Aneurysms of the aorta

is presently engaged in the private practice of cardiac, thoracic and peripheral vascular surgery and is a member of the active staffs of Norfolk General, Portsmouth General, Maryview, Leigh Memorial and DePaul hospitals. He received his M.D. from the Johns Hopkins University School of Medicine and interned in surgery at the Johns Hopkins Hospital. The following two years were spent as a research associate at the National Institutes of Health, Bethesda, Maryland, before returning to Hopkins for the completion of his residency. He then became Assistant Professor of Surgery at the University of Pittsburgh School of Medicine, specializing in cardiovascular and thoracic surgery.

is the George V. Foster Professor and Chairman of the Department of Surgery at the University of Pittsburgh School of Medicine. A graduate of Davidson College, North Carolina, Doctor Bahnson received his M.D. from Harvard Medical School in 1944. A shortened internship was followed by a brief tour in the Pacific with the United States Navy. He completed his residency training at Johns Hopkins Hospital and participated in the rapid development of cardiovascular surgery under his mentor Alfred Blalock. There Doctor Bahnson reached the rank of Professor of Surgery before going to the University of Pittsburgh in 1963. His research interests and publications have centered around cardiovascular and pulmonary surgery and physiology.

HISTORY T H E E A R L Y H I S T O R Y of the operative treatment of aneurysms of the aorta has been summarized in detail by Cooley and De Bakey, ~ Matas, 14G and by Bahnson. 7 Early attempts to treat aortic aneurysms by operation included ligation, endoaneurysmorrhaphy, wiring, wrapping, and the introduction of thrombogenic substances. Ligation of the 3

abdominal aorta was first recommended by Anel in 1710, but, like endoaneurysmorrhaphy, ligation was useful mainly in the treatment of aneurysms of peripheral arteries. In 1923, however, Matas 14.5 ligated the abdominal aorta above an aneurysm, with apparent success. The wiring of aneurysms, a technic advocated and refined by Blakemore and King, 2'~ was used during the 1940's and early 1950's and seemed to arrest the enlargement of aneurysms in which thrombosis was induced. The wrapping of aneurysms with various materials such as cellophane w ~ designed to induce fibrosis about the aneurysm, thus preventing furNer enlargement. Similarly, various sprays such as diacetylphosphate and irritating materials were tried, but as with wrapping, results were variable at best. Excision, with restoration of aortic continuity, is obviously the method of choice for treatment of aortic aneurysms. Tuffier 195 is credited with the first attemp.t, which consisted of ligation of the neck of a saccuiar aneurysm of t h e thoracic aorta. The aneurysm was not removed, and the patient died 13 days later. The first successful attempt at resection of an aortic aneurysm was by Alexander and Byron, 2 who successfully excised a thoracic aortic--aneurysm associated with aortic coarctation and oversewed the ends of the aisrta. Shumacker 179 performed the same operation, but re-established aortic continuity by endto-end anastomosis. The use of homografts to replace segments of the aorta excised for coarctation by Gross e t aI. :o4 in 1949 provided impetus for further development of excisional therapy of aortic aneurysms. Saccular aneurysms of the descending thoracic aorta were successfully excised by Ochsner ~s and by Monod, ~° both of whom clamped the base of the aneurysm and performed lateral aortorrhaphy. In 1951, Lain and Aram ~° reported excision of an aneurysm of the descending thoracic aorta, using a temporary internal shunt to preserve distal flow, and successfully restored aortic continuity with a homograft. Unfortunately, the patient died later of the consequences of a mediastinal infection. In 1952, DuBost e t al. 8z reported successful replacement of an abdominal aortic aneurysm with a homograft. This important achievement was quickly followed by the first successful excision of a fusiform aneurysm of the descending thoracic aorta with homograft replacement by Cooley and De Bakey 54 in 1953. Bahnson G advocated a direct attack and reported the first successful correction of a traumatic false aneul2y'sm of the aorta, as well as homograft replacement of the abdominal aorta for an aneurysm. By 1954, Blakemore and Voorhees 26 and Shumacker and King ~s0 had used synthetic tubes for aortic replacement; the forerunners of modern aortic prostheses. In 1954, De Bakey and Cooley vz reported the successful resection and homograft replacement of the distal aortic arch, using external hypothermia, without any sort of aortic bypass. Also in 1954, Mahorner and Spencer ~al articulated the shunt graft principle to permit aortic oc4

clusion without interruption of the distal circulation. This principle was used for total aortic arch replacement by Cooley, Mahaffey and De Bakey ~7 in 1955, but the patient died 6 days after operation without regaining consciousness. Cross and associates ~'5 in 1955 described successful laboratory use of left-heart bypass for aortic resection. A reservoir and pump were used, cannulating the'left ventricle through the left atrial appendage and returning blood via the femoral artery. Left atrial'to'femoral bypass was used for operative treatment of aneurysms of the descending thoracic aorta by Cooley and associates s~ in 1957. In 1956, Cooley and De Bakey had also reported use of total cardiopulmonary bypass, with perfusion of arch vessels for resection of aneurysms of the ascending aorta and proximal aortic arch. 53 Resection of an aneurysm of the ascending aorta with simultaneous aortic valve replacement was reported by Wheat e t aI. 2°9 in 1964.

CLASSIFICATION, ETIOLOGY AND INCIDENCE Aortic aneurysms are most common in the 5th, 6th and 7th decades of life. They may be classified according t o t y p e , location, shape and etiology (Table 1 ). Second aneurysms in other areas of the aorta occur with increased frequency in patients already k n o w n to harbor one aortic aneurysm. 204 Abdominal aortic aneurysms are the most common, making up over three quarters of the 3,000 reported by De Bakey e t al. TM Of the abdominal types, 9 6 % are due to arteriosclerosis, and 9 out of 10 are seen in males. Arteriosclerotic abdominal aneurysms commonly arise just below the renal arteries and frequently involve the aortic bifurcation. Fewer than 2% involve the renal arteries. 67 Suprarenal aneurysms are usually part of a thoracoabdominal aneurysm, although isolated aneurysms of the abdominal aorta between the renal arteries and t h e d i a p h r a g m do occur rarely. 7, sg, a00 Such isolated aneurysms are usually saccular and of syphilitic orion. Other causes of abdominai aortic aneurysms are rare.

TABLE

1.

CLASSIFICATION OF AORTIC ANEURYSMS

I

II

III

TYPE

LOCATION

SHAPE

True Dissecting False

Thoracic ascending transverse (arch) descending combination of above Thoracoabdominal Abdominal

Fusiform Saccular

5

IV ETIOLOGY

Arteriosclerosis Syphilis Trauma Cystic medial necrosis Mycotic infection Congenital malformation Aortitis Postoperation

Of thoracic aneurysms reported by DeBakey et al., TM syphilis and arteriosclerosis were equally common and together were responsible for approximately 80% of the lesions. Ten per cent were of traumatic, and the remainder were of miscellaneous or undetermined origins. Cystic medial necrosis is a prominent cause of aneurysms of the ascending aorta in some series 9, 2~. ,07 not associated with aortic dissection. Marfan's syndrome may or may not be present. TM Indeed, with the decreased incidence o f syphilitic lesions, cystic medial necrosis may now be the most common cause of aneurysms of the ascending aorta, 13GA,%rtic insufficiency with dilatation of the aortic annulus frequently accompanies aneurysms due to cystic medial necrosis A similar histologic lesion is produced in rats~ by feeding fl-aminonitrile. ~zg; 9, Also, there may be changes in the aortic valve cusps resembling the lesions of cystic medialrnecrosis,29.9~ and in this circumstance aortic regurgitation may be present without direct involvement of the aortic annulus by the aneurysm. 17° It should be noted that syphilis is a far less frequent cause of aneurysms nowadays than formerly. Older series,Z3. 60 reflect an incidence of syphilitic aneurysms of 6 2 - 8 2 % , the vast majority of which were saccutar_thoracic, involving the ascending aorta or arch. Over-all, thoracic aneurysms a~b more common in males by a ratio of 3" 1. 78 Thoracoabdominal aneurysms are less common, comprising only 42 cases of those reported by De Bakey et al. 76 Two thirds of these were caused by arteriosclerosis and the remainder by syphilis. Mycotic ~neurysms have resulted from infection by a varietY of organisms, including streptococci, salmonellae, L i s t e r i a m o n o c Y t o g e n e s and others. ~zS,~56.203. aTt Development is ordinarily associated with a recognized source of blood stream sepsis, commonly endocarditis. The organisms usually gain entry at a pre-existing aortic lesion, such as an atherosclerotic plaque or a coarctation. Mycotic aneurysms also occur as a result of infection of an aortic suture line or from direct extension to the aorta of an infection, such as a mediastinal abscess. 27 Aortitis of uncertain etiology is an occasional cause of aortic aneurysms. Congenital aortic aneurysms are most commonly associated with minor or overt coarctation of the aorta, and will not be discussed further in this monograph. The underlying defect common to all aortic aneurysms is weakening of the aortic wall due to destruction of the media, the layer containing elastic fibers. Once this has occurred, the remaining fibrous tissue graduallystretches, permitting the formation of an aneurysm. Destruction of elastic tissue by arteriosclerosis is diffuse, leading to the formation of fusiform aneurysms, whereas destruction by syphilis is usually focal, leading to the formation of saccular aneurysms,~2~. 19~ A s the aneurysm increases in diameter, wall tension increases according to the law of Laplace, promoting further enlargement, until rupture ensues. The laminated clot which lines most aneurysms provides little support to 6

FiG. 1.---Specimen showing opened aneurysm with lining clot.

the thinned-out aortic wall, as the clot usually undergoes peripheral liquefaction necrosis (Fig. 1 ).

