- Email: [email protected]
Peripheral Arterial Emergencies
Peripheral Arterial Emergencies O. ALAN ROSE, M.D., F.A.C.P.·
majority of acute peripheral arterial conditions are caused by sudden or rapidly developing occlusion. With prolongation of life due to medical advances, it may be anticipated that arterial emergencies will be seen with increasing frequency. Acute arterial occlusion was formerly considered an exclusively surgical problem. With increased knowledge of the mechanisms involved, and following the introduction of anticoagulants, the diagnosis and institution of correct therapy have become the primary or initial responsibilities of the physician who first sees the patient and is best able to start the proper early treatment. Recent developments in surgical vascular techniques have improved the efficacy and safety of surgical procedures, and have also made it possible in many instances to restore arterial circulation in vessels which were previously considered to be inoperable. Since both medical and surgical treatment are frequently required, it is advantageous for both physician and surgeon to observe, and be prepared to treat the patient from the time the diagnosis is made. Abrupt interference ,vith arterial flow may result in the loss of an extremity or its parts. Death may follow the occurrence of shock or may be due to prolonged stress or to amputation. Patients who are debilitated or suffer from chronic diseases are most subject to vascular occlusions and least able to tolerate their sequelae. The early institution of the correct therapeutic measures will usually improve, and may almost completely restore adequate arterial circulation. Too frequently, the diagnosis of sudden arterial occlusion is not made early enough for maximal therapeutic benefit.
THE
ETIOLOGY
Acute arterial occlusions may result from a number of causes and predisposing factors. These are listed in the accompanying outline. From the Department of Medicine, New York University College of Medicine and the Third (New York University) M edical Division of Bellevue Hospital, New York, N.Y.
* Assistant Professor of Clinical Medicine, New York Un1:versily College of Medicine; Attending Physician, Cardiovascular Service and Chief, Cardiac Clinic, Lenox Hill Hospital; Attending Physician, Cardiovascular Service, Veterans Administration Hospital, Kingsbridge Road, Bronx, N.Y. 629
o. Alan Rose
630
Thrombosis, secondary to previously existing partial arterial occlusion, and embolism produce acute arterial obstruction in the vast majority of cases. More than one factor frequently combine to cause acute arterial insufficiency. This is seen most commonly with resulting tissue necrosis, when a limb with obliterative arterial disease has been exposed to trauma, particularly to cold, and to badly fitting shoes. Vasospasm alone may produce profound ischemia and occasionally is the sole evident cause of gangrene of an extremity. DIAGNOSIS
The diagnosis of acute arterial occlusion usually demands no special equipment. An awareness of the possibility that the condition may exist, a good detailed history of the onset and development of the complaint, and careful observation and examination with hand and fingers will almost invariably establish the presence of arterial obstruction. The following are the symptoms and signs of acute arterial occlusion: (1) pain, (2) neuropathy, (3) skin color and temperature changes, (4) superficial veins collapsed, and (5) arterial pulsations weak or absent. Symptollls
The manifestations depend upon a number of factors, particularly the rate of development and the degree of ischemia of the part. With high sudden obstruction, especially when caused by a "saddle embolus" lodged at the aortic bifurcation, the onset is usually dramatic. The symptoms and signs develop rapidly, with abrupt onset of severe pain in the region of hips and buttocks or upper thigh. There is usually loss of motor function or extreme weakness of both lower extremities, with marked pallor, and lowering of the skin temperature. These, and the less striking manifestation of arterial insufficiency described below, are often at first believed to be due to neurological or to orthopedic disorders. Acute deep vein thrombophlebitis is sometimes nlistaken for arterial occlusion. Phlebitis can usually be differentiated by the enlarged appearance of the involved limb, the presence of engorged veins, elevated skin temperature, and normal arterial pulses. However, secondary vasospasm in thrombophlebitis may make differential diagnosis difficult. The onset of acute arterial obstruction is often insidious. Pain may be absent or insignificant and, contrary to general belief, occurs in only about 50 per cent of patients as the first evidence of sudden occlusion. Pain is frequently so diffuse and variable that the diagnosis of myositis or neuralgia is made before attention to absent pulses or other evidences of arterial occlusion indicate that emergency therapy for arterial occlusion is required. When profound ischemia persists, especially with delayed or inadequate treatment, neuropathy may result in pain which is so severe that 'it becomes the reason for amputation. Early acute rest pain often merges into the later chronic symptom, intermittent claudica-
Peripheral Arterial Emergencies
631
FACTORS WHICH CAUSE OR PREDISPOSE TO ACUTE ARTERIAI.J OCCLUSION Thrombosis Partial or Intermittent Occlusion
Arteriosclerosis obHterans Thromboangiitis obliterans Mechanical factors Shoulder girdle compression syndrome Surgery and fractures Systemic Hemodynamic Factors Heart failure Shock Trauma Extensive surgery Crushing injury Excessive exposure to heat, cold or radiation Arteritis Thromboangiitis obliterans Collagen diseases Rheumatoid arthritis Essential polyangiitis (periarteritis nodosa) Lupus erythematosus disseminatus Secondary to acute and chronic infections Intravascular H ypercoagulability Blood dyscrasias Cryoglobulinemia Thrombophilia Idiopathic "Thrombosing disease"
Embolism Cardiac-Mural Thrombosis Due to:
Heart failure Atrial fibrillation Myocardial infarction Endocarditis (nonbacterial and bacterial) Cardiac-Septal Defect From venous origin ("paradoxical") Arterial-Mural Thrombosis Due to: Obliterative arterial disease Aneurysm Endarteritis N onclot Embolism Air Fat Tumor Inorganic substance
Transection, Laceration or Perforation
Surgery Gunshot wounds Miscellaneous accidents
Vasospasm
Secondary to acute arterial or venous occlusion Due to cold, injury and other trauma
o. Alan Rose
632
tion. Numbness is the next most frequent symptom and may be the patient's only initial complaint. Paresthesias, cramps, itching, burning or a sense of weight may be present. These, with frequent loss of motor power in the involved extremity and the physical findings to be described, will usually establish the diagnosis. Signs
With sudden occlusion, the involved extremity is usually waxy pale at onset, later becoming mottled in appearance. The superficial veins are collapsed with the extremity in the horizontal or dependent position, and the temperature of the skin is lowered. Involved arterial pulsations always become diminished or disappear. Careful palpation of the major arteries (the femoral, popliteal, dorsalis pedis and posterior tibial in the lower extremities and the brachial, radial and ulnar in the upper extremities) will usually lead to the definitive diagnosis. Oscillometry may be helpful as a corroborative objective method for the determination of the presence of pulsations and the approximate level of obstruction. However, this and other instruments used to evaluate the local circulation are rarely, if ever, essential to the diagnosis of acute arterial occlusion. Lowered skin temperature can usually be easily recognized by the palpation of the involved extremity with the back of the hand and fingers and comparison of the temperatures of symmetrical parts of its mate. While it is frequently impossible to exactly localize the site of obstruction and to differentiate between thrombosis and embolism when the patient is first seen, the treatment to be initiated is the same. Any advantage which might he derived fronl initial precise evaluation is unimportant compared to the urgency of starting treatment at the earliest possible time. Because of the not infrequent absence of striking symptoms and the unfortunate tendency of the physician to neglect careful and thorough examination of the extremities, the diagnosis of acute arterial insufficiency has often gone unrecognized until much precious time has been lost. MEDICAL TREATMENT
The principal aims of medical treatment are: (1) to protect the involved extremity, (2) to promote maximum dilatation of all its remaining patent collateral vessels, and (3) to prevent further occlusion by propagated thrombus. These aims are usually best accomplished by early treatment and observation under the supervision of both physician and surgeon. Optimal therapeutic results in the restoration of circulation can usually be achieved with medical measures alone when occlusion is peripheral to the femoral arteries of the lower extremities and to the brachial arteries of the upper. The progress with medical treatment will indicate the level of obstruction and whether operative intervention will be re-
Per~pheral
Arterial Emergencies
633
quired. Embolectomy, or one of the procedures for the removal of an obstruction in a segment of a major artery, may ordinarily be postponed for sufficient time to permit adequate evaluation of medical measures. Early Treatm.ent
The patient with acute arterial occlusion is usually best cared for in a hospital. However, whether the diagnosis is established or is only strongly suspected, treatment should be instituted wherever he is and as soon as possible after the patient is first seen. Pain and anxiety which reflexly produce vasoconstriction should be relieved with reassurance by the physician, the use of opiates (morphine 15 to 30 mg., Demerol 75 to 100 mg.) and other sedation, particularly rapidly acting barbiturates (parenterally sodium Luminal or Seconal or pentobarbital 0.1 gram per os). Alcohol by Inouth (V\rhisky or brandy-30 cc. or more) is also recommended for this purpose and as a mild vasodilator agent. The extremity should be maintained in a some,vhat dependent position. This is best accomplished by raising the entire head of the bed 4 to 6 inches on books, blocks or other support. The optimal position is that ,vhich nearly produces the normal pink color in the distal portions of the involved limb. Protection, and Avoidance of Harm.ful Measures
Commonly used measures which may cause irreparable damage should be sedulously avoided. These include the local application of various medications, massage, heat, cold, and elevation of the involved extremity. The ischemic limb is extremely sensitive to trauma due to pressure and to degrees of heat and cold which are well tolerated by normal tissues. Protection of the extremity is therefore of the utmost importance and is achieved by covering it gently with bland oil or lanolin and wrapping it in bulky, soft, porous material such as cotton or a light, soft blanket. A cradle should be used if available. The best type is that which is inserted under the mattress. It serves only to protect the extremity from the pressure of bedclothes and from drafts and should therefore be covered with a sheet and not contain a heating element. A bolster placed at the foot of the bed will reduce trauma to the feet, and is especially important when the head of the bed is elevated. Vasodilator Measures
Local, and sometimes widespread vasospasm follows rapid occlusion of arteries and veins, which at the outset may make it difficult or impossible to identify the exact site and extent of organic obstruction. Of far more importance is the less recognized fact that, if secondary vasoconstriction is allowed to persist, extensive thrombosis will result when the circulation eventually begins to be re-established. This is believed to be the result of ischemic changes in the intima of involved vessels. 1 Specific
634
o. Alan Rose
