling, muscular weakness, and paralysis. When complete occlusion occurs in a patient who has a slowly developing arterial occlusive process, the collateral circulation may have been sufficiently developed so that only mild discomfort, coldness, and paresthesias may be present. The location of the occlusion is also a factor in development of the symptoms. Acute occlusion of the smaller distal arteries is frequently better tolerated with only mild symptoms than acute occlusion of large, more proximal arteries. In the experience of AlIen et aLI the upper extremity has a better ability than the lower extremity to survive acute arterial occlusion. A renal artery occluded by embolism or other causes may be accompanied by flank pain and hematuria. If it is unrecognized, acute hypertension may result.
OCCLUSIVE ARTERIAL EMERGENCIES
337
An acute abdominal condition may result from mesenteric artery embolism or thrombosis. Symptoms from cerebral embolism depend on the location and the size of the artery occluded.
PHYSICAL EXAMINATION In the extremities, the absence of pulses helps to confirm the diagnosis of arterial occlusion. Anatomical variation in the position of arteries and the presence of previous occlusive arterial disease and edema may make it impossible to determine the presence or absence of pulsations and to arrive at any final conclusion concerning the cause or location of the arterial block. In the involved extremity, pallor of the skin usually appears early and cyanosis later. There may be grooving of the superficial veins resulting from lack of blood. There may be decrease in skin temperature, loss of sensation, diminution or loss of reflexes, rigidity, and loss of muscle function. Loss of sensation, of reflexes, and of muscle function with muscle rigidity are indicative of severe ischemia, and if some degree of circulation is not re-established, gangrene and loss of the extremity will usually result.
TREATMENT Maintenance of life must be the first consideration. The general state of health with specific reference to cardiac and generalized vascular disease must be considered in deciding the extent and degree of treatment of the patient with an acute arterial occlusion. If acute clot embolism occurs, embolectomy is usually indicated, unless the general state of health of the patient would be jeopardized by surgery. Failure to remove the clot may result in impaired function of the extremity and tissue necrosis, which in itself could be a serious threat to the patient. The clot embolus will lodge at points of bifurcation or anatomical or atheromatous narrowing of an artery. Darling et al.,4 in a review of 260 patients, noted that 68.1 per cent of emboli involved the bifurcation of the aorta or major peripheral· arteries, 22.6 per cent involved cerebral arteries, and 11.3 per cent involved visceral arteries. It is generally agreed that patients with arterial emboli should receive heparin as soon as the diagnosis is considered. This gives protection from propagation of the embolism by thrombosis both proximal and distal to the site of the embolism. It also provides time to evaluate the patient's condition with specific reference to the cardiac status and to the possible source of the embolism. It also provides time to institute appropriate therapy in an attempt to improve the patient's general state of health before any surgical procedure is attempted. Because of the high mortality rate, especially in patients with arteriosclerotic heart disease, careful evaluation is mandatory. The mortality rates for those with rheumatic heart disease vary from 20.4 to 26.6 per cent and for arteriosclerotic heart disease from 34.0 to 74.2 per cent. 4. 6
338
CARL C. BARTELS
In patients with clot embolism, early operation usually off~rs the best results. The best limb survival rate is obtained by surgery performed within 12 hours of the occlusion. 4,1O The results of embolectomy are poorer the longer the embolism remains in an artery, but this does not indicate that embolectomy should not be attempted. In a series of 11 patients who underwent embolectomy 4 days to a month after embolism, only one failure was experienced. Cranley et al,3 reported reviving a limb in the presence of rigor mortis of the muscles. Billig et al,2 reported the case of one patient in whom the extremity was improved after a bypass procedure that was performed for a saddle embolism of the aortic bifurcation 5 months after embolization. The use of the Fogarty7 catheter for removing emboli has been primarily responsible for the improvement in the results of embolectomy in recent years. By this technique, making a relatively simple surgical incision in both inguinal regions and opening the femoral arteries, it is possible to remove emboli from the bifurcation of the aorta down to and including the common femoral artery. In some cases it is possible to remove emboli from the superficial femoral artery. Once the embolus is removed, the possibility of the existence of a more distal thrombosis or embolism must be considered and can best be determined by arteriography or by the extent of the retrograde blood flow from the distal part of the artery. A small suction catheter passed down