ABDOMINAL ANEURYSMS SYMPTOMS AND DIAGNOSIS

Although pain in the abdomen or back is noted at some time in about half of the patients with abdominal aortic aneurysm, patients frequently have no symptoms even when the aneurysm is large, and the diagnosis is often made as a result of a physical examination or x-ray of the abdomen done for other reasons. Nowadays, an increasing number of small aortic aneurysms are discovered incidental to aortography for visualization of various branches of the abdominal aorta. Large aneurysms may cause vague epigastric discomfort or mild low back pain, and an occasional patient becomes aware of prominent abdominal pulsations. Vascular insufficiency in the legs is more common in patients with abdominal aneurysms than in the normal population, but provides no diagnostic help. Embolism of debris from the aneurysm is unusual. More impressive symptoms occur if the aneurysm enlarges rapidly. This often causes back pain and epigastric discomfort, presumably due to increasing tension on surrounding structures. Leakage of blood into the retroperitoneal space causes worsening of these symptoms, ls3 often 7

with radiation of pain into the groin. Finally, with sufficient blood loss, shock and death may ensue. Retroperitoneal leakage of blood has also been thought to cause "autosympathectomy" so that one foot becomes warmer and drier than the other, s4 although this is not commonly of diagnostic value. One fourth to one half of patients with abdominal aortic aneurysms ( A A A ) are symptomatic prior to rupture. TM a43 Although catastrophic rupture with immediate death may occur, it should be emphasized that the pain o~ rupture is frequently intermittent and may be associated with intermittent nausea or faintness. Transient episodes of hypotension are not unusual. TM It is not possible to distinguish with certainty between the patient with pain due to a rapidly enlarging aneurysm and the patient with pain due to retroperit~neal leakage of blood. Thus, the onset of back pain a n d / o r pain radiating to the groin in a patient with an aneurysm is an indication for emergency operation. A more obvious emergency exists in the patient with Shock as well as pain. A ruptured aneurysm may or may not be palpable. Tenderness over the aneurysm or in the flank with blood below the :inguinal ligament may be present, resembling a Pott's abscess or hernia'. ~1 Unusual forms of rupture o c c u r ; a s into the gastrointestinal tract, resulting in hematemesis or melena~ With rupture into the vena cava, an abdominal murmur may be present together with venous engorgement of the legs, widened pulse pressure and perhaps cardiac failure.44,115 Szilagyi and associates ls9 have pointed out that leakage of blood.into the retroperitoneum can cause a mild to moderate systemic reaction simulating sepsis, with fever, leukocytosis and anemia. The presence of the characteristic pain is helpful in distinguishing this picture from sepsis, as, of course, is the ability to palpate an aneurysm or see it on radioloNc examination. On physical examination, the ordinary fusiform aneurysm presents as an expansile mass between the umbilicus and xyphoid process. This location often leads the inexperienced examiner to believe that the aneurysm is unusually high, involving the renal arteries. In truth, thoracoabdominal aneurysms or ancurysms localized above the renal arteries are seldom palpable. Depending on the build of the patient, an abdominal aneurysm has to be 4 to 5 cm. in diameter to be palpable. Both hands should be used to confirm that the mass is expansile, to avoid mistaking for an aneurysm the normal aortic pulse transmitted through an abdominal mass. Such a mistake is more common when there is a lumbar lordosis or when the aorta is elongated and tortuous from hypertension. Physical examination is all that is necessary for diagnosis in most instances, and this should, of course, include thorough evaluation of the enlirc cardiovascular system. Lateral x-ray films of lhc abdomen taken with the technic used for examination of tile lumbar spine may 8

Fro. 2 . ~ A , lateral abdominal x-ray showing aneurysm wall. B, view of aortogram showing straight channel.

show a curvilinear calcification outlining the aneurysm wall in about half of the patients with an abdominal aneurysm (Fig. 2, A).ls-z Bone erosion is unusual with fusiform arteriosclerotic aneurysms, but common with those of saccular syphilitic origin. 59 We feel, as do most surgeons, 62, ~'a that aortography is unnecessary in the uncomplicated case. If the location of the aneurysm is unusuaI, if there is evidence of peripheral vascular occlusion or if the examiner is uncertain whether the aorta is simply tortuous or is aneurysmal, aortography is indicated. Most arteriosclerotic abdominal aneurysms are filled with clot, save for a central channel, and the aortogram frequently does not demonstrate the dilatation (Fig. 2, B ) . 62, 1G9 This is less true o f false aneurysms, saccular aneurysms or thoracoabdominal aneurysms, which are more easily demonstrable by aortography.

NATURAL HISTORY AND RESULTS OF OPERATIVE TREATMENT Unlike thoracic aneurysms, which frequently cause death by compression of surrounding structures, arteriosclerotic aneurysms of the abdominal aorta cause death mainly by rupture. Distal embolism of aneurysmal contents occurs, '°9 as does thrombosis 9~, ~,z and bacterial infection of an untreated aneurysm, '7' but these problems are rare. The only accepted treatment for abdominal aneurysms is operative. Decisions concerning therapy, then, must be ba~ed upon knowledge of survival figures with and without operation, recognizing that although pain and other symptoms may be relieved, the sole value of operation, 9

insofar as survival is concerned, is the prevention and treatment of rupture,

UNRUPTURED ABDOMINAL AORTIC ANEURYSMS In the mid 1950's, when excision and graft replacement of abdominal aneurysms became widespread practice, the yardstick against which the results of resection were measured was the data provided by Estes in 1~50. s9 This series of 10I cases of untreated abdominal aneurysms, alnhost all arteriosclerotic, was collected immediately prior to the development of modern su~ical therapy. Only 18.9% of the patients survived 5 years after diagnosis,: compared to the 79.1% expected 5-year survival rate in a normal population of the same mean age (65 years). Of patieiats for whom the cause of death was known, 63.3% died of rupture of the aneurysin; Thus, Estes documented the poor prognosis of patients with abdominal aneurysms and showed that the aneurysm itself caused death by rupture in about two thirds of his patients. This incidence of rupture may be inaccurate, however, as the cause of death is unknown in 15 of hisj patients: Subsequently, in the 1950's, other studies of untreated A A A 5 9 . 60. lo2. ~83. 212. z14 confirmed the poor prognosis and the high incidence of rupture. It was also appreciated that associated cardiovascular disease was a major reason for the shortened life expectancy of patients with A A A and that the aneurysm was a "local expression of a' generalized disease. T M By the mid 1960's, numerous reports of long-term results of resec, tion of A A A had been published. These documented the improved long-term survival resulting from resection (Fig. 3).4°, 177.197 During this time, however, controversy ....not yet settled arose concerning the indications for surgery in patients with associated cardiovascular disease, or small or asymptomatic aneurysms. Statistical evaluation of the results of resection of such lesions was difficult because of: 1 ) the statistical impossibility of comparing diverse groups of patients treated in different institutions and 2) dramatically decreasing operative mortality rates resulting from experience 199 and from improved technics, ~, laZ including abandonment of the use of homografts. 177 In 1964, De Bakey et a[. 75 reported 1,449 surgically treated patients with AAA, followed from 1 to ! 1 years postoperatively, with an over-all survival of 63% (including those with ruptured aneurysms). Their data indicated that the coexistence of cardiovascular disease decreased survival in surgically tre~ated patients but that survival in th~s group was nevertheless much greater than in patients without operation (Fig. 4). By /966, the series from Baylor consisted of 3,000 patients, 12 with an over-all survival of 58% at 5 years. The operative mortality in elective cases was 7% over-all, 15% in patients with hypertension and heart disease, 13 % in those with heart disease only, 10

,oo %

8o! ~

~

65%

31%

(Resec,ed)

10%

i

o

2

3

4

5

Yeors

6

7

B

NO HYPERTENSION OR HEART DISEASE. 0 ALL RESECTED CASES.

~%1II IIIll I~,

90

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o

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i

c~. ~'",,,,,,

~ I " ~ ? ,77~

60

83 __

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"

,,.....74

"..

" ~

HYPERTENSION AND HEART DISEASE

~..~

"'"'®"',,,,,,. 79 -

-

~'~-~. ",~..,..

~,44

-- NON-- RESECTED CASES.

s,

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%

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I

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6

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7

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8

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9

I0

PERIOD OF SURVIVAL IN YEARS

FIG. 3 ( t o p ) . .... Comparison of survival of normal population and of patients with abdominal aneurysm untreated and resected. Other reported survival rates of untreated patients are even less than that shown. The majority of late deaths in the treated patients were caused by complications of arteriosclerosis. Data for treated patients represent percentage survival of those patients operated on long enough prior to 1960 to have been followed up for the times indicated. (Reprinted with permission J97) FIo. 4 ( b o t t o m ) . Life expectancy of all patients with abdominal aortic aneurysm in this series: those -without hypertension or heart disease, those with hypertension and heart disease and the nonresected cases of Estes and Wright. (Reprinted with permission.7~)

4% in those with hypertension only and 3% in those with neither heart disease nor hypertension. As reflected by these figures, the major causes of operative mortality following resection of an AAA relate to complications of arteriosclerotic cardiovascular disease. Age alone correlates with surgica! risk only in that the incidence of arteriosclerotic cardiovascular disease (ASCVD) is greater in older patients. Esselstyn 11

reviewed a series of 152 patients 75 years of age or older who had AAA. Of the 69 untreated patients, 37% went on to die of a ruptured aneurysm, whereas the operative mortality for elective resection was 14 % of 3 7 patients. They concluded that age alone is no contraindication to resection of an A A A but that the presence of associated diseases, the general physical status of the patient and the size of the aneurysm nmst be carefully evaluated in determining operative treatmerit. In a series of 100 consecutive patients with su~ically treated AAA, Friedman et aI. 94 noted that 47% had clinically evident coronary artery disease, as compared to an expected incidence of about 10% in a comparable segment of the population. The incidence of coexisting cardiovascular disease, in their series is summarized in Table 2. Postoperative morbidity, manifested by peripheral arterial occlusion, stroke and myocardial infarction, correlated Well with clinical evidence of pre-existing arteriosclerotic occlusive disease. Angina pectoris was especially important in this ,respect. None of the 4 deaths, however, occurred in patients with symptomatic heart disease. Postoperative renal failure, a frequent cause of deati~in the e~rly years of excision of AAA, seldom occurs nowadays in elective cases. 11° Despite these excellent surgical results, however, several authors have cautioned against resection of small or asymptomatic aneurysms, especially in patients with associated cardiovascu!ar disease, because death is more likely to result from cardiovascular problems than from rupture of the aneurysm, zT, ~ . ~99.zn This remains a difficult problem both in terms of statistical evaluation and of therapeutic decisions regarding an individual patient. No randomized series of aneurysms treated with and without operation is available, and none is likely to be. Thus, the available figures must be analyzed critically for insight. The data usually cited in support of nonoperative management of A A A are those of Schatz e t of., 175 W o l f e and Colcherfl ~ Klippel and Butcher, z7 and Bernstein e t al. ~9 The first three of these series suggested that the incidence of death e t al. ss

I

I II

T A B L E 2.

I

I

I

I

II

I

I

II Im

II

II

II

I

II

I

PRESENCE OF O T H E R CARDIOVASCULAR DISEASE IN 1 0 0 CASES TM CORONARY ARTERY DISEASE

PERIPHERAL ARTERIAL OBSTRUCTION

47 18 4 19

18 43 6 15

Coronary artery disease Peripheral arterial obstruction Cerebrovascular disease Hypertension Total with cardiovascular disease

CEREBROVASCULAR DISEASE

4 6 8 5

HYPERTENSION

19 I5 5 34

88

*The n u m b e r in each box represents the n u m b e r of instances of coexistence of the disease listed above and the disease listed to the left. I

IIII

II

Ik~

I

p

I

~

w

. . . . . . .