vasodilator therapy is urgently indicated in addition to the relief of pain and anxiety, and treatment of other factors which predispose to vasoconstriction. Reflex vasodilatation is the simplest and one of the best methods of dilating peripheral vessels, and is so effective that it is one of the few reliable tests for the evaluation of peripheral vasoconstriction. It is the physiological mechanism which reflexly induces peripheral vasodilatation when the body temperature is elevated. Its simplicity is an important additional advantage because it can be easily instituted when the patient is first seen and continued thereafter. Reflex vasodilatation is induced as follows: the body and uninvolved extremities of the patient are covered with blankets, while the involved limb is protected as described above, and is maintained at average room temperature (60 to 800 F.) to minimize its local tissue metabolism and circulatory requirement. Hot water bottles or electric pads are applied to the abdomen or back. The temperature, taken rectally, should be raised and maintained at one or more degrees above normal (more than 1000 F.). Orally administered agents should be used to aid in the maintenance of maximum vasodilatation and for this purpose mild dilator medications are advisable to avoid side effects which may complicate treatment. In addition to alcohol, papaverine which also has a sedative effect is recommended. The dose should be a relatively large one (0.1 to 0.2 gram). Tolazoline hydrochloride (Priscoline hydrochloride) is a more powerful agent and is usually well tolerated in doses of 25 lUg. Dosage may be cautiously increased to 50 or to 75 mg. depending upon the development of side effects. Phenoxybenzamine (Dibenzyline) is more effective than Priscoline but side effects are also more common. The dosage is 10 mg. or more. Phenyl-I-butyl-norsuprifen (Arlidin), a new vasodilator agent which is reported to affect predominantly the deep arterial circulation, has not as yet been adequately evaluated. The above drugs are given at four to six hour intervals. Hexamethonium and other ganglionic blocking agents are liable to produce effects which are too widespread to be practical or safe for use in the dosage required to relieve spasm in acute local arterial occlusion. The response to potent vasodilator medications when given orally or intravenously is maximal upon the most normal vessels and may therefore actually shunt blood away from diseased or partially occluded arteries. Patients with peripheral arterial occlusion often have concomitant recognized or occult vascular disease involving vital areas, particularly the cerebral, coronary and renal circulations. Vasodilator agents are thus capable of actually increasing vascular insufficiency in these as well as in more acutely involved areas. The intra-arterial route of administration is theoretically best for the emergency use of vasodilator agents in acute arterial occlusion because the effect is attained at the earliest possible time and is achieved with
Peripheral Arterial Emergencies
635
maximal concentration of therapeutic agents where they are most needed. The almost exclusively local effect of intra-arterial therapy has been found to be safe for patients with diffuse vascular involvement and to be relatively free from the systemic side reactions which are frequent when a general route of administration is used. 2 It has been demonstrated that vasodilator medication given intra-arterially can duplicate the response to adequate sympathetic block and that this effect is ,velllocalized.8 TIle only equipment required is the material to be administered and syringe and needle which may be carried in the physician's bag with his other emergency medications. The injection is most often given into the femoral artery because of the frequency of obstruction distal to this vessel, and the ease with ,vhich it can be entered. The brachial and other vessels can also be used. The technique for intra-arterial administration is easily mastered. When the femoral artery is used, the injection is given just below the inguinalligament. The arterial pulsation must be palpable. Two fingers are placed on the pulsating longitudinal axis of the vessel and the needle is inserted at right angles to the artery between the palpating fingers until the return of bright red arterial blood (which usually enters the syringe under positive pressure) indicates that the needle has entered the lumen of the artery. A small (22 or 23 gauge) needle is best used to minimize local arterial trauma, and pressure is applied firmly at the site immediately following injection. While the vasodilator effect is of relatively short duration following the intra-arterial administration of present dilator agents, the method is valuable for emergency use. Priscoline (12.5 to 50 mg., 0.5 to 2 cc.) has been shown to be effective and well tolerated when given intraarterially.3. 4 It is given slowly over a period of several minutes, at a rate of about 1 cc. per minute. Newer vasodilator agents have been studied2 and investigation is being continued in an effort'to discover vasodilator medications which whe.n given by the intra-arterial route most nearly approach the ideal of prolonged action and minimal side effects. Sympathet~c blockade by the injection of local anesthetic agents in autonomic ganglia, in the region of the cauda equina or in the spinal canal will effectively release local spasm 'for six or more hours. The disadvantages of this form of therapy are: (1) an experienced anesthesiologist is required, (2) there is almost always a delay before this treatment can be started, and (3) the danger of deep local injections after anticoagulant therapy has been instituted. If the patient is hospitalized when acute occlusion occurs and block can be performed promptly, it is a -:valuable adjunct in treatment. This applies particularly to patients with ~rial embolism where angiospasm is most severe and early surgery may be anticipated. Blocks or sympathectomy may also be valuable at tthe time of surgery to aid in optimal vasodilatation.
636
o. Alan Rose
Anticoagulant Therapy
The object in the use of anticoagulants is to prevent propagation of thrombus distal and proximal to the site of obstruction with occlusion of essential collateral vessels. Anticoagulation therapy is recognized as one of the major factors in the improved results of medical treatment of acute vascular occlusion. Heparin is the only anticoagulant which is effective within minutes following administration and it is therefore the drug of choice for the institution of emergency anticoagulation therapy. If it is technically possible, heparin is given intra-arterially usually in a dose of 25 mg. Injection proximal to the site of obstruction may be precluded by high occlusion or inability to palpate the arterial pulsation. Whether heparin is administered intra-arterially or not, it is given by the intravenous route as soon as possible after occlusion. The initial intravenous dose of heparin is usually 100 mg. followed by doses of 50 to 75 mg. every four to six hours. We use the aqueous preparation with concentration of 50 mg. per cc. and follow the initial intravenous dose with 50 or 75 mg. given subcutaneously every six hours. Extensive experience with the intermittent method of heparin administration indicates that adequate anticoagulant effect is achieved despite long periods when the clotting time is only slightly prolonged or normal. i For this reason clotting times are usually not necessary when heparin is used alone. This is an advantage in the use of heparin compared to the coumarin derivatives and is particularly important when adequate laboratory facilities are not available. We prefer the subcutaneous route for the continued use of heparin following the initial intravenous dose because (1) it has been found to be satisfactory over a number of years, (2) it eliminates the possibility of producing a large occult deep hematoma which we have seen following intramuscular injection and (3) it permits the regular administration of heparin by nurses, by a member of the family or even by the patient himself. While ecchymoses often occur with subcutaneous heparin administration, they cause no significant distress or serious sequelae. Heparin is expensive and it must be administered parenterally at intervals with some discomfort to the patient. Anticoagulant effect is usually required for days or weeks after acute vascular occlusions and in some cases is continued for much longer periods on an ambulatory basis. For these reasons, the longer acting, easily administered coumarin preparations are usually started soon after the first dose of heparin. Heparin is discontinued only when the prothrombin time has reached the therapeutic range (usually 48 to 72 hours). If emergency surgery is to be performed, Dicumarol is usually not given and the effect of heparin is neutralized with protamine. The dosage for protamine is that of the heparin which has been administered in the previous four hours. Our experience is in agreement with others that it is rarely necessary
Peripheral Arterial Emergencies
637
to use agents other than Dicumarol and heparin. 6 Proficiency increases with the use of these preparations. There is no space here for a detailed discussion of drugs and methods of administration. It is stressed however, that, anticoagulant therapy should not be undertaken without a thorough knowledge of the correct use of these agents, the contraindications to anticoagulation and the treatment of excessive effect from heparin or the coumarins. These extremely important aspects are now well established and information concerning them is readily available in the literature and recent texts. The physician who institutes this treatment must accept complete responsibility for administration and control of the agents used. A suggested method for the use of anticoagulants for acute arterial occlusion is included in the outline of treatment at the end of this section. Treatment of Systemic Disease
Treatment of concomitant systemic disease is, of course, urgently required. This is particularly true of congestive heart failure and of cardiac conditions which may predispose to embolism. Emboli most frequently arise from the heart in rheumatic disease particularly when mitral stenosis and atrial fibrillation are present. Here, both medical and surgical treatment are frequently necessary. Medical therapy is directed at heart failure, arrhythmias and carditis. Prophylactic use of anticoagulants may also be indicated. Surgical treatment for embolism will be discussed below. A small embolus frequently warns of the occurrence of larger, more serious and possibly fatal emboli to follow. This applies to atrial fibrillation and other paroxysmal arrhythmias and to embolism from an aneurysmal sac and similar sources. When emboli result from bacterial endocarditis, acute or subacute, anticoagulants are contraindicated. Here, of course, the early institution of adequate penicillin or other antimicrobial therapy is required to treat the disease and to prevent the damaging effects of infected emboli. Arterial occlusion due to emboli indicates immediate search for the source because the process which is responsible may itself require emergency treatment or may considerably influence the form of therapy to be used. Myocardial infarction with mural thrombosis may be responsible for embolism. Here, treatment for the cardiac condition is usually more urgent than that for the embolic phenomenon and at least temporarily precludes surgery. This is illustrated by the following case: CASE I. A 59 year old Negro clerk was admitted to the hospital complaining of severe pain in the right thigh and calf of 2 days' duration. Sudden onset of pain obliged him to stop walking. Severe rest pain had persisted despite repeated treatment opiates and other medications. Hot and cold soaks had been prescribed by his family physician and these had exaggerated the pain. Examination on admission revealed absence of all arterial pulsations below
638
o. Ala1L' Rose
the right femoral artery which was pulsating strongly. Pallor and lowered temperature were noted in the leg below the knee. Routine electrocardiograms taken soon after admission revealed the presence of a recent anteroseptal myocardial infarct, which had apparently been asymptomatic. The diagnosis of embolism to the right superficial femoral artery secondary to myocardial infarction was made. Because of the interval following onset and the patient's cardiac status, surgical intervention was not considered. Heparin and Dicumarol were started. Priscoline, 25 mg., was administered in the right femoral artery. Additional measures as included in the outline for treatment were followed. Intra-arterial vasodilator medication was given twice daily for the first several days and daily thereafter. Papaverine 0.1 gram four times daily and alcohol 30 cc. three times daily were also given by.mouth. The temperature of the extremity improved progressively within 24 hours, with return in sensation and motor power and progressive decrease in pain. The cardiac status improved with the disappearance of minimal failure which had been present on admission. The electrocardiogram showed evolutionary changes. The patient was discharged from the hospital in 6 weeks. He remained on maintenance Dicumarol therapy and vasodilator medications for 6 months during which time initial claudication of one or two blocks improved to walking tolerance of 10 blocks which has persisted to the present. Recent femoral arteriogram performed 3 years after embolism reveals complete obstruction of the right superficial femoral artery and the development of extensive collateral circulation (Fig. 85).