the femoral artery may pick up a distal clot. It may be necessary to expose the popliteal artery to attempt retrograde flushing. If the embolism is located at the bifurcation of the popliteal artery, exposure of that artery and removal of the embolism may be all that is necessary. Exposure of the posterior tibial artery and retrograde flushing with heparin solution will help to confirm the patency of the tibial artery. The restoration of the pedal pulses is a reassuring sign that circulation has been re-established. Pedal pulses may be absent immediately after operation, but may appear within an hour or two. Emboli in the upper limbs are more likely to lodge in the subclavian, axillary, or brachial arteries. The upper extremity seems to tolerate embolic occlusion better than the legs. Darling et al.,4 in a series of 59 patients treated conservatively for embolic occlusion involving the upper extremity, had two patients who required amputation. Mesenteric and cerebral emboli accounted for one third of the deaths from embolism in their series. Results of both surgery and conservative management in patients with these two problems have been poor. In the postoperative period, the patients who have had embolectomy must be given anticoagulation therapy. Previously the use of heparin after abdominal operation to remove a saddle embolus or an embolus from an iliac artery was somewhat hazardous, because hemorrhage could occur and remain undetected. Incisions required to use the Fogarty catheter are usually superficial, and should hemorrhage occur, it can usually be detected. Anticoagulation therapy should be started with heparin, and as soon as the patient is able to take oral medication, prothrombin depressant agents should be used. Once the therapeutic prothrombin level has been
OCCLUSIVE ARTERIAL EMERGENCIES
339
obtained, administration of heparin can be discontinued but oral anticoagulant should be continued. If the embolism has resulted from a myocardial infarction, anticoagulation should be maintained for a period of 3 to 6 months, and then it can gradually be terminated. If embolism has resulted from auricular fibrillation and fibrillation persists, anticoagulation therapy should be continued indefinitely. Recurrent embolism is common; Darling et al. 4 reported a rate of 45.5 per cent. Adequate anticoagulation must be maintained if there is to be any hope of reducing this. Acute occlusion, whether thrombotic or embolic, in an artery in which there has been slowly progressive arteriosclerotic occlusive disease is less likely to result in severe ischemic changes than acute occlusion of a normal vessel. Because of the gradual narrowing from arteriosclerotic occlusive disease, collateral circulation usually has developed. An arteriogram is of value in determining the degree of arteriosclerotic disease and determining whether a good vessel exists below the block. It also helps to indicate the extent of the block. If a good runoff exists below and the block is of short length, endarterectomy with removal of the clot and the arteriosclerotic process may produce a good result with the return of peripheral pulses. If the disease process in the artery is extensive, a vein bypass graft may be necessary. If an acute occlusion occurs in a patient with extensive arteriosclerotic occlusive disease and the extremity is not in jeopardy, it is frequently better to follow a conservative course of treatment. Anticoagulation therapy may be of value in preventing further thrombosis. Adequate medication should be given for relief of pain. Heat should never be applied to an ischemic part. The involved extremity should never be elevated. The extremity should be in a slightly dependent position; this will help to increase the amount of arterial blood in the extremity. Frequently the patient will have already found that by sitting on the side of the bed and hanging his legs over the edge he will have some diminution in the pain, but this may cause edema of the legs. If the patient is given adequate medication for pain so that he can tolerate having the leg in only a slightly dependent position, the edema will usually subside in 24 to 48 hours. Vasodilators such as tolazoline hydrochloride (Priscoline, 25 mg.) or papaverine hydrochloride, 100 mg., given intra-arterially above the block, may be of value in relieving spasm and symptoms of ischemia. If effective, medication can be repeated as indicated. The patient should be kept warm. He should be advised never to smoke. Buerger's exercises may give some relief of pain and should be used if the patient is physically able to accomplish them. As the patient improves, exercise of the legs with the use of a stationary bicycle and walking will help to improve collateral circulation. Lumbar sympathectomy is of value in a patient who has extensive arteriosclerotic occlusive disease and ischemic pain and in whom arterial surgery is not possible. It will frequently relieve ischemic pain but is of little help in relieving claudication. Limb survival rates vary. Darling et al. l reported a 91.4 per cent limb survival regardless of treatment. Edwards et al. 6 reported an 18.4 per cent limb loss in their series of patients.