12

m

I

I

,

Jl

by rupture of AAA, especially small ones, was less than the incidence of death due to arteriosclerotic cardiovascular disease, and recommended operation only for symptomatic or rapidly enlarging lesions. Wolfe and Colcher's series consisted of 35 cases, of which 25 were aneurysms of less th:an 4.5 cm. in diameter. None was operated on and none ruptured. Klippel and Butcher reported 30 patients followed 5 years or until death. Two aneurysms, one 6 cm. in diameter and one 10 cm. in diameter, ruptured, whereas patients with severe ASCVD died of causes other than rupture. Resection of aneurysms over 6 cm. in size in patients free of ASCVD was recommended, along with resection of enlarging and symptomatic ones. Schatz e t al. 175 studied 141 untreated patients, with follow-up data on 137 of them. The 5-year survival of those with other ASCVD was 20%, whereas 50% of those free of ASCVD at the time of diagnosis survived 5 years. The over-all incidence of rupture was 14 %. Szilagyi TM has questioned the value of these data because 80.8% of the patients were rejected for operation, implying that many were thought to have extensive ASCVD. Foster e t al. 93 believed that the results in these three series were at variance w~th their own findings, and with those of others (see below) because of: 1 ) a low incidence of large aneurysms; 2 ) questionable documentation of diagnosis, especially for small aneurysms; 3 ) inaccurate methods of determining the cause of death; 4) short or indeterminate lengths of follow-up in certain instances; 5) lack of standardization of extent of associated diseases; and 6) the method used to select patients for inclusion in the study. Bernstein e t al. 19 collected all the previously available data on the natural history of AAA together with results of operation. Using these combined data they concluded that "the incidence of rupture in the small aneurysm is considerably less than the risk of elective operation." They considered that the elderly patient with severe ASCVD should be operated upon only for a "large aneurysm (7 cm. or greater), recent growth, or progressive symptomatology, particularly pain." The interpretation of these data, as it applies to present-day problems, has been criticized 93, ~9~ because 1 ) important figures are drawn from the three previously criticized series, and 2) conclusions should be based upon the present operative mortality rates for elective resection of small aneu~,sms ( 2 . 5 - 3 % ) , not upon the 5 - 1 8 % operative mortality rate for elective resection of A A A of all sizes. It should be clearly noted, however, that all authors agree that large AAA (more than 6-7 cm.) should be aggressively resected, since the danger of rupture is great (Table 3 ). It is apparent that the study which sets the standard is that of Szilagyi e t al. ~9~ Theirs is the only study based on sizeable numbers of patients, from the same period and the same institution, with careful follow-up and thorough statistical analysis. The treated and untreated groups are not randomized, but this is acknowledged by the authors 13

TABLE

3., UNTREATED ABDOMINAL AORTIC A N E U R Y S M

Importance of SizelO DEATFI D U E TO RUPTURE ( % ) < 7 cm. > 7 cm.

AUTHORS Cralle

Bleidman and associates Sommerville and associates Szilagyi and associates

4

82

18 10 20

72 83 43*

~" "~'Based o n 6 c m .

and appropriate measures are taken to eliminate resultant bias insofar as possible. Szilagyi compared 480 patients who underwent resection of A A A with 223 untreated patients, all seen at the Henry Ford Hospital between 1944 a n d 1965. Surgically and nonsurgically treated patients were selected for comparability on the basis of numerous factors, such as heart disease, hypertension, age, an'd size o[the aneurysm. Figure 5 illustrates the cumulative survival of comparable groups of treated and untreated patients. Figure 6 illustrates survival of treated and untreated patients with small aneurysms. It should be recognized that these results (Fig. 6) undoubtedly apply to a population of patients free of severe complicating disease. That is, resection of small aneurysms in patients with severe ASCVD would not improve s u r v i v a l rather it would likely worsen it as compared to an untreated population with similar severity of ASCVD. Table 4 indicates the effect of associated diseases and surgical experience on operative mortality rates. Finally, Table 5 shows the causes of death in resected and in untreated patients. The data of Szilagyi et aI., I9t i n o u r opinion, provide the m o s t useful information on which to base decisions concerning treatment of AAA. Their data correlate well with those of Foster et al. 93 SOMMARY.--In summary are the following data: L a r g e a n e u ~ , s m s (larger than 6-7 cm. in d i a m e t e r ) . - - ( 1 ) The risk of rupture is 4 5 - 5 0 % '(of all cases observed during a 10-year period). (2) Operative mortality is about 10-15 %, influenced by presence or absence of associated factors affecting risk. (3) Five-year survival without resection is 5 - 1 0 % ; with resection, about 50%. One-year survival without resection is about 5 0 % . S m a l l a n e u r y s m s (less t h a n 6 cm. in d i a m e t e r ) . - - ( 1 ) The risk of rupture is 15-20% (of all cases observed during a 10-year period). (2) Operative mortality in patients free of serious associated disease is about 3 % . (3) Five-year survival with resection is about 6 5 - 7 0 % and without resection about 50%, in comparable groups of good-risk patients. 14

"'~. , ~ , , , , , .

POPtlLAT~0~ ,'~MPL.E,.,.m..,Ir,~C~

POPUL~WO~ S~PLE. %, NON-SURGICAL * ~,.,,,

% SURVIVAL RATE

"-,,, *"%,,

PATIENTS,SURCaC~

NON-St~IGICAL

2

3

4

S 6 7 S LENGTH OF SURVIVAL (YEARS)

S

~

tl

=

t3

A,A.A. R - 2 8 - 6 6

I00 i

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6cm~, SURG1CAL

% SURVIVAL RATE

( 6cm., NON'SURGICAL D

40

30.

20-

0

!

2

3

4

5

6

7

8

Q

•

9

10

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LENGTH OF SURVIVAL (YEARS)

FIG. 5 (top). Observed cumulative 13-year-survival experience of 244 surgically and 105 nonsurgically treated cases of abdominal aortic aneurysm standardized for age, card~.c status, blood pressure and renal function, and calculated survival experience of general-population samples compiled for corresponding sex and age distribution. (Reprinted with permission, Szilagyi, et al.Z91) FIc. 6 (bottom). -Observed cumulative 13-year-surviva! experience of 44 cases of small ( < 6 cm.) abdominal aortic aneurysm treated nonsurgically and 74 cases of small abdominal aortic aneurysm treated surgically; both groups standardized for age, cardiac status, blood pressure and renal function. (Reprinted with permission, Szilagyi, et al.191)

15

O~

12/110

1/37 6/51 5/22

2.7 11.8 22.7

150 150-200 200-250 >250 TOTAL

SYST. B.P, (MM. HG)

0.0 13.0 9.6 16.7 0.0

15/'139 22/131 4/14 0/0 41/284

NO.

10.8 16.8 28.6 0.0

.

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%

TOTAL

i

i

1952-5 1956-7 1958-9 1960-1 1962--3 1964--5

"EXPERIENCE" OBSER. PERIOD

8.8 19.2 21.4 50.0 0.0

OPER. MORTAL*YY

10/113 5/26 3/14 1/2 0/0 19/155

OPER. MORTALITY No. ~

Normal Class I Class II Class III Class IV TOTAL

CARDIACSTATUS

*Groups standardized for age, cardiac status, hypertension and renal and pulmonary function, as the case may be.

TOTAt.

Small ( < 6 era.) Medium (6-10 cm.) Large ( > 10 cm. )

SIZE ANEUR.

0/2 7/54 8/83 3 / 18 0/1 18/158

%

OPER. MORTALITY

No.

OPER. MORTALITY No. ~

40-50 51-60 61-70 71-80 80+ TOTAL

AGE (YR.)

AND EXPERIENCE ON OPERATIVE MORTALITY .191

TABLE 4.~ EFFECT OF AGE, CARDIAC STATUS, SIZE OF ANEURYSM, HYPERTENSION

i

2/3 9/20 I3/48 4/59 7/70 3/86 38/286

66.7 45.0 27.1 6.8 10.0 3.5

%

OPER. MORTALITY

No.

T A B L E 5.- CAUSES OF DEATH (NONOPERATIVE AND TOTAL OPERATIVE MORTALITY IN 434 SURGICAL CASES) 19.1.

%

No. CASES

CAUSE OF DEATH

Operative mortality* Postoperative mortality Coronary atherosclerosis Cerebral atherosclerosis Graft failure Malignancy Renal failure Other

59 107

14.7 24.6 41 12 10 7 4 33

166

TO'rAL

9.4 2.8 2.3 1.6 0.9 7.6 39.3

223 NONSURGICAL CASES CAUSE OF DEATH

N o . CASES

%

Rupture Coronary atherosclerosis Cerebral atherosclerosis Malignancy Renal failure Other

78 38 11 I1 6 30 174

34.9 17.0 4.9 4.9 2.7 13.5 77.9

TOa'AL *Ruptured aneurysms not included.

All aneucvsms..~ T h e most c o m m o n cause of operative and late deaths is associated A S C V D (especially coronary arteriosclerosis). It must be emphasized that statistical data should be applied with understanding in decisions regarding surgical treatment of the individual patient. Clearly there are situations, especially in the case of small aneurysms, in which associated factors make operative risk prohibitive. Also, patients with severe A S C V D are more likely to die of this than of a small A A A . However, available data clearly indicate that large aneurysms are a serious threat and should be aggressively resected. Small aneurysms should likewise be resected in good-risk patients. Szilagyi has advocated resection of small aneurysms in otherwise healthy patients who have a life expectancy of ] 0 or more years (up to 76 years of age). This seems to be a reasonable approach.

RUPTURED ABDOMINAL AORTIC ANEURYSMS Arteriosclerotic abdominal aortic aneurysms most commonly rupture into the retroperitoneum, about 2 - 4 cm. distal to the renal arteries, on the posterolateral aspect of the sac. 1~5 This is usually near the region of greatest diameter of the aneurysm, where, according to Laplace's law, wall tension is greatest, ~s3 and where the wall is unsupported by the peritoneum. 1°~ Rupture may also occur into the free peritoneal cavity, or, rarely, into adjacent structures such as the vena cava, 17

renal vein 1as or bowel. TM 10.~These latter forms of spontaneous rupture are rare. The developmen t of an A-V fistula was noted by Beall e t al. ~5 in 4 out of 130 patients admitted with ruptured AAA. In a more typical series of 107 ruptured AAA, 15 ruptured free into the peritoneal cavity, whereas the remaining 92 ruptured into the retroperitoneum, l°a It is a common and probably accurate clinical observation that rapidly enlarging aneurysms are prone to rupture, although statistical confirmation is lacking. Szilagyi a91 believes that all aneurysms enlarge progressively, b u t , a t w i d e i y differing rates, and that progressive enlargement with evgntual rupture is the natural history of the lesion. Presumably, rapidly enlarging ane~urysms tend to cause pain, ~°s and it is documented that symptomatic aneurysms are prone to rupture. 1°2, ~sa Symptoms are often associated with leakage of blood into the retroperitoneum, however, and thus symptoms may be a result of rupture, rather than antecedent to it. This makes the s[atistical differentiation of ruptured from symptomatic aneurysms difficult or impossible, but from a clinical point of view imparts ominous significance to symptomatic aneurysms. Blum a~ has appropriately suggested that the term "ruptured" be restricted to those critically ill patiems in whom large amounts of blood are found when the abdomen is opened. S3,mptoms do not always precede frank rupture, however. ~97 In one series ~°s only 6 of 26 patients were aware of their aneurysm prior to rupture, and BarrattBoyes x2 noted that only one-half of his patients complained of pain prior to rupture. Gardner, 9s by contrast, found that only 2 of 24 patients were free of symptoms prior to rupture. Rupture of an AAA can be catastrophic, with death rapidly occurring from exsanguination, especially if the lesion ruptures into the free peritoneal cavity. TM More commonly, however, rupture is heralded by the onset of severe pain or hypotension, with temporary survival. Barratt-Boyes, az in 1957, reported 18 patients with ruptured AAA, carefully observed, only 6 of whom were operated on by earlier methods. Survival following admission ranged from 6 hours to 17 days, and all but 2 of these were apparently in sbock during the first 12 hours. Similar findings were reported by Crane. 59 Nowadays, such patients would be operated on promptly, as untreated rupture probably is uniformly fatal, ~2 although an occasional patient may develop a retroperitoneal false aneurysm and survive for an unusual length of time. aS, sos Operative treatment of ruPtured AAA has resulted in significant survival. A collective review of 756 patients surgically treated for ruptured A A A between 1953 and 1968 showed an over-all mortality rate of 56%. ~°a Operative mortality rates as low as 34% have been reported in one large series of patients with ruptured AAA. 62 The results are highly dependent on the state of the patient when surgically treated. Such factors as shock, renal failure or cardiac arrest exert a profoundly deleterious effect, and the results are markedly inferior to those obtained by operating on patients who have only a small retroperitoneal 18

hemorrhage, but no alteration of vital signs. 98, 103. 197 Major causes of death i n the postoperative period are roughly evenly divided between renal failure, continued hypotension and cardiopulmonary problems, 43 all a result of blood loss. Thus, the presence of a ruptured or symptomatic abdominal aortic aneurysm is a clear indication for operation.