This case also illustrates that medical treatment alone may be adequate in the treatment of embolism even with relatively high arterial occlusion. The unusual collateral supply which developed in this instance has made it unnecessary to consider late surgery. Diabetic patients are likely to develop complications in the presence of sudden arterial occlusion. Adequate control of diabetes may be difficult but is essential, as dehydration, acidosis and coma predispose to thrombotic occlusion, infection and a high mortality. Infection should be vigorously treated with antimicrobial agents. General and Supportive Measures
Adequate hydration and nutrition are extremely important, particularly in patients who are old and debilitated. Hemoconcentration may be an important predisposing factor in thrombotic arterial occlusion. Hydration may be accomplished with administration of sodium-free fluids. Two liters or more each 24 hours should be given pa.renterally or orally even in the presence of severe cardiovascular disease. Necessary nutrition should not be neglected. Additional Conditions Which Require Individual Treatlllent
Factors which increase the thrombosing tendency, particularly blood dyscrasias, must of course be treated individually with an attempt at correction of the factor which predisposes to thrombosis. Polycythemia
Peripheral Arterial Emergencies
639
Fig. 85. Femoral arteriogram in a case of embolus to superficial femoral artery, showing site of obstruction of right superficial femoral artery (arrow) with collateral vessels to the considerably enlarged profunda femoris. The deep femoral artery supplies large collateral vessels peripherally. Extensive collateral circulation about the knee is visualized with return of flow below.
vera, thrombophilia, cryoglobulinemia and so-called "thrombosing disease" sometimes respond to the prophylactic use of anticoagulants. Thrombotic occlus~:on due to the arteritides is extremely difficult to control. We have seen a young Negro girl with known lupus erythematosus who had extensive thrombosis involving both arteries and veins of the leg below the knee which resulted in amputation. The process did not respond to medical treatment. Section of the amputated extremity showed suggestive evidence of involvement due to lupus erythematosus. Treatment should be directed at the cause of arteritis if known, particularly predisposing infections. Thromboangiitis obliterans may respond simply to the discontinuance of the use of tobacco. Arteritis related to collagen diseases may respond to the steroids. IIovv"'ever, there is evidence which suggests that these compounds themselves predispose to thrombosis. 7 Arterial thrombosis related to exposure to heat, cold and moisture, including frostbite, "trench foot," "immersion foot" and related syndromes, and arterial involvement secondary to radiation are usually treated with the
o.
Alan Rose
conservative measures which have already been outlined. 1'1he involved extremity is protected and nlaintained at a constant environment of 70 to 80° F. The use of anticoagulants and vasodilator agents lnay aid by preventing extension of thrombus, particularly during the stage vvhen severe vasospasm plays an inlportant part in the occlusive process. SURGICAL TREA rMEN1' r
The increasing etIectiveness and safety of vascular surgery has made it possible to consider this treatment for most patients with high arterial occlusion. Vascular surgical procedures even when extensive are essentially local and minor, and are generally very well tolerated. Embolectomy is usually the treatment of choice vvith involvement of the lower abdominal aorta, the iliac or femoral arteries, or the lnajor arteries of the upper extremities. When indicated, embolectomy should be performed within six hours after occlusion if possible. While the likelihood of re-establishing adequate circulation decreases progressively with time, embolectomy has been successful in some cases when performed 24 or more hours after occlusion. As previously indicated, medical treatment should be evaluated if possible before a surgical procedure is undertaken, as vasospasm following acute occlusion commonly presents the picture of arterial obstruction at a much higher level than that which is caused by the embolus. We have seen a number of instances ,vith the manifestations of iliofemoral or lower abdominal aortic occlusion, when the site was at or below the popliteal artery. Medical measures alone in these cases frequently resulted in almost complete return of the arterial circulation. The decision to operate, can, as previously emphasized, best be lllade with the frequent observation of the patient by both physician and surgeon. Embolectomy may be indicated or operative treatment of the source of emboli may be useful when the patient has recovered from the initial acute occlusion and his general condition is optimal to withstand such procedures. These include resection of aneurysm, and in some cases, cardiac surgery. Excellent long-term surgical results have been attained in the treatment of emboli due to rheumatic heart disease with mitral stenosis and atrial fibrillation. This is illustrated by the follo,ving case: CASE 11. The patient, a 44 year old secretary, had longstanding rheumatic heart disease, with mitral stenosis and atrial fibrillation. There had been progressive reduction in cardiac reserve over the previous several years, with two brief episodes of pulmonary edema in the preceding three months. She was admitted to the hospital because of severe lower back and abdominal pain and diffuse pain in both lower extremities accompanied by numbness, paresthesias, and complete loss of motor power. All arterial pulses of the lower extremities were absent including the iliac and femoral pulsations. The extremities were cool below midthigh, with marked diminution in sensory perception and absent reflexes. Six hours after onset a saddle embolus was removed transperitoneally. Heparin was injected into the aorta before closure and given postoperatively
Peripheral Arterial Emergencies
641
for the first three days when the prothrombin time reached the therapeutic range with Dicumarol. There was improvement in color, temperature and return of sensation and motor power within 24 hours postoperatively. All arterial pulsations gradually returned. The patient's cardiac status became progressively worse despite digitalization, dietary restriction of salt, and mercurial diuretics. Clinical evidence supported by cardiac catheterization indicated that mitral stenosis was the predominant or exclusive lesion, and mitral commissurotomy was performed three months after embolectomy. There has subsequently been considerable improvement in the cardiac status, the patient is able to work regularly, walks at an average pace and climbs two flights of stairs without dyspnea. Dicumarol, which had been administered until commissurotomy, was discontinued postoperatively. The patient has not required medication except for digitalis. There have been no further embolic manifestations.
The results of surgery, both for the source and the embolus itself, were unusually successful in this case. Emboli of this size are relatively uncommon as a result of rheumatic heart disease. Rarely, emboli from a venous source produce occlusion of peripheral arteries. This so-called "paradoxical" embolus indicates the presence of an interatrial septal opening, which has permitted an embolus to pass from the right to the left heart. This may occur with a patent foramen ovale or a larger congenital atrial septal defect. Large atrial defects may be considered for surgical treatment. When the cause of high occlusion is rapidly progressive thrombosis, vascular surgery may be considered. Removal of the thrombus and a portion of the inner wall of the artery (thromboendarterectomy), section of the occluded segment with graft replacement, or a by-pass procedure may be possible. These surgical measures are frequently successful in the treatment of relatively chronic high segmental arterial occlusion and they may occasionally be performed with dramatic improvement in arterial flow in patients with acute thrombosis. When such surgical procedures are considered in acute as well as chronic cases, it must be established that there is adequate arterial outflow below the obstructed portion before they are attempted. This is likely to be true when occlusion is due to embolism, particularly when it occurs in relatively young people. With thrombotic occlusion, and in older individuals, arteriography is extremely helpful for the identification of the exact location and extent of occlusion, as well as the presence of necessary patent peipheral arteries. We have seen several patients who while under direct observation have developed such occlusions and ,vho have been operated upon successfully. The results in a patient with right iliac thrombosis is demonstrated in Figure 86. Surgical intervention is of course urgently indicated when arterial obstruction is due to injury with transection, laceration or perforation. Fractures compressing lnajor vessels must be immediately treated. Injured vessels may be repaired by suture and large damaged sections may
o. Alan Rose
Fig. 86. Right iliofemoral thrombosis with thromboendarterectomy. A 53 year old laborer with intermittent claudication of 2 weeks' duration in region of right hip and upper thigh. Rapid progression in symptoms over -several days with complete obstruction at right iliofemoral level (aortagrams A and lE). Thromboendarterectomy resulted in marked improvement in arterial flow to below popliteal level (aortagrams and D). The patient is now almost completely asymptomatic.