340
CARL C. BARTELS
CONCLUSIONS Sudden arterial occlusion must be considered an emergency problem. The underlying disease responsible for the occlusion is frequently of sufficient seriousness to jeopardize the life of the patient. If clot embolism occurs, embolectomy is indicated in most instances, unless the general state of the patient would be jeopardized by surgery. The patient with generalized arteriosclerotic occlusive disease in whom acute occlusion develops frequently has good collateral circulation, so that the occlusion is often accompanied by only mild symptoms of vascular insufficiency. Furthermore, because extensive arteriosclerotic disease already is present in the extremity, vascular surgery of any type is less successful than in an extremity in which arteriosclerosis is not present. The use of the Fogarty catheter has helped to reduce the operative mortality and morbidity associated with clot embolism. Most arterial emboli are intracardiac in origin. Recurrent embolism is a serious hazard and is best avoided by adequate anticoagulation therapy. Prevention of recurrent embolism, more adequate treatment of heart disease responsible for clot embolism, and prompt recognition and treatment of the initial embolism will help to reduce the morbidity and mortality resulting from clot embolism.
REFERENCES 1. Allen, E. V., Barker, N. W., and Hines, E. A., Jr.: Peripheral Vacular Diseases. Philadel-
phia, W. B. Saunders Co., 1966, pp. 386-402. 2. Billig, D. M., Hallman, G. L., and Cooley, D. A.: Arterial embolism. Surgical treatment and results. Arch. Surg., 95:1-6 (July), 1967. 3. Cranley, J. J., Krause, R. J., Strasser, E. S., et al.: Peripheral arterial embolism: Changing concepts. Surgery, 55:57-63 (Jan.), 1964. 4. Darling, R. C., Austen, W. G., and Linton, R. R.: Arterial embolism. Surg. Gynec. Obstet., 124:106-114 (Jan.), 1967. 5. Durant, T. M., Oppenheimer, M. J., Webster, M. R., et al.: Arterial air embolism. Amer. Heart J., 38:481-500 (Oct.), 1949. 6. Edwards, E. A., Tilney, N., and Lindquist, R. R.: Causes of peripheral embolism and their significance. J.A.M.A., 196: 133-138 (April 11), 1966. 7. Fogarty, T. J., Cranley, J. J., Krause, R. J., et al.: A method for extraction of arterial emboli and thrombi. Surg. Gynec. Obstet., 116:241-244 (Feb.), 1963. 8. Gill, T. J., Ill, and Dammin, G. J.: Paradoxical embolism with renal failure caused by occlusion of the renal arteries. Amer. J. Med., 25 :780-787 (Nov.), 1958. 9. Haimovici, H.: The ischemic forms of venous thrombosis. 1. Phlegmasia cerulea dolens. 2. Venous gangrene. J. Cardiovasc. Surg., Suppl., 164-173 (Sept. 5-18), 1965. 10. Hardin, C. A., and Hendren, T. H.: Arterial embolism. Vase. Dis., 2:11-13 (Jan.), 1965. 11. Ingham, D. W.: Paradoxical embolism. Amer. J. Med. Sci., 196:201-207 (Aug.), 1938.