AORTIC PROSTHESES By the late 1950's, it was recognized that aortic homografts were subject to late failure characterized by the development of atherosclerotic degeneration with subsequent occlusion, aneurysm formation or rupture.67. 119.12s. 177. ,90 The failure rate of aortic homografts for a 10'year period in one study was 4.1% per year. 1~9 Various aortic prostheses were developed and substituted for homografts. Early prostheses, such as Vinyon N, zS'e6 nylon and Orlon were unsatisfactory because of a tendency to fragment, rupture or thrombose and were quickly discarded in favor of Teflon or Dacron. 75, 197 Using modern aortic prostheses, the long-term failure rate has been about 2 % . 7~, 191 With present technics, failure will likely be even less frequen(. Failure has resulted largely from infection, thrombosis of the prosthesis, suture line disruption, or formation of a false aneurysm. Rupture of the prosthesis itself has rarely been a problem. False aneurysms may result from" 1 ) f r a y i n g of the prosthesis; 2) leaking anastomosis with suture line hematoma and failure to heal; 3) infection; 4) use of inappropriate suture material; ~92,z°~ or 5) distraction of sutures from the aorta or iliac arteries because of small bites when suturing, poor quality vessel wall, or aseptic necrosis due to excessive dissection of the proximal cuff and destruction of its blood supply. It is clear that the integrity of an anastomosis between a vessel and a prosthesis depends in part on the continued integrity of the sutures used for anastomosis. The ingrowth of tissue per se is not sufficiently strong to secure the anastomosis. This is apparent to anyone who has stripped a prothesis from its bed and noted the ease with which this can be accomplished, even years after implantation. Silk sutures used for anastomosis eventually fragment, permitting disruption of the suture line and formation of a false aneurysm 42. 1~9. ~z. ~s8 (Fig. 7). At the time of reoperation for removal of such a false aneurysm, the fragmented silk sutures are readily observed, with the prosthesis lying partially or totally free within the lumen of the aneurysm. NonabsorbabIe synthetic vascular sutures, of which a variety are now available, should therefore be used for suturing vascular prostheses, as they are more durable than silk. Presently, surgeons may choose between a variety of prostheses for aortic replacement. The most common are made of Dacron or Teflon, either woven or knitted, and are available in various weights. The most widely used are crimped, to provide elasticity and permit bending with19

Fro. 7., .....F a l s e a n e u r y s m at p r o x i m a l e n d o f prosthesis.

out kinking. Uncrimped prostheses in which the elasticity is a property of the yarn have been used~with success. 192 This type of prosthesis has been criticized on the theoretical basis that pore size varies with varying degrees of stretch, unlike the crimped prostheses. 2°8 Pore size and the nature of the material used for construction influence the manner and degree of incorporation of the prosthesis ~by the host. Nonporous or slightly porous prostheses are prone to thrombosis, presumably because ingrowth of living tissue through interstices of the prosthesis is necessary" for the development o f a lining (neointima or pseudointima).-~°~- Following implantation of a porous prosthesis its interstices become filled with clot. ONanization follows, permitting living tissue to reach the luminal surface. In the meantime, a thin layer o f fibrin or thrombus is deposited upon the luminal surface. This eventually organizes into a layer of fibrous tissue, stabilized by continuity with the tufts of fibrous tissue growing through the interstices. ~'I9 A mature such fibrous layer is present 6 to 12 months after implantation, but endothelium extends only a few millimeters from the suture lines into the prosthesis. ~92 Arteriosclerotic plaques have been observed within such a pseudointima but have not been a clinical problem. Formation of pseudointima is inconstant, however, and areas of the prosthesis bare of lining are common. 11:~Warren e t al. 2o2 suggest that the organized pseudointima forms not as a result of organization of a 20

fibrinous lining, but as a direct result of ingrowth of fibrous tissue through interstices of the prosthesis, thus explaining the sometimes spotty nature of the lining. At any rate, stability of this lining is dependent on its continuity with the capsule of fibrous tissue outside the prosthesis. In the absence of such continuity, the poorly supported pseudointima may peel free of the prosthesis and form an obstructing flap, with subsequent thrombosis of the graft, Thus, pore size, as previously noted, is important. For example, woven grafts, having small pores, develop a less stable pseudointima than do knitted ones, whichhave l a ~ e r pores. 95, 114 The stability of the pseudointima is also influenced by the type of fabric used for the prosthesis. Teflon prostheses are quite unreactive in tissue and seem to develop a less stable pseudointima than Dacron.46, 100.1~4. lsl Also, the weight (thinness) of the particular fabric may be important, and Wesolowski e t a / . 2°6, 2o7 suggest that the use of a smaller diameter yarn, permitting construction of thinner walled prostheses, will permit better tissue ingrowth for a given pore size. Davila e t al. 6s suggest Dacron felt for construction of prostheses, in the belief that compression and shearing o f tissue growing through interstices is a characteristic of k n i t t e d a n d woven material that wilI always lead to instability of the pseudointima. Experimental studies of various other materials, including those of biologic derivation, are being carried out, but will not be discussed here. It should be noted, when evaluating experimental studies, that a stable, living pseudointima forms more readily in the dog than in the human being. 67, 192,202 At present, knitted Dacron appears to be the best choice for clinically useful ~rterial prostheses, and should be used where possible. The lightweight knitted material may prove best of all, because of its porosity and thinness, coupled with adequate stren~h and ease of handling. These prostheses must be preclotted to reduce initial blood loss. In situations requiring an unusually long prosthesis or complete heparinization of the patient, woven prostheses should be used to avoid excessive bleeding. COMPLICATIONS OF PROSTHESES AND THEIR MANAGEMENT

THROMBOSIS. Late thrombosis of a prosthesis may result from local factors, such as obstruction by a flap of pseudointima, infection, or kinking, or may be due to poor run-off. Thrombosis in the immediate postoperative period is unusual, and should arouse suspicion of either faulty operative technic or distal arterial obstruction. Immediate re-exploration is indicated in this circumstance, and operative arteriography is often helpful. In late thromboses, usually only one limb of a prosthesis is involved, and usually there is sufficient collateral circulation to maintain viability

21

of the extremities while preoperative studies are done. Understanding the cause of late thrombosis is important and is the basis for decisions regarding therapy: Basically, evidence of infection should be sought, and an arteriogram m~ide. The arteriogram defines the site of occlusion and, if sufficient Collateral circulation is present, may demonstrate the state of the distal circulation. For the latter purpose, operative arteriography mayalso be necessary. Treatment, except in the presence of infection, generally consists of repl/:ce,ment of the prosthesis or a limb of it, together with restoration of distal~ circulation if run'off is poor. FALSE A N E U R ¥ S M . -U -The development of a false aneurysm requires re-establishment of continuity between the prosthesis and the host artery. This usually necessitates rep!iacement of all or part of the prosthesis, using synthetic material. Preoperative aortography is sometimes desirable, to define ~the nature and location o f the lesion, but is not always necessary as this informaiion is readily apparent in the operating room. These aneurysms are often multiple, and replacement of the entire prosthesis is frequently required. AORTOENTERIC FISTULA. Acrrtoenterjc fistulas occur most commonly at the proximal suture line, where the infrarenal aorta and the prosthesis have been joined. Such fistulas are likely due to rupture of a suture line, in the same sense that false aneurysms are, but in this case rupture occurs into an adjacentlportion of the small bowel, usually the duodenum. Spontaneous fistulas between untreated aneurysms and an adjacent hollow viscus have been reported, s: and fistulas do occasionally occur between an iliac artery anastomosis and the ileum. Fistulas also may be due to direct rupture of a degenerated homograft into the intestine. 117 One fistula has been reported at the site of aortic cross clamping, 42 proximal to the suture line. To our knowledge, none has been reported involving the colon. The presence of an aortoenteric fistula is manifested by the onset of gastrointestinal hemorrhage. The average time of onset in those patients developing a fistula unassociated with infection is about 6 months following operation, 1:7 but such a fistula may first appear several years afterward. TM A fistula due to infection of the prosthesis will usually develop more rapidly, 'although administration of antibiotics may cause delay. The gastrointestinal hemorrhage may be Catastrophic, but there is usually time for treatment prior to exsanguination. Indeed, some patients may have melena for 4 to 6 weeks. 7°. ::7 Death from exsanguination is inevitable if the fistula is not repaired. TM a:7, 159 Diagnosis is aided by the demonstration of a false aneurysm by palpation or aortography. A gastrointestinal series may show displacement of the duodenum (by hemorrhage or by a false aneurysm), extravasation of barium or, as pointed out by Humphries, :~7 a different cause of the bleeding. When there is time, therefore, a gastrointestinal 22

series should be done. Aortogi'aphy is of less value but may demonstrate an unrecognized false aneurysm or, occasionally, the fistula itself, s~ Treatment should consist of immediate operation, with control of the bleeding, incision of the fistula and repair or resection of the involved bowel. If infection is clearly present, the therapy must follow the guidelines outlined below. However, there is usually uncertainty of the presence or absence of bacterial contamination, and the proper method of repair is controversial. Clearly, many have been successfully treated by simple closure of the leak between the aorta and the prosthesis; or more commonly by orthotopic replacement of the prosthesis, in the uninfected false aneurysm. 11.~Viable tissue should be interposed between the new suture line and the bowel if possible. O~hers have suggested that all aortoenteric fistulas should be regarded as infected and treated accordingly. Certainly if strong suspicion of infection exists, the latter philosophy should apply. The mortality rate for operative treatment o f 13 aort0enteric fistulas reported by De Bakey in 196370 was 3 8 % . Recurrence and infections of prostheses following repair have been noted. ~17 Both the incidence of aortoenteric fistulas and the mortality rate following their repair have undoubtedly declined during recent years. IYrECTrON.--The incidence of infection of aortic prostheses is approximately 1 % - 6 % . 4~. 96 There is evidence that the use of prophylactic antibiotics, either systemically ~35 or by soaking the prosthesis in a solution of antibiotics 4, tvz may lessen the incidence of infection. Predisposing factors include debilitation of the patient, steroid or immunosuppressive therapy and, of course, direct operative contamination. 45 The use of prophylactic antibiotics not only seems to influence the type of the infecting organism, but also may prolong the interval between operation and manifestation of infection. Infection may become manifest in a variety of ways. The most obvious is a wound infection with direct extension to the prosthesis, though this is unusual when the prosthesis is confined to the abdomen. More common is delayed abscess formation, hemorrhage, false aneur3'sm, thrombosis of the graft, aortoenteric fistula or sepsis. Usually, the infection is obvious. Infection should always be suspected when a vascular anastomosis fails to heal properly, ~37 and cultures of adjacent tissues should be taken at reoperation, even if infection is not apparent. Although many cases have not been reported, two principles regarding the management of infected prostheses have become clear: first, in order to cure the infection, the infected prosthesis must be removed; second, a new prosthesis cannot be placed in an infected field without virtually certain recurrence of t h e infection. Homografts are affected similarly when placed in an infected field and should not be used. TM Autogenous tissue tubes may resist infection when placed in an in23