o
Peripheral Arterial Emergencies be replaced by arterial grafts. 8 The physician who initiates treatment for arterial injury should be extremely careful in the use of tight tourniquets and their prolonged applications because they may produce considerable trauma to uninvolved vessels and nerves. The surgical treatment of the shoulder girdle compression syndromes is frequently difficult and inadequate. While newer procedures have been devised for these conditions, 9 medical measures, especially postural exercises and muscle training, are usually effective and obviate the need for surgery. Amputation is the final admission of both medical and surgical failure. It is indicated when necrosis is extensive or cannot be controlled. This occurs most frequently with progression of gangrene from digits to involve the more proximal portions of extremities. The fullest possible evaluation of medical and other surgical measures should precede consideration of amputation. However, when the condition is hopeless, delay in radical surgery may threaten further vascular impairment or the life of the patient. When indicated, amputation should of course be at the lowest possible level including transmetatarsal resection or below-knee amputation in lo"\\~er extremities. Medical treat.ment when only digits or small areas of extremities or other portions of the body are involved should include protective dressings, scrupulous cleanliness of the involved part, the prophylactic use of antimicrobial agents, and vasodilator measures as outlined above. Refrigeration should be used only for areas of necrosis or those which are obviously compromised, and is indicated solely to prevent absorption and for local anesthetic effect prior to operation. An outline for the treatment of acute arterial occlusion is presented on the following page. PROPHYLAXIS
Arterial occlusion both acute and chronic is in the majority of instances related to atherosclerosis. This process is no longer accepted as the inevitable result of degenerative change3 and a more dynamic approach has stimulated intensive investigation of possible etiological factors. While the results of these studies have as yet no definite clinical application, there is considerable hope that they will lead to measures which will aid in the prevention of this most prevalent vascular disease. Significant findings to date apply to dietary factors and suggest the advisability of low caloric, nutritious diets and of weight reduction for obesity. Surgical treatment of evident or potential sources of embolism including procedures to improve or repair intracardiac abnormalities, the excision of aneurysms, and the treatment of abnormal vascular communications has been indicated. Surgical measures are frequently efficacious in the prophylactic treatment of carefully selected cases with high level segmental arterial obstruction.
o. Alan Rose GENERAL PLAN AND OUTLINE FOR THE TREATMENT OF ACUTE ARTERIAL OCCLUSION l. Treatlllent of Pain and Anxiety A. Morphine 8ulfate 15 to 30 mg. or Demerol, 100 mg. B. Sedation-rapid acting barbiturate-reassurance I L Protection of Extrelllity and Optimal Position A. Cover lightly with mineral oil..or lanolin and protect distal portions
B. Position of extremity below heart level
Ill. Vasodilator Measures A. Heat body with blankets and hot water bottles or electric pads (maintain involved extremity at 60 to 80° F.) B. Intra-arterial-PriscoIine 12.5 to 50 mg. Repeat 1 to 3 times daily (heparin may be given in same syringe with initial dose) c. Oral-alcohol 30 cc. or more, papaverine 100 to 200 mg. every 4 hours, PriscoIine 25 to 50 mg. or dibenzyline 10 mg. (These vasodilator agents can also be given by other routes.) D. Sympathetic block-paravertebral, caudal, spinal anesthesia (if it can be performed promptly)
IV. Initiate Anticoagulant Therapy A. Heparin 100 mg. intravenously and, if possible, 25 mg. intra-arterially, followed by heparin 50 to 75 mg. intravenously or subcutaneously every 4 to 6 hours B. Dicumarol 300 mg. followed by daily doses depending upon prothrombin times V. General Measures
A. Prompt adequate treatment of concomitant infection and acute systemic diseases (congestive heart failure, shock, diabetic coma or hypertensive crisis) B. Hydration-2000 to 3000 cc. of low sodium fluids each 24 hours (increased if fever present) c. Nutrition including necessary proteins and vitamins particularly for old and debilitated patients VI. Surgical Treatm.ent
A. Measures to improve arterial flow 1. Embolectomy-within 6 hours if possible 2. l'hromboendarterectomy or graft 3. Relief of compression from fractures, shoulder girdle compres.. sion and other mechanical factors B. Amputation-early if condition of extremity is hopeless. Refrigeration of necrotic and compromised parts only and only preliminary to amputation.
Prophylactic medical measures are specifically required vvhen there is evidence of partial peripheral arterial occlusion demonstrated by diminished arterial pulses, and/or a history of claudication or other manifestations of arterial insufficiency. At this time, the patient's condition and the need for prophylaxis should be carefully explained, and reassurance given that, with proper care, serious consequences can usually be avoided. Written instructions regarding foot care, the avoidance of trauma, the use of vasodilator measures, and weight reduction with adequate diet and hydration are useful in the institution and maintenance of a prophylactic regimen. The use of tobacco must of course be forbidden. Regular
Peripheral Arterial Emergencies follow-up examinations for evaluation of the progress of arterial occlusion and the adequacy of prophylactic measures are essential. When there is definite evidence of rapid progression of peripheral arterial occlusion despite all the usual medical measures, prophylactic surgery or anticoagulant therapy should be considered. Surgical procedures to relieve arterial occlusion and to prevent thromboembolism have been cited. Anticoagulants have been shown experimentally to retard intravascular thrombosis and possibly to hasten recanalization of thrombosed arteries. IO These medications are now of accepted value in the treatment and prevention of thromboembolism, and increasing recent evidence indicates that the long-term use of anticoagulants effectively reduces the incidence of recurrent coronary artery occlusion. 11 - I2 Because the accessibility of peripheral vessels makes it easy to recognize beginning or "impending" arterial occlusion, the possible indication for anticoagulant agents is usually readily apparent. In preliminary observations with prophylactic anticoagulant therapy ",re have noted apparent control of rapidly advancing arterial occlusion of the extremities and, in some instances, unexpected regression of the signs of arterial insufficiency. The theoretical indications and the clinical results to date justify further trial and evaluation of the prophylactic use of anticoagulants for both embolic and thrombotic acute arterial occlusion. SUMMARY
An increase in the relative incidence and occurrence of acute arterial occlusion may be anticipated. The importance of early diagnosis and treatment and the joint participation of the physician and the surgeon in observation and therapy have been indicated. Therapeutic and prophylactic measures have been outlined. Acknowledgments
The author gratefully acknowledges the helpful advice and perlnission to use case material of Drs. John J. Kneisel and Jere W. Lord Jr., and thanks Drs. Karl Harpuder and Herhert C. Maier for aid and suggestions in the writing of this article. REJ?ERENCES 1. AlIen, E. V.: Emergency Treatment of Vascular Occlusion. J.A.M.A. 135: 15, 1947. 2. Rose, o. A. and Ebel, A.: Intra-arterial Vasodilator Agents in Treatlnent of Advanced Occlusive Arterial Disease of Extreluities. J. An!. Geriatric Soc. 4: 142, 1956. 3. Prandoni, A. G. and Moser, M.: Clinical Appraisal of Intra-arterial Priscoline Therapy in Management of Peripheral Arterial Diseases. Circulation 9: 73, 1954. . 4. Lippmann, H. I.: Intra-arterial Priscoline Therapy for Peripheral Vascular Disturbances. Angiology 3: 69, 1952. 5. Bauer, G.: Nine Years Experience with lIeparin in Acute Venous Throlnbosis. Angiology 1: 161, 1950.
646
o. Alan Rose
6. Allen, E. v., Barker, N. W. and Hines, E. A. Jr.: Peripheral Vascular Diseases. 2nd Ed. Philadelphia, W. B. Saunders Co., 1955. 7. Gosgriff, S. W.: Thromboembolic Complications Associated with ACTH and Cortisone Therapy. J.A.M.A. 147: 924, 1951. 8. Humphries, A. W., deWolfe, V. G. and LeFevre, F. A.: Analysis of 120 Consecutive Cases of Major Arterial Grafts. J.A.M.A. 161: 953, 1956. 9. Lord, J. W. Jr.: Surgical Management of Shoulder Girdle Syndromes. New Operative Procedure for Hyperabduction, Costoclavicular, Cervical Rib and Scalenus Syndromes. Arch. Surg. 66: 69, 1953. 10. Wright, H. P. and Kubik, M. M.: Recanalization of Thrombosed Arteries Under Anticoagulant Therapy. Brit. M. J. 1: 1021, 1953. 11. Suzman, M. M., Ruskin, H. D. and Goldberg, B.: Evaluation of Effect of Continuous Long-term Anticoagulant Therapy on Prognosis of Myocardial Infarction. Circulation 12: 338, 1955. 12. Keyes, J. W., Drake, E. H. and Smith, F. J.: Survival Rates After Acute Myocardial Infarction with Long-Term Anticoagulant Therapy. Circulation 14: 254, 1956. 815 Park Avenue New York 21, N.Y.
majority of acute peripheral arterial conditions are caused by sudden or rapidly developing occlusion. With prolongation of life due to medical advances, it may be anticipated that arterial emergencies will be seen with increasing frequency. Acute arterial occlusion was formerly considered an exclusively surgical problem. With increased knowledge of the mechanisms involved, and following the introduction of anticoagulants, the diagnosis and institution of correct therapy have become the primary or initial responsibilities of the physician who first sees the patient and is best able to start the proper early treatment. Recent developments in surgical vascular techniques have improved the efficacy and safety of surgical procedures, and have also made it possible in many instances to restore arterial circulation in vessels which were previously considered to be inoperable. Since both medical and surgical treatment are frequently required, it is advantageous for both physician and surgeon to observe, and be prepared to treat the patient from the time the diagnosis is made. Abrupt interference ,vith arterial flow may result in the loss of an extremity or its parts. Death may follow the occurrence of shock or may be due to prolonged stress or to amputation. Patients who are debilitated or suffer from chronic diseases are most subject to vascular occlusions and least able to tolerate their sequelae. The early institution of the correct therapeutic measures will usually improve, and may almost completely restore adequate arterial circulation. Too frequently, the diagnosis of sudden arterial occlusion is not made early enough for maximal therapeutic benefit.