~/",

(

~

,L Ax. K

,.-

Pectoraiis Major

Fern Art

"

"

L e a p Femora/

/ lJ

Fro. 8.- Diagram of the technic of insertion of an axillofemoral graft. A preclolted, knitted Dacron graft is tunneled between the axillary and femoral incisions and is then sutured end-to-side to the first portion of the axillary artery and to tile common femoral artery. (Reprinted with permission, Mannick and Nabseth.14~) fected area, 4°. ,3, but none is large enough to be useful for replacement of infected aortic prostheses. Shaw and B a u e 176 note that sepsis remains localized to the area of direct involvement of a prosthesis which has been in place long enough to become firmly encapsulated. However, sepsis propagates throughout the length of a thrombosed graft, or of one freshly placed. Thus, it may be possible to remove Only a portion (e.g., one limb) of a prosthesis with established infection if it is not thrombosed, rather than removing it entirely. The treatment, then, of the infected prosthesis consists of the following: 1 ) administration of appropriate antibiotics to control sepsis; 2) removal of the prosthesis or appropriate portion thereof; 3) re-establishment of the circulation via an alternate, uncontaminated route. Suggested alternate routes for bypass of infected abdominal aortic prostheses include: I) thoracic aorta-to-iliac artery bypass via the retroperitoneal gutter; 2'. '~6 2) transrectus sheath bypass from the proximal aorta to an iliac artery; 2'° and 3) axillofemoral bypass. 22. 4~.,4., Axillofemoral bypass (Fig. 8) apparently is the preferred method at present because of the ease with which the infected area can be avoided and the operation accomplished. 24

OPERATIVE TECHNIC Administration of antibiotics is begun preoperatively, as there is evidence that protection is provided against infection of prosthetic materials in:tplanted in the bloodstream.!aa A Foley catheter is inserted into the bladder for continuous monitoring of urine output and the patient is draped for access to both femoral arteries at the groin. Our preference is for a midline incision, from xiphoid to the pubis. The small bowel is placed in a Lahey bag and retracted to the right, while the omentum and transverse colon are lifted superiorly. The retroperitoneum is incised longitudinally over the aneurysm and control of the common iliac arteries obtained~ usually by encircling them with umbilical tapes. If these vessels are difficult to free from the adjacent iliac veins, which are a source of dangerous hemorrhage if injured, the iliac arteries can be clamped without complete mobilization. The ureters must be avoided in this area. The presence of iliac aneurysms, or occlusive disease, may dictate a more distal dissection for implantation of the graft. The circulation to at least one internal iliac artery should be preserved if possible. Next, the retroperitoneal incision is carried upward to the left renal vein and the duodenum is retracted to the right following dissection of the ligament of Treitz. The inferior mesenteric artery is located, divided and ligated near the aneurysm. The proximal inferior mesenteric vein may either be retracted or divided. Dissection is then carried about the neck of the aneurysm; that is, about the segment of normal caliber aorta between the aneurysm and the renal arteries. This procedure is begun by sharp dissection of the anterior and lateral portions of the aorta and is usually completed by blunt dissection of the retroaortic portion with the fingers. This is facilitated by the bulk of the aneurysm pushing the aorta away from the spine, creating a space between the aorta, the aneurysm and the spine, through which a finger is easily passed. If the renal vein is manipulated unduly during this dissection, troublesome hemorrhage may result from tearing of its tributaries immediately to the left of the aorta. If this appears likely, the left spermatic vein and any other branch in that area should be divided and ligated. The left renal vein apparently may be divided and ligated with impunity, a0 although we have not found this necessary and have carefully avoided it. It should be noted that the left renal vein occasionally courses behind the aorta. Renal arteries are easily palpated or visualized during dissection, and their injur 3, should be avoided. The location of the renal arteries should routinely be ascertained prior to clamping the aorta. At this point it must be decided whether the aneurysm is to be removed or treated by an intra-aneurysmal approach. Some aneurysms are easily excised, in which case the aneurysm is dissected from the retroperitoneal tissues as completely as convenient prior to clamping the aorta. Undue manipulation prior to clamping should be avoided, for 25

fear of dislodging aneurysmal contents with embolism into the legs. Removal of the sac is completed after transection of the aorta, with anterior traction on the aneurysm. Numerous authors have pointed out the advantages of the intrasaccular approach, Ga, 11-°,194 This permits definitive treatment of the lesion with decreased operating time, decreased blood loss and less frequent interference with sexual function; also a higher percentage of aneurysms can be replaced with a straight, instead of a bifurcation, prosthesis. 6a. 19a An abdominal lymphocele has been reported subsequent to excision of an A A A and this rare complication, too, should be avoidable with the intrasaccular approach. ~9 Reluctance ito leave the aneurysm wall in place is based on fear of subsequent'infection. This stems from case reports~ early in the experience with:operative treatment of aortic aneurysms, of four instances of infection:after incomplete resection of aneurysms:7.55, la0, 195 The residual aneuwsm wall is viable tissue, and the use of this technic has not resulted in! any recognized increase in infection in many cases since that early time. Ordinarily, then, the intrasaccular approach is preferable. Thirty milliliters of blood is withdrawn and a lightweight knitted Dacron prosthesis is precl0tted. Five thousand units of heparin is administered intravenously or 500 um,s ".* may be injected in each external iliac artery to avoid clotting of the blood in the legs. Heparinization may also decrease the incidence of pulmonary microembolism by prevention of intravascular clotting. -*a The aorta is clamped just below the renal arteries using a large De Bakey-type vascular clamp, and the iliac arteries are clamped using straight vascular clamps or De Bakey bulldogs. The aneurysm is opened longitudinally from just below its upper end to just short of the aortic bifurcation. The contents are readily scooped out by hand, leaving the viable wall in place; Back bleeding from lumbar arteries is controlled with a laparotomy pad, while each bleeding orifice is closed with a suture from within the sac. The incision in the aneurysm is then extended proximally to the normal caliber aorta, usually about 1 cm. below the clamp. Distally, the excision may sometimes be terminated just short of the aortic bifurcation, so that a straight prosthesis can be used. If the iliac arteries are aneurysmal', the incision is extended into each, forming a y, until a site suitable for anastomosis is reached. At each site of anastomosis one may then cut transversely either partially or completely around the circumference of the vessel, to provide suitable exposure. Usually hal~fwa.y around is sufficient (Figs. 9 and 10). The proximal anastomosis' is then made with nonabsorbable suture. The suture technic should be continuous, with large bites of aorta, providing maximal anastomotic strength. 1~7 The use of large-diameter suture, 3 - 0 to 4-0, minimizes tearing of the aorta. The suturing is usually begun in the midpoint posteriorly, with a single mattress suture, one {~_

J,

26

FI6. 9 (leJt).--The orifices of lumbar arteries are closed with figure-of-eight

sutures. Circumferential incisions are made at the junction of the aorta with the aneurysm above and below. These incisions are greatly facilitated by dissection from within as well as from outside the aneurysm. When the aneurysm begins abruptly, the graft can be sewn to the aorta without first incising the wall circumferentially (inset). (Reprinted with permission. Creech.63) Fro. 10 (rigizt).. A knitted Dacron graft is used to bridge the defect. (Reprinted with permission, Creech.6~) end of which is run in each direction as an over-and-over stitch to complete the anastomosis. Blood is then allowed to flow momentarily into the graft, with the distal graft clamped, to provide further clotting of the interstices. The clamp is then shifted to the graft just below the anastomosis, which is checked for leaks. The distal anastomoses are made in similar fashion using 4 - 0 suture if a bifurcation prosthesis is placed. Back bleeding from each iliac artery, should be checked prior to completion of the distal anastomoses. After the anastomosis of the first limb of the prosthesis is complete, the prosthesis is flushed with blood to remove any retained clots, and flow is established into the leg, while the opposite anastomosis is completed. The second iliac anastomosis is flushed from above and below iust prior to completion of the suture line, and flow is re-established. If back bleeding is poor from one or both iliac arteries, the legs may be compressed or Fogarty catheters may be used to insure removaI of any clots that may be present in He arteries to the legs. The patient's blood volume should be adequate prior to release of the aortic clamp and the clamp should be released slowly with continuous monitoring of the arterial pressure, to avoid declamping hypotension. If the pressure does not remain satisfactory despite slow release of the clamp and adequate volume replacement, sodium bicarbonate should be administered. Control of aortic flow with the clamp itself is difficult. It is preferable to occlude the prosthesis with the fingers, removing the clamp entirely and re-establishing flow by gradual release of the pros27'

thesis. With experience, the surgeon can exercise precise control of the flow, evaluating aortic pressure at the same time. Femoral pulses should be palpated after flow is re-established. Next, excess aneurysmal wall is excised. The remaining aneurysmal watl may be left in place or sutured closely around thegraft to separate it from the viscera. Pedicle flaps of the aneurysm wall can usually be mobilized and joined to cover the suture lines. The retroperitoneum is closed and the viscera returned to the abdomen. The appearance of the sigmoid colon is noted prior to closure of the abdomen.

TECHNIC

RUPTURED ABDOMINAL AORTIC ANEURYSM

The patient with a ruptured AAA should be moved to the operating room with a minimum of delay, with :the intention of establishing proximal control of the aort- as soon as possible. Large-bore plastic catheters for administration of'blood should obviously be in place, together with a means of monitoring central venous pressure, if possible. Time usually permits routine-preparation a~ddraping prior to incision of the abdomen. In the occasional patient in whom-~he blood pressure is unobtainable and cannot be restored by transfusion, it may be advisable to perform a lower left thoracotomy without skin preparation and place a clamp on the distal thoracic aorta. The abdomen is meanwhile rapidly prepared and opened, and the' thoracic clamp removed as soon as proximal control of the abdominal aorta is obtained. This procedure may save time compared to making a midline incision and occluding the aorta just below the diaphragm. Its main advantage is in allowing proper preparation of the abdomen. Ethacrynic acid, 50 mg., and mannitol, 25 mg., are administered as soon as feasible, together with intravenously administered antibiotics. A mid!ine incision is clearly indicated, because of the speed with which it can be made. As soon as the abdomen is entered, the intestines are retracted to the right and, if the patient is hypotensive, the aorta proximal to the aneurysm is compressed against the spine until continued transfusion restores the Mood pressure. If the patient's condition is stable, with the usual retroperitoneal hematoma, control of the iliac arteries should be obtained before proximal control is attempted. Back bleeding through ~the rupture is ~ereby avoided when the hematoma is opened. Then; the duodenum is reflected and the retroperit0neum over the neck of the aneurysm is incised. Thereafter, because of the hematoma, finger dissection about the neck of the aneurysm is easy, and a clamp cfin be applied below the renal arteries. Heparin should be administered as usual before clamping if conditions permit or, if not, as soon after clamping as possible. From this point, the operation proceeds in the same manner as the elective one. 28

SPECIAL PROBLEMS RENAL FAILURE.- Postoperative renal failure due to acute tubular

necrosis is seldom a problem nowadays following elective resection of AAA. 110 During the early years of operative treatment of AAA, however, acute tubular necrosis (ATN) was frequent. The reason for this change is not entirely clear, but it is probably due to improved operative technics with less blood loss, less hypotension, and decreased operating time, plus better hydration of patients undergoing general anesthesia. Acute tubular necrosis remains a problem fo~lowing treatment of ruptured aneurysms. The induction of general anesthesia in the presence of usual mild preoperative dehydration causes a decrease in renal blood flow from 20% to 40% of preoperative values. TM 1~7,ls6 This is well tolerated by patients with good renal function, but may cause difficulty in those in whom renal function is already depressed. Moreover, it has been suggested that cross clamping the aorta below the renal arteries causes a reflex drop in renal blood flow, 16 although this effect has not been confirmed by all investigators. Mannitol,administered immediately prior to an insult to the kidneys, can prevent acute tubular necrosis in experimental animals. ~62,168 Administration of mannitol causes an increase in renal blood flow, an effect likely related to an increase in plasma volume, caused by withdrawal of extravascular fluid into the vascular space. 6G Additionally, mannitol causes a decrease in renal vascular resistance, either directly or as a result of augmentation of plasma volume, 49 thus enhancing renal blood flow, even if the mean systemic arterial pressure remains unaltered. Hydration alone will reproduce these same effects on plasma volume, but the effects are better sustained with the addition of mannitol.la For these reasons, mannitoI has enjoyed wide clinical use and is reportedly effective in decreasing the incidence of postoperative renal failure. 1Gs Others have not demonstrated any clinical superiority of mannitol used for this purpose over adequate hydration alone. 16 Recently Stahl and Stone 186 suggested that the combination of mannitol, plus either ethacrynic acid or furosemide, caused a decrease in renal vascular resistance and protected against the development of postoperative renal failure. They suggested the use of such a regimen in surgical patients with already compromised renal function and demonstrated its clinical effectiveness in preventing depression of the glomerular filtration rate during and after operation. In summary, it seems to us unnecessary to use mannitol or diuretics during the elective resection Of an AAA in a patient with good renal function. Adequate hydration should always be assured both preoperatively and intraoperatively. However, in patients with already compro29

mised renal function or in those subjected to hypovolemia, the early administration of 50 rag. of ethacrynic acid plus 25 Gin. of mannitol seems a reasonable precaution. DECLAMPING SHOCK.---Sudden release of an aortic clamp after a period of occlusion causes hypotension. The severity varies but is, in general, directly proportional to the duration of clamping prior to release and to the degree of hypovolemia. Associated with the decrease in blood pressure is decreased venous return, decreased cardiac output and a drop in blood pH levels. It has beeff,suggested that these effects are related to washout of acid products of metabolism which have accumulated in the legs during the ischemic period. ~7 Also, hypoxic vasodilatation of the vascular tree of the legs tends to create a relative hypovolemia. Vetto and Brant ~gs showed that the pH of iliac venous blood of patients averaged 7.13 after declamping and that systemic arterial pH values fell from 7.42 to 7.24. There was transi;cnt hypoxia o f iliac venous blood (average Poe, 20.5 mm. Hg) immediately a:fter declamping followed by a rise in Po.., to greater than normal levels, suggestive of A-V shunting. In addition to acidosis, Brant et aI.34 have reported that a vasodepressor substance is found in effluent blood from the lower extremities of dogs during declamping hypotension. This appears to be a protein, molecular weight 60,000 to ! 00;000. Ten milliliters of serum containing this substance was sufficient to cause hypotension when injected into another dog. Treatment or avoidance of declamping hypotension is accomplished by" 1) slow release of aortic occlusion; 2) full-restoration of blood volume prior to release of occlusion; and 3) administration of sodium bicarbonate if hypotension occurs despite these measures. Some authors recommend the administration of a vasopressor when declamping, 1os but we have not found this necessary and believe that the resultant vasoconstriction is undesirable. COLON ISCHEMIA.- Resection of an abdominal aortic aneurysm ordinarily involves interruption of the inferior mesenteric artery and sometimes one or both hypogastric arteries as well Following interruption of the inferior mesenteric artery,i circulation to the rectosigmoid must come from the superior mesenteric artery via the marginal artery of the colon, and from the hypogastric arteries via collaterals among the hemorrhoidal arteries. Thus, it is desirable to leave at least one internal iliac artery patent, 3s, ~sz although both can be ligated in patients with otherwise unimpaired circulation. TM Also dissection of the sigmoid mesocolon should be minimized, and to avoid interruption of collateral pathways, the inferior mesenteric artery should be ligated near the aorta, z13 Ischemia of the rectosigmoid after resection of an abdominal aortic aneurysm may occur in up to 10% of patients, ~sz although this is a higher figure than others have reported, z~a The incidence of this com30

plication is lower following operation for aortoiliac occlusive disease, presumably because of extensive collateral circulation. ~sz,zl~ The colon is usually involved distal to the splenic flexure, and the damaged area is commonly visible through a sigmoidoscope. The severity ranges from frank necrosis manifested by peritonitis and shock, to milder forms with only mild diarrhea or persistent abdominal distention. Intermediate degrees of ischemia may lead to chronic ulceration and stricture, zt3 Severe involvement is usually manifested in the early postoperative period by bloody diarrhea, fever, distention, pain and abdominal tenderness. Sigrnoidoscopy is usually diagnostic, TM and operation is urgently indicated: Later onset of symptoms is usually associated with lesser degrees of involvement, z° Although the circulation to the colon may not appear to be compromised at aneurysmectomy, the appearance of the colon should routinely be observed prior to closure of the abdomen. An enlarged, tortuous inferior mesenteric artery, noted either on preoperative arteriography or in the operating room, suggests that the superior mesenteric artery is obstructed and that the inferior mesenteric artery is providing circulation to the proximal bowel. Such a situat i.on demands reimplantation of the inferior mesenteric artery, for if it is Iigated, extensive bowel infarction can be expected. It has been suggested that preoperative sterilization of the bowel with antibiotics will lessen the incidence of colonic necrosis after resection of AAA, ls~- but others have not found it to be of value, z° It is not our practice to prepare the colon prior to resection of an aneurysm. EFFECT ON SEXUAL FUNCTION. Changes in sexual function following operation for abdominal aneurysm were well documented in a series of 26 male patients studied by May, DeWeese and Rob. ~47 Eight per cent of these patients had preoperative difficulty with erection. Of those with no such preoperative difficult3,, 25 % who had aneurysms resected suffered impaired ability to have an erection, in contrast to 13 % of those whose aneurysms were treated by insertion of a graft without resection of the entire aneurysrn (endoaneurysmorrhaphy or intrasaccular approach). None had an abnormality of ejaculation preoperatively, but over half had difficulty postoperatively, mainly with retrograde ejaculation. This suggests that the intrasaccular approach is less likely to impair sexual function, as would be expected, although the series is small. PARAPLEGIA.. ParapleNa is always of concern after resection of aneurysms of the descending thoracic aorta, but on rare occasions it has also been reported to follow resection of an AAA. Zuber, Gaspar and Rothschild 21;; reported 5 cases following abdominal aortic surgery, and found 8 more in the literature. Eight followed resection of a ruptured aneurysm, 3 followed elective operation for aneurysm and 2 followed aortoiliac bypass for occlusive disease. Most of these were associated with operative hypotension and suprarenaI aortic cross clamping..The .

.

.

.

31

arteria magna l may arise anywhere between T 10 and L 4, or, if occluded by atherosclerosis, may be supplied by collaterals from the lower tumbar arteries~ thus creating the possibility of spinal cord damage when the usual technics are used. It should be emphasized, however, that this is an extremely rare complication of operation for AAA. Unusually large lumbar arteries should be preserved when possible. HORSESHOE KIDNEY AND ANOMALOUS R E N A L ARTERIES.~Cohn~

Stoney and Wylie41 report 3 cases of successful abdominal aneurysmectomy in the presence of a horseshoe kidney, with 7 reported previously. They-~uggest that ih ~most cases, access to the aneurysm can be gained simply by mobilization of the kidney, without interruption of its blood supply. There often is an artery to the isthmus arising from the aneurysm. However, this may be ligated with impunity if the right and left renal arterial supply seems normal. Division of the isthmus may also be carried out to provide access if the arterial supply to either side will not be interrupted ~hereby. 139 If the presence of a horseshoe kidney is known preoperatively, angiography is indicated, 139 because over two thirds of the cases will have anomalies of the renal vasculature. 41 The venous drainage is similarly variable. The presence of a patent major anomalous renal vessel arising from the aneurysm, whether to a horseshoe or a normal kidney, requires reimplantation of that artery for preservation of the blood supply. Anastomosis is facilitated by preservation of a cuff of tissue about the orifice of the vessel when it is excised from the wall of the aneur3,sm.