THE
ETIOLOGY
Acute arterial occlusions may result from a number of causes and predisposing factors. These are listed in the accompanying outline. From the Department of Medicine, New York University College of Medicine and the Third (New York University) M edical Division of Bellevue Hospital, New York, N.Y.
* Assistant Professor of Clinical Medicine, New York Un1:versily College of Medicine; Attending Physician, Cardiovascular Service and Chief, Cardiac Clinic, Lenox Hill Hospital; Attending Physician, Cardiovascular Service, Veterans Administration Hospital, Kingsbridge Road, Bronx, N.Y. 629
o. Alan Rose
630
Thrombosis, secondary to previously existing partial arterial occlusion, and embolism produce acute arterial obstruction in the vast majority of cases. More than one factor frequently combine to cause acute arterial insufficiency. This is seen most commonly with resulting tissue necrosis, when a limb with obliterative arterial disease has been exposed to trauma, particularly to cold, and to badly fitting shoes. Vasospasm alone may produce profound ischemia and occasionally is the sole evident cause of gangrene of an extremity. DIAGNOSIS
The diagnosis of acute arterial occlusion usually demands no special equipment. An awareness of the possibility that the condition may exist, a good detailed history of the onset and development of the complaint, and careful observation and examination with hand and fingers will almost invariably establish the presence of arterial obstruction. The following are the symptoms and signs of acute arterial occlusion: (1) pain, (2) neuropathy, (3) skin color and temperature changes, (4) superficial veins collapsed, and (5) arterial pulsations weak or absent. Symptollls
The manifestations depend upon a number of factors, particularly the rate of development and the degree of ischemia of the part. With high sudden obstruction, especially when caused by a "saddle embolus" lodged at the aortic bifurcation, the onset is usually dramatic. The symptoms and signs develop rapidly, with abrupt onset of severe pain in the region of hips and buttocks or upper thigh. There is usually loss of motor function or extreme weakness of both lower extremities, with marked pallor, and lowering of the skin temperature. These, and the less striking manifestation of arterial insufficiency described below, are often at first believed to be due to neurological or to orthopedic disorders. Acute deep vein thrombophlebitis is sometimes nlistaken for arterial occlusion. Phlebitis can usually be differentiated by the enlarged appearance of the involved limb, the presence of engorged veins, elevated skin temperature, and normal arterial pulses. However, secondary vasospasm in thrombophlebitis may make differential diagnosis difficult. The onset of acute arterial obstruction is often insidious. Pain may be absent or insignificant and, contrary to general belief, occurs in only about 50 per cent of patients as the first evidence of sudden occlusion. Pain is frequently so diffuse and variable that the diagnosis of myositis or neuralgia is made before attention to absent pulses or other evidences of arterial occlusion indicate that emergency therapy for arterial occlusion is required. When profound ischemia persists, especially with delayed or inadequate treatment, neuropathy may result in pain which is so severe that 'it becomes the reason for amputation. Early acute rest pain often merges into the later chronic symptom, intermittent claudica-
Peripheral Arterial Emergencies
631
FACTORS WHICH CAUSE OR PREDISPOSE TO ACUTE ARTERIAI.J OCCLUSION Thrombosis Partial or Intermittent Occlusion
Arteriosclerosis obHterans Thromboangiitis obliterans Mechanical factors Shoulder girdle compression syndrome Surgery and fractures Systemic Hemodynamic Factors Heart failure Shock Trauma Extensive surgery Crushing injury Excessive exposure to heat, cold or radiation Arteritis Thromboangiitis obliterans Collagen diseases Rheumatoid arthritis Essential polyangiitis (periarteritis nodosa) Lupus erythematosus disseminatus Secondary to acute and chronic infections Intravascular H ypercoagulability Blood dyscrasias Cryoglobulinemia Thrombophilia Idiopathic "Thrombosing disease"
Embolism Cardiac-Mural Thrombosis Due to:
Heart failure Atrial fibrillation Myocardial infarction Endocarditis (nonbacterial and bacterial) Cardiac-Septal Defect From venous origin ("paradoxical") Arterial-Mural Thrombosis Due to: Obliterative arterial disease Aneurysm Endarteritis N onclot Embolism Air Fat Tumor Inorganic substance
Transection, Laceration or Perforation
Surgery Gunshot wounds Miscellaneous accidents
Vasospasm
Secondary to acute arterial or venous occlusion Due to cold, injury and other trauma
o. Alan Rose
632
tion. Numbness is the next most frequent symptom and may be the patient's only initial complaint. Paresthesias, cramps, itching, burning or a sense of weight may be present. These, with frequent loss of motor power in the involved extremity and the physical findings to be described, will usually establish the diagnosis. Signs
With sudden occlusion, the involved extremity is usually waxy pale at onset, later becoming mottled in appearance. The superficial veins are collapsed with the extremity in the horizontal or dependent position, and the temperature of the skin is lowered. Involved arterial pulsations always become diminished or disappear. Careful palpation of the major arteries (the femoral, popliteal, dorsalis pedis and posterior tibial in the lower extremities and the brachial, radial and ulnar in the upper extremities) will usually lead to the definitive diagnosis. Oscillometry may be helpful as a corroborative objective method for the determination of the presence of pulsations and the approximate level of obstruction. However, this and other instruments used to evaluate the local circulation are rarely, if ever, essential to the diagnosis of acute arterial occlusion. Lowered skin temperature can usually be easily recognized by the palpation of the involved extremity with the back of the hand and fingers and comparison of the temperatures of symmetrical parts of its mate. While it is frequently impossible to exactly localize the site of obstruction and to differentiate between thrombosis and embolism when the patient is first seen, the treatment to be initiated is the same. Any advantage which might he derived fronl initial precise evaluation is unimportant compared to the urgency of starting treatment at the earliest possible time. Because of the not infrequent absence of striking symptoms and the unfortunate tendency of the physician to neglect careful and thorough examination of the extremities, the diagnosis of acute arterial insufficiency has often gone unrecognized until much precious time has been lost. MEDICAL TREATMENT
The principal aims of medical treatment are: (1) to protect the involved extremity, (2) to promote maximum dilatation of all its remaining patent collateral vessels, and (3) to prevent further occlusion by propagated thrombus. These aims are usually best accomplished by early treatment and observation under the supervision of both physician and surgeon. Optimal therapeutic results in the restoration of circulation can usually be achieved with medical measures alone when occlusion is peripheral to the femoral arteries of the lower extremities and to the brachial arteries of the upper. The progress with medical treatment will indicate the level of obstruction and whether operative intervention will be re-
Per~pheral
Arterial Emergencies
633
quired. Embolectomy, or one of the procedures for the removal of an obstruction in a segment of a major artery, may ordinarily be postponed for sufficient time to permit adequate evaluation of medical measures. Early Treatm.ent
The patient with acute arterial occlusion is usually best cared for in a hospital. However, whether the diagnosis is established or is only strongly suspected, treatment should be instituted wherever he is and as soon as possible after the patient is first seen. Pain and anxiety which reflexly produce vasoconstriction should be relieved with reassurance by the physician, the use of opiates (morphine 15 to 30 mg., Demerol 75 to 100 mg.) and other sedation, particularly rapidly acting barbiturates (parenterally sodium Luminal or Seconal or pentobarbital 0.1 gram per os). Alcohol by Inouth (V\rhisky or brandy-30 cc. or more) is also recommended for this purpose and as a mild vasodilator agent. The extremity should be maintained in a some,vhat dependent position. This is best accomplished by raising the entire head of the bed 4 to 6 inches on books, blocks or other support. The optimal position is that ,vhich nearly produces the normal pink color in the distal portions of the involved limb. Protection, and Avoidance of Harm.ful Measures
Commonly used measures which may cause irreparable damage should be sedulously avoided. These include the local application of various medications, massage, heat, cold, and elevation of the involved extremity. The ischemic limb is extremely sensitive to trauma due to pressure and to degrees of heat and cold which are well tolerated by normal tissues. Protection of the extremity is therefore of the utmost importance and is achieved by covering it gently with bland oil or lanolin and wrapping it in bulky, soft, porous material such as cotton or a light, soft blanket. A cradle should be used if available. The best type is that which is inserted under the mattress. It serves only to protect the extremity from the pressure of bedclothes and from drafts and should therefore be covered with a sheet and not contain a heating element. A bolster placed at the foot of the bed will reduce trauma to the feet, and is especially important when the head of the bed is elevated. Vasodilator Measures
Local, and sometimes widespread vasospasm follows rapid occlusion of arteries and veins, which at the outset may make it difficult or impossible to identify the exact site and extent of organic obstruction. Of far more importance is the less recognized fact that, if secondary vasoconstriction is allowed to persist, extensive thrombosis will result when the circulation eventually begins to be re-established. This is believed to be the result of ischemic changes in the intima of involved vessels. 1 Specific
634
o. Alan Rose
vasodilator therapy is urgently indicated in addition to the relief of pain and anxiety, and treatment of other factors which predispose to vasoconstriction. Reflex vasodilatation is the simplest and one of the best methods of dilating peripheral vessels, and is so effective that it is one of the few reliable tests for the evaluation of peripheral vasoconstriction. It is the physiological mechanism which reflexly induces peripheral vasodilatation when the body temperature is elevated. Its simplicity is an important additional advantage because it can be easily instituted when the patient is first seen and continued thereafter. Reflex vasodilatation is induced as follows: the body and uninvolved extremities of the patient are covered with blankets, while the involved limb is protected as described above, and is maintained at average room temperature (60 to 800 F.) to minimize its local tissue metabolism and circulatory requirement. Hot water bottles or electric pads are applied to the abdomen or back. The temperature, taken rectally, should be raised and maintained at one or more degrees above normal (more than 1000 F.). Orally administered agents should be used to aid in the maintenance of maximum vasodilatation and for this purpose mild dilator medications are advisable to avoid side effects which may complicate treatment. In addition to alcohol, papaverine which also has a sedative effect is recommended. The dose should be a relatively large one (0.1 to 0.2 gram). Tolazoline hydrochloride (Priscoline hydrochloride) is a more powerful agent and is usually well tolerated in doses of 25 lUg. Dosage may be cautiously increased to 50 or to 75 mg. depending upon the development of side effects. Phenoxybenzamine (Dibenzyline) is more effective than Priscoline but side effects are also more common. The dosage is 10 mg. or more. Phenyl-I-butyl-norsuprifen (Arlidin), a new vasodilator agent which is reported to affect predominantly the deep arterial circulation, has not as yet been adequately evaluated. The above drugs are given at four to six hour intervals. Hexamethonium and other ganglionic blocking agents are liable to produce effects which are too widespread to be practical or safe for use in the dosage required to relieve spasm in acute local arterial occlusion. The response to potent vasodilator medications when given orally or intravenously is maximal upon the most normal vessels and may therefore actually shunt blood away from diseased or partially occluded arteries. Patients with peripheral arterial occlusion often have concomitant recognized or occult vascular disease involving vital areas, particularly the cerebral, coronary and renal circulations. Vasodilator agents are thus capable of actually increasing vascular insufficiency in these as well as in more acutely involved areas. The intra-arterial route of administration is theoretically best for the emergency use of vasodilator agents in acute arterial occlusion because the effect is attained at the earliest possible time and is achieved with
Peripheral Arterial Emergencies
635
maximal concentration of therapeutic agents where they are most needed. The almost exclusively local effect of intra-arterial therapy has been found to be safe for patients with diffuse vascular involvement and to be relatively free from the systemic side reactions which are frequent when a general route of administration is used. 2 It has been demonstrated that vasodilator medication given intra-arterially can duplicate the response to adequate sympathetic block and that this effect is ,velllocalized.8 TIle only equipment required is the material to be administered and syringe and needle which may be carried in the physician's bag with his other emergency medications. The injection is most often given into the femoral artery because of the frequency of obstruction distal to this vessel, and the ease with ,vhich it can be entered. The brachial and other vessels can also be used. The technique for intra-arterial administration is easily mastered. When the femoral artery is used, the injection is given just below the inguinalligament. The arterial pulsation must be palpable. Two fingers are placed on the pulsating longitudinal axis of the vessel and the needle is inserted at right angles to the artery between the palpating fingers until the return of bright red arterial blood (which usually enters the syringe under positive pressure) indicates that the needle has entered the lumen of the artery. A small (22 or 23 gauge) needle is best used to minimize local arterial trauma, and pressure is applied firmly at the site immediately following injection. While the vasodilator effect is of relatively short duration following the intra-arterial administration of present dilator agents, the method is valuable for emergency use. Priscoline (12.5 to 50 mg., 0.5 to 2 cc.) has been shown to be effective and well tolerated when given intraarterially.3. 4 It is given slowly over a period of several minutes, at a rate of about 1 cc. per minute. Newer vasodilator agents have been studied2 and investigation is being continued in an effort'to discover vasodilator medications which whe.n given by the intra-arterial route most nearly approach the ideal of prolonged action and minimal side effects. Sympathet~c blockade by the injection of local anesthetic agents in autonomic ganglia, in the region of the cauda equina or in the spinal canal will effectively release local spasm 'for six or more hours. The disadvantages of this form of therapy are: (1) an experienced anesthesiologist is required, (2) there is almost always a delay before this treatment can be started, and (3) the danger of deep local injections after anticoagulant therapy has been instituted. If the patient is hospitalized when acute occlusion occurs and block can be performed promptly, it is a -:valuable adjunct in treatment. This applies particularly to patients with ~rial embolism where angiospasm is most severe and early surgery may be anticipated. Blocks or sympathectomy may also be valuable at tthe time of surgery to aid in optimal vasodilatation.
636
o. Alan Rose
Anticoagulant Therapy
The object in the use of anticoagulants is to prevent propagation of thrombus distal and proximal to the site of obstruction with occlusion of essential collateral vessels. Anticoagulation therapy is recognized as one of the major factors in the improved results of medical treatment of acute vascular occlusion. Heparin is the only anticoagulant which is effective within minutes following administration and it is therefore the drug of choice for the institution of emergency anticoagulation therapy. If it is technically possible, heparin is given intra-arterially usually in a dose of 25 mg. Injection proximal to the site of obstruction may be precluded by high occlusion or inability to palpate the arterial pulsation. Whether heparin is administered intra-arterially or not, it is given by the intravenous route as soon as possible after occlusion. The initial intravenous dose of heparin is usually 100 mg. followed by doses of 50 to 75 mg. every four to six hours. We use the aqueous preparation with concentration of 50 mg. per cc. and follow the initial intravenous dose with 50 or 75 mg. given subcutaneously every six hours. Extensive experience with the intermittent method of heparin administration indicates that adequate anticoagulant effect is achieved despite long periods when the clotting time is only slightly prolonged or normal. i For this reason clotting times are usually not necessary when heparin is used alone. This is an advantage in the use of heparin compared to the coumarin derivatives and is particularly important when adequate laboratory facilities are not available. We prefer the subcutaneous route for the continued use of heparin following the initial intravenous dose because (1) it has been found to be satisfactory over a number of years, (2) it eliminates the possibility of producing a large occult deep hematoma which we have seen following intramuscular injection and (3) it permits the regular administration of heparin by nurses, by a member of the family or even by the patient himself. While ecchymoses often occur with subcutaneous heparin administration, they cause no significant distress or serious sequelae. Heparin is expensive and it must be administered parenterally at intervals with some discomfort to the patient. Anticoagulant effect is usually required for days or weeks after acute vascular occlusions and in some cases is continued for much longer periods on an ambulatory basis. For these reasons, the longer acting, easily administered coumarin preparations are usually started soon after the first dose of heparin. Heparin is discontinued only when the prothrombin time has reached the therapeutic range (usually 48 to 72 hours). If emergency surgery is to be performed, Dicumarol is usually not given and the effect of heparin is neutralized with protamine. The dosage for protamine is that of the heparin which has been administered in the previous four hours. Our experience is in agreement with others that it is rarely necessary
Peripheral Arterial Emergencies
637
to use agents other than Dicumarol and heparin. 6 Proficiency increases with the use of these preparations. There is no space here for a detailed discussion of drugs and methods of administration. It is stressed however, that, anticoagulant therapy should not be undertaken without a thorough knowledge of the correct use of these agents, the contraindications to anticoagulation and the treatment of excessive effect from heparin or the coumarins. These extremely important aspects are now well established and information concerning them is readily available in the literature and recent texts. The physician who institutes this treatment must accept complete responsibility for administration and control of the agents used. A suggested method for the use of anticoagulants for acute arterial occlusion is included in the outline of treatment at the end of this section. Treatment of Systemic Disease
Treatment of concomitant systemic disease is, of course, urgently required. This is particularly true of congestive heart failure and of cardiac conditions which may predispose to embolism. Emboli most frequently arise from the heart in rheumatic disease particularly when mitral stenosis and atrial fibrillation are present. Here, both medical and surgical treatment are frequently necessary. Medical therapy is directed at heart failure, arrhythmias and carditis. Prophylactic use of anticoagulants may also be indicated. Surgical treatment for embolism will be discussed below. A small embolus frequently warns of the occurrence of larger, more serious and possibly fatal emboli to follow. This applies to atrial fibrillation and other paroxysmal arrhythmias and to embolism from an aneurysmal sac and similar sources. When emboli result from bacterial endocarditis, acute or subacute, anticoagulants are contraindicated. Here, of course, the early institution of adequate penicillin or other antimicrobial therapy is required to treat the disease and to prevent the damaging effects of infected emboli. Arterial occlusion due to emboli indicates immediate search for the source because the process which is responsible may itself require emergency treatment or may considerably influence the form of therapy to be used. Myocardial infarction with mural thrombosis may be responsible for embolism. Here, treatment for the cardiac condition is usually more urgent than that for the embolic phenomenon and at least temporarily precludes surgery. This is illustrated by the following case: CASE I. A 59 year old Negro clerk was admitted to the hospital complaining of severe pain in the right thigh and calf of 2 days' duration. Sudden onset of pain obliged him to stop walking. Severe rest pain had persisted despite repeated treatment opiates and other medications. Hot and cold soaks had been prescribed by his family physician and these had exaggerated the pain. Examination on admission revealed absence of all arterial pulsations below
638
o. Ala1L' Rose
the right femoral artery which was pulsating strongly. Pallor and lowered temperature were noted in the leg below the knee. Routine electrocardiograms taken soon after admission revealed the presence of a recent anteroseptal myocardial infarct, which had apparently been asymptomatic. The diagnosis of embolism to the right superficial femoral artery secondary to myocardial infarction was made. Because of the interval following onset and the patient's cardiac status, surgical intervention was not considered. Heparin and Dicumarol were started. Priscoline, 25 mg., was administered in the right femoral artery. Additional measures as included in the outline for treatment were followed. Intra-arterial vasodilator medication was given twice daily for the first several days and daily thereafter. Papaverine 0.1 gram four times daily and alcohol 30 cc. three times daily were also given by.mouth. The temperature of the extremity improved progressively within 24 hours, with return in sensation and motor power and progressive decrease in pain. The cardiac status improved with the disappearance of minimal failure which had been present on admission. The electrocardiogram showed evolutionary changes. The patient was discharged from the hospital in 6 weeks. He remained on maintenance Dicumarol therapy and vasodilator medications for 6 months during which time initial claudication of one or two blocks improved to walking tolerance of 10 blocks which has persisted to the present. Recent femoral arteriogram performed 3 years after embolism reveals complete obstruction of the right superficial femoral artery and the development of extensive collateral circulation (Fig. 85).