THORACIC ANEURYSMS

DIAGNOSIS Thoracic aneurysms cause symptoms by: ! ) compression of adjacent structures; 2) rupture, either free or into adjacent structures; 3) erosion of bone with pain; 4)enlargement, with pain presumably due to the stretching of surrounding soft tissue; or 5) heart failure due to aortic regurgitation or to a fistula between the aorta and an adjacent vascular structure. Many are found incidentally on chest x-rays taken for other reasons. Aneurysms found incidentally probably represent the largest group nowadays, in view of the number of x-rays taken for other reasons, although many a supposed thoracic aneurysm turns out to be simply a dilated tortuous aorta. Thus, smaller aneurysms are discovered more often today, and the massive aneur3,sms eroding through the chest wall, familiar to clinicians of a generation ago, are seldom seen (Fig. 1 1 ). This may also be due to the lessened incidence of saccular aneurysms that seem particularly inclined to erode the vertebral column or chest wall. Chest pain is probably the most common symptom associated with thoracic aneurysms, followed by symptoms related to impingement on 32

FI6. 1 I. A n e u r y s m of ascendin.~ aorta eroding through the anterior chest wall as a pulsating mass.

adjacent structures, such as the bronchus or recurrent laryngeal nerve, causing hoarseness, stridor or dyspnea. Hemoptysis too is common, especially with arch or descending aortic aneurysms. This may be related to direct tracheobronchial erosion 3G or more commonly to erosion into the parenchyma of the lung. 80 Superior vena cavaI obstruction also occurs, usually in association with aneurysms of the ascending aorta. Rupture may occur into any area of the chest depending on the location of the aneurysm. Bizarre patterns have occurred z3 (Table 6). Rupture is most common, however, into the mediastinum, pleural space, pericardium or respiratory system (either lung or tracheobronchial tree). Rupture always causes death if untreated, but occasionally there is time for treatment before massive hemorrhage ensues. The presence of chest pain with hemothorax, hemoptysis or hemopericardium demands consideration of immediate operation. Rupture into a lower pressure portion of the vascular system, such as the pulmonary artery, may be associated with the appearance of a continuous murmur, but not always. TM The diagnosis of aortic insufficiency, associated with ascending aortic aneurysms, is based on the recognition of the characteristic decrescendo diastolic murmur with widened pulse pressure. Cardiac failure may be present in either of these situations. Aside from auscultation to detect murmurs, physical ex.amination is 33

T A B L E 6.--THORACIC ANEURYSMS: RUPTURE INTO VARIOUS ORGANS33 Pericardium Left pleura Esophagus Right pleura Left bronchus Trachea Externally Pulmonary a r t e ~ Sup. vena cava Left lung Mediastinum Right auricle

No.

%

3 69 174 112 88 85 74 61 45 44 40 20 13

31.0 14.6 9.4 7.4 7.1 6.2 5.1 3~7 3.7 3.3 1.6 1.0 TOTAL

No.

Right lung Right bronchus Right ventricle Left auricle Descending vena Left ventricle Spinal column Hematoma, thorax Stomach Both pleura Hematoma, neck

12 12 12 9 8 5 4 4 3 2 1

% 1.0 1.0 1.0 0.7 0.6 0.4 0.3 0.3 0.2 0.1 0.8

1,197 ruptures

of little value in the diagnosis of most thoracic aneurysms. It cannot be overemphasized however, that inany patients with thoracic aneurysms have associated cardiovascular disease. This must be carefully evaluated, for it plays a major role in decisi0n~g regarding therapy. The two most valuable diagnostic studies are roentgenography of the chest and aortography. Aortograpt~y should be done in all cases, with the exception of the patient in extremis who has a recognizable aneurysm on the chest film and needs immediate operation. Typically, on the standard posterior;anterior (P-A) chest film, aneurysms of the. ascending aorta present to the right side of the medias,~ tinum, and aneurysms of the descending thoracic aorta appear on the left (Fig. 12). Arch aneurysms may appear on either or both sides depending on their size and whether they are more proximal or distal in the arch. Aneurysms limited to the descending aorta may present enFro. 12. A and B, ascending aortic aneurysm extending into the right hemithorax. C, upper thoracic aortic aneurysm, previously partially wired, extending into the left hemithorax.

34

FIG. 13. Aneurysm of the aortic a r c h extending into both hemithoraces and compressing the trachea to the right. ,4, plain:roentgenogram. B, a0rtogram. The contrast-filled lumen constitutes only part of the larger mass.

tirely on the right side, 142 although that is unusual. Calcification of all or a part of the aneurysm wall may be visible. In general, as pointed out by De Bakey, 6'~ arteriosclerotic aneurysms tend to be restricted to characteristic areas; e.g., the ascending aorta, the arch or the descending aorta, and do not tend to overlap into adjacent areas. Exceptions, of course, occur. Aortography provides accurate information regarding the location of aneurysms, but allowance must be made for the presence of clot lining the aneurysm in judging its size and shape (Fig. 13 ). The contrast study should include the entire aorta and its major branches, Associated arteriosclerotic occlusive disease is common and abdominal, as well as thoracic, aneurysms are present in up t o 6% of patients, z°4 Visualization of the extracranial cerebral circulation should also be provided if there is any suggestion of cerebrovascular occlusive disease. Likewise, coronary arteriography should probably b e done if there is angina and operative treatment of the aneurysm is contemplated. Arteriosclerotic aneurysms o f the thoracic aorta have been termed a "late stage of a diffuse disease, ''39 and thorough evaluation of the cardiovascular system is essential for the assessment of operative risk. Evaluation of other major organ systems, such as the lungs, kidneys, and liver should be as for any major cardiovascular procedure. NATURAL HISTORY The only sound basis for making a decision for or against resection of an aneurysm is knowledge of the natural history of the unoperated 35

lesion together with knowledge of the results of operative treatment. Unfortunately, relatively little information is available concerning the natural history of thoracic aneurysms. Kampmeier, 12a Cranley, 60 and Boyd aa published reports which contained high percentages of syphilitic aneurysms. This information is of little help today because of the relative rarity o f syphilis. However, it should be noted that the usual saccular syphilitic aneurysms generally pose a greater threat of progressive enlargement and rupture than those of arteriosclerotic origin.C0, 155 Of Kampmeier's seri~s, 60% of the 633 patients had a positive Wasserman"teSt, while only 112 had neither a positive serology nor a history of syphilis. Thirty-nine iaer cent of the deaths were from rupture of the aneur-ysm, An additional ~18% died from respiratory obstruction by the aneurysm and 11.5% died of cardiac failure. Patients with symptomatic aneurysms died an/average of 6 to 9 months from the onset of symptoms. Crawford e t al. .G1 described 97 patients with thoracic aortic aneurysms 0bservedi before the advent of corrective surgery', of whom 91 died during the:subsequent 5-year period. No details were provided. Fomon e t at. 9z reviewed the autopsy reeQrds of 7,642 patients and found 249 aneurysms of the aorta or its major br-~inches in 192 patients. Unfortunately, determination of the! etiology was impossible and no distinction was made between saccular and fusiform thoracic aneurysms. Aneurysms of the ascending aorta were the most common thoracic type, comprising 22.1% of theJ total. Of these aneurysms, 31.4% caused death either by rupture ( 1 8 . 5 % ) or by compression of surrounding structures, such as the tracheobronchial tree or pulmonary artery ( 1 2 . 9 % ) . Aortic insufficiency is not specifically mentioned, but dilatation of the aortic annulus was noted in 2 patients. In 18 of 28 cases ( 6 4 . 3 % ) aortic arch aneurysms either caused death by rupture (32.1% ) or contributed to death by compression of surrounding structures (32.1% ). Of descending thoracic aortic aneurysms, 3 of 19 ( 1 5 . 8 % ) caused death by rupture, and none contributed to death by compression of other structures. At all levels the risk of rupture and the frequency of compression of surrounding structures were clearly related to the size of the aneurysm. Aneurysms over 10 cm. in diameter either caused or contributed tO death in a high percentage of cases. Conversely, aneurysms:under 5 cm. caused or contributed to death in only 0 to 8 % of cases. Perhaps the most useful natural history study was made by Joyce e t a l az0 who obtained data on 107 cases of untreated thoracic aortic aneurysms. Ninety,eight patients (91% ) were traced for 5 years, and of the 64 who could have survived 10 years, 57 ( 8 8 % ) were traced. Eighty of the aneurysms were fusiform, 20 were saccular and 9 were of indeterminate shape. In contrast to the study of Fomon e t al., 9z the most common location was in the descending thoracic aorta (48 / 109 ), in keeping with the high percentage of fusiform aneurysms. On the 36

basis of available information 78 ( 7 3 % ) were t h o u g h t t o be arteriosclerotic, 20 ( 1 9 % ) syphilitic, 5 ( 5 % ) traumatic and 2 ( 2 % ) congenital. This distribution more closely approximates that seen in clinical practice today, and thus this study is of particular interest. Twenty-six per cent were symptomatic at the time of diagnosis and of these, only 26.9% survived 5 years, in contrast to 58% of those without symptoms at the time of diagnosis. Those with symptoms usually had large aneurysms, a factor which also had an adverse effect on survival. These facts, together with the deleterious effects of associated cardiovascular disease, hypertension and age can be seen in Table 7. Associated cardiovascular disease was recognized in 37% of patients at the time of diagnosis. The shape and location of the aneurysms exerted little influence on survival. Over-all, 19 of the 59 deaths ( 3 2 % ) were from rupture of the aneurysm, whereas at least half of the deaths were from associated cardiovascular disease, figures which agree closely with those of F o m o n e t al. 9z It is not clear from the study of Joyce e t al. leo whether the patients with symPtomatic aneurysms all died of rupture of the aneurysm. Also the problem of aortic valvular insufficiency is not specifically discussed, and deaths from congestive heart failure may include patients dying o f aortic regurgitation due to aneurysms. Aortic regurgitation may properly be considered an effect of the aneurysm and may rapidly lead to death from.heart failure if uncorrected. Blunt chest trauma may cause rupture of the aorta. This most commonly consists of a transverse tear, circumferential or partial, of the descending thoracic aorta just distal to the ligamentum arteriosum. Of patients suffering such injuries, about 20% will survive to reach the hospital and about 2 % , untreated, will form a false aneurysm at the site of trauma. 1G1 Rupture of the ascending aorta due to blunt trauma also occurs, but survival with formation of a false aneurvsm has not, to our knowledge, been reported. P e n e t r a t i n g t r a u m a seldom causes false aneurysm formation because the tissues surrounding the aortic wound are disrupted, and hemorrhage is not well contained. 16° False aneurysms may, however, form at the site of avulsion of a major artery, usually the innominate, from the aortic arch following blunt trauma.13~, aG5

Bennett and Cherry is published a thorough study of the natural history of traumatic false aneurysms of t h e a o r t a . Groves I°G pointed out that a true fibrous false aneurysmal s a c . m a y b e present as early as 23 days following injury. However, Bennett and Cherry selected an interval of 3 months after injury as a more usual period for the formation of a fully developed fibrous aneurysm. They.evaluate the controversy that has existed over the natural history of these leSions and conclude that there is little evidence that even the calcified ones are ever stabilized and that the patient who harbors such a lesion is subject to an ever present threat of rupture. Some pro37

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"FABLE 7.- FrYE-YEAR SUI~VlVAL RATES FOLLOWING DIAGNOSIS OF THORACIC AORTIC A N E U R Y S M 120 LIVED BEYOND 5-YR. PERIOD

PATIENTS

L~ATEGORYOF PATIENTS AT TIME OF DIAGNOSIS

All patients Sex Male Female Shape of anem-~ysm Saccular Fusiform Roentgenogram unavailable Location of aneurysm Ascending Arch Descending Entire Age, years 40 40 49 50-59 60-69 70-79 80+ Width of aneurysm 6 cm. or less 6 cm. Not available Associated cardiovascular disease Without With Hypertension (diastolic, 95 ram. Hg) Without With Symptoms Without With