This case also illustrates that medical treatment alone may be adequate in the treatment of embolism even with relatively high arterial occlusion. The unusual collateral supply which developed in this instance has made it unnecessary to consider late surgery. Diabetic patients are likely to develop complications in the presence of sudden arterial occlusion. Adequate control of diabetes may be difficult but is essential, as dehydration, acidosis and coma predispose to thrombotic occlusion, infection and a high mortality. Infection should be vigorously treated with antimicrobial agents. General and Supportive Measures
Adequate hydration and nutrition are extremely important, particularly in patients who are old and debilitated. Hemoconcentration may be an important predisposing factor in thrombotic arterial occlusion. Hydration may be accomplished with administration of sodium-free fluids. Two liters or more each 24 hours should be given pa.renterally or orally even in the presence of severe cardiovascular disease. Necessary nutrition should not be neglected. Additional Conditions Which Require Individual Treatlllent
Factors which increase the thrombosing tendency, particularly blood dyscrasias, must of course be treated individually with an attempt at correction of the factor which predisposes to thrombosis. Polycythemia
Peripheral Arterial Emergencies
639
Fig. 85. Femoral arteriogram in a case of embolus to superficial femoral artery, showing site of obstruction of right superficial femoral artery (arrow) with collateral vessels to the considerably enlarged profunda femoris. The deep femoral artery supplies large collateral vessels peripherally. Extensive collateral circulation about the knee is visualized with return of flow below.
vera, thrombophilia, cryoglobulinemia and so-called "thrombosing disease" sometimes respond to the prophylactic use of anticoagulants. Thrombotic occlus~:on due to the arteritides is extremely difficult to control. We have seen a young Negro girl with known lupus erythematosus who had extensive thrombosis involving both arteries and veins of the leg below the knee which resulted in amputation. The process did not respond to medical treatment. Section of the amputated extremity showed suggestive evidence of involvement due to lupus erythematosus. Treatment should be directed at the cause of arteritis if known, particularly predisposing infections. Thromboangiitis obliterans may respond simply to the discontinuance of the use of tobacco. Arteritis related to collagen diseases may respond to the steroids. IIovv"'ever, there is evidence which suggests that these compounds themselves predispose to thrombosis. 7 Arterial thrombosis related to exposure to heat, cold and moisture, including frostbite, "trench foot," "immersion foot" and related syndromes, and arterial involvement secondary to radiation are usually treated with the
o.
Alan Rose
conservative measures which have already been outlined. 1'1he involved extremity is protected and nlaintained at a constant environment of 70 to 80° F. The use of anticoagulants and vasodilator agents lnay aid by preventing extension of thrombus, particularly during the stage vvhen severe vasospasm plays an inlportant part in the occlusive process. SURGICAL TREA rMEN1' r
The increasing etIectiveness and safety of vascular surgery has made it possible to consider this treatment for most patients with high arterial occlusion. Vascular surgical procedures even when extensive are essentially local and minor, and are generally very well tolerated. Embolectomy is usually the treatment of choice vvith involvement of the lower abdominal aorta, the iliac or femoral arteries, or the lnajor arteries of the upper extremities. When indicated, embolectomy should be performed within six hours after occlusion if possible. While the likelihood of re-establishing adequate circulation decreases progressively with time, embolectomy has been successful in some cases when performed 24 or more hours after occlusion. As previously indicated, medical treatment should be evaluated if possible before a surgical procedure is undertaken, as vasospasm following acute occlusion commonly presents the picture of arterial obstruction at a much higher level than that which is caused by the embolus. We have seen a number of instances ,vith the manifestations of iliofemoral or lower abdominal aortic occlusion, when the site was at or below the popliteal artery. Medical measures alone in these cases frequently resulted in almost complete return of the arterial circulation. The decision to operate, can, as previously emphasized, best be lllade with the frequent observation of the patient by both physician and surgeon. Embolectomy may be indicated or operative treatment of the source of emboli may be useful when the patient has recovered from the initial acute occlusion and his general condition is optimal to withstand such procedures. These include resection of aneurysm, and in some cases, cardiac surgery. Excellent long-term surgical results have been attained in the treatment of emboli due to rheumatic heart disease with mitral stenosis and atrial fibrillation. This is illustrated by the follo,ving case: CASE 11. The patient, a 44 year old secretary, had longstanding rheumatic heart disease, with mitral stenosis and atrial fibrillation. There had been progressive reduction in cardiac reserve over the previous several years, with two brief episodes of pulmonary edema in the preceding three months. She was admitted to the hospital because of severe lower back and abdominal pain and diffuse pain in both lower extremities accompanied by numbness, paresthesias, and complete loss of motor power. All arterial pulses of the lower extremities were absent including the iliac and femoral pulsations. The extremities were cool below midthigh, with marked diminution in sensory perception and absent reflexes. Six hours after onset a saddle embolus was removed transperitoneally. Heparin was injected into the aorta before closure and given postoperatively
Peripheral Arterial Emergencies
641
for the first three days when the prothrombin time reached the therapeutic range with Dicumarol. There was improvement in color, temperature and return of sensation and motor power within 24 hours postoperatively. All arterial pulsations gradually returned. The patient's cardiac status became progressively worse despite digitalization, dietary restriction of salt, and mercurial diuretics. Clinical evidence supported by cardiac catheterization indicated that mitral stenosis was the predominant or exclusive lesion, and mitral commissurotomy was performed three months after embolectomy. There has subsequently been considerable improvement in the cardiac status, the patient is able to work regularly, walks at an average pace and climbs two flights of stairs without dyspnea. Dicumarol, which had been administered until commissurotomy, was discontinued postoperatively. The patient has not required medication except for digitalis. There have been no further embolic manifestations.
The results of surgery, both for the source and the embolus itself, were unusually successful in this case. Emboli of this size are relatively uncommon as a result of rheumatic heart disease. Rarely, emboli from a venous source produce occlusion of peripheral arteries. This so-called "paradoxical" embolus indicates the presence of an interatrial septal opening, which has permitted an embolus to pass from the right to the left heart. This may occur with a patent foramen ovale or a larger congenital atrial septal defect. Large atrial defects may be considered for surgical treatment. When the cause of high occlusion is rapidly progressive thrombosis, vascular surgery may be considered. Removal of the thrombus and a portion of the inner wall of the artery (thromboendarterectomy), section of the occluded segment with graft replacement, or a by-pass procedure may be possible. These surgical measures are frequently successful in the treatment of relatively chronic high segmental arterial occlusion and they may occasionally be performed with dramatic improvement in arterial flow in patients with acute thrombosis. When such surgical procedures are considered in acute as well as chronic cases, it must be established that there is adequate arterial outflow below the obstructed portion before they are attempted. This is likely to be true when occlusion is due to embolism, particularly when it occurs in relatively young people. With thrombotic occlusion, and in older individuals, arteriography is extremely helpful for the identification of the exact location and extent of occlusion, as well as the presence of necessary patent peipheral arteries. We have seen several patients who while under direct observation have developed such occlusions and ,vho have been operated upon successfully. The results in a patient with right iliac thrombosis is demonstrated in Figure 86. Surgical intervention is of course urgently indicated when arterial obstruction is due to injury with transection, laceration or perforation. Fractures compressing lnajor vessels must be immediately treated. Injured vessels may be repaired by suture and large damaged sections may
o. Alan Rose
Fig. 86. Right iliofemoral thrombosis with thromboendarterectomy. A 53 year old laborer with intermittent claudication of 2 weeks' duration in region of right hip and upper thigh. Rapid progression in symptoms over -several days with complete obstruction at right iliofemoral level (aortagrams A and lE). Thromboendarterectomy resulted in marked improvement in arterial flow to below popliteal level (aortagrams and D). The patient is now almost completely asymptomatic.
o
Peripheral Arterial Emergencies be replaced by arterial grafts. 8 The physician who initiates treatment for arterial injury should be extremely careful in the use of tight tourniquets and their prolonged applications because they may produce considerable trauma to uninvolved vessels and nerves. The surgical treatment of the shoulder girdle compression syndromes is frequently difficult and inadequate. While newer procedures have been devised for these conditions, 9 medical measures, especially postural exercises and muscle training, are usually effective and obviate the need for surgery. Amputation is the final admission of both medical and surgical failure. It is indicated when necrosis is extensive or cannot be controlled. This occurs most frequently with progression of gangrene from digits to involve the more proximal portions of extremities. The fullest possible evaluation of medical and other surgical measures should precede consideration of amputation. However, when the condition is hopeless, delay in radical surgery may threaten further vascular impairment or the life of the patient. When indicated, amputation should of course be at the lowest possible level including transmetatarsal resection or below-knee amputation in lo"\\~er extremities. Medical treat.ment when only digits or small areas of extremities or other portions of the body are involved should include protective dressings, scrupulous cleanliness of the involved part, the prophylactic use of antimicrobial agents, and vasodilator measures as outlined above. Refrigeration should be used only for areas of necrosis or those which are obviously compromised, and is indicated solely to prevent absorption and for local anesthetic effect prior to operation. An outline for the treatment of acute arterial occlusion is presented on the following page. PROPHYLAXIS
Arterial occlusion both acute and chronic is in the majority of instances related to atherosclerosis. This process is no longer accepted as the inevitable result of degenerative change3 and a more dynamic approach has stimulated intensive investigation of possible etiological factors. While the results of these studies have as yet no definite clinical application, there is considerable hope that they will lead to measures which will aid in the prevention of this most prevalent vascular disease. Significant findings to date apply to dietary factors and suggest the advisability of low caloric, nutritious diets and of weight reduction for obesity. Surgical treatment of evident or potential sources of embolism including procedures to improve or repair intracardiac abnormalities, the excision of aneurysms, and the treatment of abnormal vascular communications has been indicated. Surgical measures are frequently efficacious in the prophylactic treatment of carefully selected cases with high level segmental arterial obstruction.
o. Alan Rose GENERAL PLAN AND OUTLINE FOR THE TREATMENT OF ACUTE ARTERIAL OCCLUSION l. Treatlllent of Pain and Anxiety A. Morphine 8ulfate 15 to 30 mg. or Demerol, 100 mg. B. Sedation-rapid acting barbiturate-reassurance I L Protection of Extrelllity and Optimal Position A. Cover lightly with mineral oil..or lanolin and protect distal portions
B. Position of extremity below heart level
Ill. Vasodilator Measures A. Heat body with blankets and hot water bottles or electric pads (maintain involved extremity at 60 to 80° F.) B. Intra-arterial-PriscoIine 12.5 to 50 mg. Repeat 1 to 3 times daily (heparin may be given in same syringe with initial dose) c. Oral-alcohol 30 cc. or more, papaverine 100 to 200 mg. every 4 hours, PriscoIine 25 to 50 mg. or dibenzyline 10 mg. (These vasodilator agents can also be given by other routes.) D. Sympathetic block-paravertebral, caudal, spinal anesthesia (if it can be performed promptly)
IV. Initiate Anticoagulant Therapy A. Heparin 100 mg. intravenously and, if possible, 25 mg. intra-arterially, followed by heparin 50 to 75 mg. intravenously or subcutaneously every 4 to 6 hours B. Dicumarol 300 mg. followed by daily doses depending upon prothrombin times V. General Measures
A. Prompt adequate treatment of concomitant infection and acute systemic diseases (congestive heart failure, shock, diabetic coma or hypertensive crisis) B. Hydration-2000 to 3000 cc. of low sodium fluids each 24 hours (increased if fever present) c. Nutrition including necessary proteins and vitamins particularly for old and debilitated patients VI. Surgical Treatm.ent
A. Measures to improve arterial flow 1. Embolectomy-within 6 hours if possible 2. l'hromboendarterectomy or graft 3. Relief of compression from fractures, shoulder girdle compres.. sion and other mechanical factors B. Amputation-early if condition of extremity is hopeless. Refrigeration of necrotic and compromised parts only and only preliminary to amputation.
Prophylactic medical measures are specifically required vvhen there is evidence of partial peripheral arterial occlusion demonstrated by diminished arterial pulses, and/or a history of claudication or other manifestations of arterial insufficiency. At this time, the patient's condition and the need for prophylaxis should be carefully explained, and reassurance given that, with proper care, serious consequences can usually be avoided. Written instructions regarding foot care, the avoidance of trauma, the use of vasodilator measures, and weight reduction with adequate diet and hydration are useful in the institution and maintenance of a prophylactic regimen. The use of tobacco must of course be forbidden. Regular
Peripheral Arterial Emergencies follow-up examinations for evaluation of the progress of arterial occlusion and the adequacy of prophylactic measures are essential. When there is definite evidence of rapid progression of peripheral arterial occlusion despite all the usual medical measures, prophylactic surgery or anticoagulant therapy should be considered. Surgical procedures to relieve arterial occlusion and to prevent thromboembolism have been cited. Anticoagulants have been shown experimentally to retard intravascular thrombosis and possibly to hasten recanalization of thrombosed arteries. IO These medications are now of accepted value in the treatment and prevention of thromboembolism, and increasing recent evidence indicates that the long-term use of anticoagulants effectively reduces the incidence of recurrent coronary artery occlusion. 11 - I2 Because the accessibility of peripheral vessels makes it easy to recognize beginning or "impending" arterial occlusion, the possible indication for anticoagulant agents is usually readily apparent. In preliminary observations with prophylactic anticoagulant therapy ",re have noted apparent control of rapidly advancing arterial occlusion of the extremities and, in some instances, unexpected regression of the signs of arterial insufficiency. The theoretical indications and the clinical results to date justify further trial and evaluation of the prophylactic use of anticoagulants for both embolic and thrombotic acute arterial occlusion. SUMMARY
An increase in the relative incidence and occurrence of acute arterial occlusion may be anticipated. The importance of early diagnosis and treatment and the joint participation of the physician and the surgeon in observation and therapy have been indicated. Therapeutic and prophylactic measures have been outlined. Acknowledgments
The author gratefully acknowledges the helpful advice and perlnission to use case material of Drs. John J. Kneisel and Jere W. Lord Jr., and thanks Drs. Karl Harpuder and Herhert C. Maier for aid and suggestions in the writing of this article. REJ?ERENCES 1. AlIen, E. V.: Emergency Treatment of Vascular Occlusion. J.A.M.A. 135: 15, 1947. 2. Rose, o. A. and Ebel, A.: Intra-arterial Vasodilator Agents in Treatlnent of Advanced Occlusive Arterial Disease of Extreluities. J. An!. Geriatric Soc. 4: 142, 1956. 3. Prandoni, A. G. and Moser, M.: Clinical Appraisal of Intra-arterial Priscoline Therapy in Management of Peripheral Arterial Diseases. Circulation 9: 73, 1954. . 4. Lippmann, H. I.: Intra-arterial Priscoline Therapy for Peripheral Vascular Disturbances. Angiology 3: 69, 1952. 5. Bauer, G.: Nine Years Experience with lIeparin in Acute Venous Throlnbosis. Angiology 1: 161, 1950.
646
o. Alan Rose
6. Allen, E. v., Barker, N. W. and Hines, E. A. Jr.: Peripheral Vascular Diseases. 2nd Ed. Philadelphia, W. B. Saunders Co., 1955. 7. Gosgriff, S. W.: Thromboembolic Complications Associated with ACTH and Cortisone Therapy. J.A.M.A. 147: 924, 1951. 8. Humphries, A. W., deWolfe, V. G. and LeFevre, F. A.: Analysis of 120 Consecutive Cases of Major Arterial Grafts. J.A.M.A. 161: 953, 1956. 9. Lord, J. W. Jr.: Surgical Management of Shoulder Girdle Syndromes. New Operative Procedure for Hyperabduction, Costoclavicular, Cervical Rib and Scalenus Syndromes. Arch. Surg. 66: 69, 1953. 10. Wright, H. P. and Kubik, M. M.: Recanalization of Thrombosed Arteries Under Anticoagulant Therapy. Brit. M. J. 1: 1021, 1953. 11. Suzman, M. M., Ruskin, H. D. and Goldberg, B.: Evaluation of Effect of Continuous Long-term Anticoagulant Therapy on Prognosis of Myocardial Infarction. Circulation 12: 338, 1955. 12. Keyes, J. W., Drake, E. H. and Smith, F. J.: Survival Rates After Acute Myocardial Infarction with Long-Term Anticoagulant Therapy. Circulation 14: 254, 1956. 815 Park Avenue New York 21, N.Y.