TRACED 98

Number 49

Per Cent 50.0

72 26

33 16

45.8 61.5

14 74 l0

7 35 7

50.0 47.3 70.0

24 31 40 3

I3 16 20 0

54.2 51.6 50.0 0

9 11 ..? 32 20 3

7 10 10 15 5 "

77.8 90.9 43.5 46.9 25.o 0

!8 :34 46

11

6!.1

13 25

38.2 54.3

58 40

38

65.5

11

27.5

54 44

33 16

61.] 36.3

72 26

42 7

58.3 26.9

gressively enlarge; whereas, as pointed out by others, 1°6,122, a85 some r e m a i n s t a b l e for years, then f o r n o a p p a r e n t reason begin to enlarge and r u p t u r e . E i s e m a n s7 reported a patient whose traumatic aneurysm was present 43 years after injury and was foIlowec] for the last 9 years, with evidence of m a r k e d progressive enlargement over the last 4 years. E n l a r g e m e n t o f such aneurysms usually causes chest pain (the most frequent s y m p t o m ) , is and, d u e t 9 their location, m a y also cause hoarseness, cough and dyspnea from c o m p r e s s i o n of the adjacent bronchus and recurrent laryngeal nerve. Symptoms usually precede rupture, although t h e interval between onset and rupture may be short. A t least one case has been reported in which rupture occurred without antecedent symptoms, l~s Bacterial infection of these lesions has been 38

described, but Bennett and Cherry 19 could find no reported instance of embolism from traumatic aortic aneurysms. Few such aneurysms are found to contain clot at operation. Thus, the behavior of an individual traumatic false aneurysm of the aorta is highly unpredictable. Progressive enlargement may occur from the beginning, or there may be a stable period of any length followed by progressive enlargement. Indeed, this is probably true of aortic aneurysms of'all types.

RESULTS OF OPERATIVE TREATMENT AND INDICATIONS FOR OPERATION The results of resection of aneurysms limited to the ascending aorta have been excellent as, for the most part, have been those for resection of aneurysms of the descending thoracic aorta. Resection of aneurysms of the aortic arch involving the origins of the innominate and left carotid arteries, however, carries considerable risk. Bloodwell et ai.29 reported am.""8.3% operative mortality for resection of aneurysms of the ascending aorta in 36 patients With associated aortic regurgitation. Twenty-four of these aneurysms were due to cystic medial necrosis, 10 to arteriosclerosis and 2 to syphilis. Six were chronic dissecting aneurysms. Aortic valve replacement was required in all. In 1971, another report 7z described 56 cases of chronic aneurysms of the ascending aorta, of which 22 were fusiform, and 34 were chronic dissections. Forty-two of these required aortic valve replacement. There were 10 deaths (17% ) among the 56 patients, 5 from cerebral and cardiac complications, 3 from postoperative dissection of the aorta and 2 from hemorrhage. Mulder 1~3 reported 9 surgically treated patients, with 3 deaths. Others sr, 10t have reported smaller series of ascending aortic replacements for aneurysms with repair or replacement oI the aortic valve, with low operative mortality. Resection o[ aneurysms of the aortic arch proximal to the origin of the left subcIavian artery is hazardous. Those of "distal arch," i.e., those which can be managed by cIamping between the left carotid artery and left subclavian artery, are more in the category of aneurysms of the descending thoracic aorta, with regard to operative risk. In 1958, De Bakey e t al. 73 reported operative treatment of 50 arch aneurysms (35 syphilitic, 10 arteriosclerotic and 5 other). Twenty-six were saccular, and were resected with an operative mortality of 2 8 % , but the mortality for resection of the fusiform type was 75%. These results emphasize that aneurysms that can be treated by tangential excision can be operated o n with far less risk than can those that require aortic replacement, These resultsare also influenced by the fact that patients with syphilitic aneurysms, the most common saccular type, are less likely to have associated cardiovascular disease than are patients with arteriosclerotic aneurysms, which are usually fusiform. 39

In 1962, De Bakey e t al. ~ reported resection of 50 arch an eurysms, with an over-all operative mortality of 42%. Heart failure accounted l~or approximately one-half of the deaths, with cerebral damage responsible for another one-quarter, lit is not possible to tell from the data presented how many were fusiform and how many were saccular. In 1966, De Bakey e t al. 71 indicated that the survival rate for patients opei'ated on for aneurysms of the aortic arch was about 80%. Details are not provided, but this series included a number of saccular aneurysms and may i.nclude aneurysms of the distal arch. Survival up to 9 years following operataon is noted. Bloodwell e t al. ~° reported 10 patients who underwent resection of arch aneurysms. Of 6 having perfusion of tl~e cerebral vessels through the opened aortic arch (see Technic), 5 survived operation. The operative death was due to cerebral damage. One survivor died of hepatitis 3 months after operation. Of ~- subsequent! patients with perfusion in order to avoid subclavian steal (see Technic), all survived operation, but I suffered hemiparesis, and 1 died 5 months later of a myocardial infarction from thrombus on the aortic valve. Aneurysms of the distal arch (only the left subclavian arte~3r involved) and descending thoracic aorta have been resected more frequently than arch aneurysms, and with better results. De Bakey e t al. = reported a 12% operative mortality for these lesions in 1962. Two patients showed transient evidence of postoperative spinal cord damage. Twenty-two cases were due to trauma, with no surgical mortality. Cooley 5° reported a remarkable series of 60 cases of traumatic aneurysms of the isthmus of the aorta, all resected without a death. Smaller series14S, ~s5 also indicate that traumatic aneurysms of the aortic isthmus can be resected with low risk. Unlike patients with arteriosclerotic aneurysms, those with traumatic aneurysms are less likely to have associated cardiovascular disease and tend to be younger. Also, the adjacent aorta is healthy and the lesions are localized. Thus, in interpreting operative results, distinction must be made between traumatic and nontraumatic aneurysms. In 1961, Groves ~°~ reported resection of 13 aneurysms of the descending thoracic aorta, 2 of which were traumatic. Ten patients survived to leave the hospital, with 3 late deaths. Dillon e t a L so reported 34 patients with aneurysms of the descending thoracic aorta. Of 16 arteriosclerotic patients, 3 had lateral aortorrhaphy and 13 were resected. There were 2 operative deaths and 2 late deaths, 1 from a pulmonary embolus 2 months postoperatively and ! from a coronary occlusion 3 years after operation. Mulder e t al. ~ 3 reported resection of 5 arteriosclerotic aneurysms of the descending aorta. One case was ruptured preoperatively, and the patient did not survive. The remainder survived up to 1 ~½ years postoperatively, although one became paraplegic following operation. Using their graphite-benzalkoniumheparin external shunt tubing, Valiathan e t at. ~:'~' successfully resected 40

4 aneurysms of the descending aorta: 1 traumatic and 3 fusiform arterioscler,otic. Their patients have done well up to 18 months postoperatively. Thus, the available data suggest that even arteriosclerotic aneurysms of the descending thoracic aorta can b e resected with a n acceptable operative risk. De Bakey and associates have pointed out that the mortality rate for the operative treatment of thoracic aneurysms is decreasing, from an over-all rate of approximately 40% in their early experience to 19% in 1970.74 Technical expertise in the management of complex problems in vascular surgery has increased enormously in recent years and accounts for much of the improvement. Patient selection is terribly important, however, as it is clear that associated cardiovascular disease is as common a cause of death among patients with thoracic aneurysms as is the aneurysna itself. Indeed, associated disease is probably a more common cause of death in patients with arteriosclerotic aneurysms. The coexistence of heart disease increased the risk of resection of a thoracic aneurysm as much as 4 to 5 times zs, v7 compared to the risk in patients free of such problems. This consideration is obviously critical in selecting patients for operation. Several points seem clear. Patients with symptomatic or rapidly enlarging thoracic aneurysms should undergo resection unless associated problems render operative risk prohibitive. This group will usually include those with very large aneurysms. Similarly, good risk patients with traumatic aneurysms of the isthmus should undergo operation, as should patients with ascending aortic aneurysms and severe aortic regurgitation. In patients with associated arteriosclerotic heart disease, thoracic aneurysms should be resected only for clear indications, such as rapid enlargement, progressive symptoms, etc. Extreme caution should be exercised in deciding to operate on patients with proximal aortic arch aneurysms. In the most experienced hands operative mortality is high, and a great many patients probably have died following resection of these lesions without being reported in the literature. Decisions concerning operative therapy for patients in intermediate categories are difficult and must be individualized.

OPERATIVE TECHNIC- CONTROL OF THE CIRCULATION Clamping of the ascending aorta without rerouting of the blood will cause rapid overdistention of the heart and irreversible left ventricular failure. In addition, interruption of the circulation to the brain and spinal cord will cause ischemic damage unless circulation is promptly restored or hypothermia is used to slow metabolism. Even clamping of the thoracic aorta distal to the left subclavian artery can dangerously overload the arteriosclerotic heart, although a healthy heart will usually tolerate clamping at this level. The factor limiting clamping of the 41

TABLE

8. -METHODS OF MANAGEMENT OF THE CIRCULATION DURING RESECTION OF THORACIC ANEURYSMS

I. Aortic clamping without bypass (not recommended) II. Aortic clamping plus external hypothermia (not recommended) III. Shunts 1) Internal 2) External a) Tubing inserted into aorta b) Prosthetic graft sewed to aorta Temporary Permanent IV. Partial left-heart bypass 1) Inferior cava (via femoral vein) to femoral artery 2) Left heart (usuaIly left atrium) to femoral artery Circuits: a) Direct b) With reservoir c) With oxygenator V. Conventional cardiopulmonary bypass VI. Perfusion hypothermia (15-20 ° C.) and circulatory arrest

descending aorta thus becomes spinal cord ischemia. Paraparesis has followed clamping of the descending aortd for as little as 1 8 minutes, 3 although p e r i o d s of 45 minutes to over an h o u r have been toleratedSS. 141 Patients with c0arctation of the aorta are an exception because of their extensive collateral circuiafion. Thus, in order to protect the h e a r t from overdistention and to protect the brain and spinal cord from ischemic damage, special technics are necessary. A variety of methods are available (Table 8). FIG. 14.~The shunt, with the graft passed over it, is inserted into the aorta through short transverse incisions in the aortic wail. With the shunt functioning, the aneurysm is completely divided and the ends are oversewn. (Reprinted with permission, Keon and Trimble.124)

..

•

I

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42

The use of external cooling to lower the body temperature to 30 ° C permits safe occlusion of the descending thoracic aorta for about one hour.47.166 However, this method is cumbersome, the time of circulatory interruption is limited and the risk of overdistention of the heart remains, especially in patients likely to have arteriosclerotic heart disease. Various types o f shunts have been successfully used to conduct blood around the site of aortic occlusion. Internal shunts, consisting of tubing inserted between the ends of the opened aorta (Fig. 14), can be used. TM These seem technically inferior to external shunts, however, because they are in the way and must be withdrawn from the aorta before the final anastomosis is completed. External shunts are of two types: prosthetic grafts, which are sewed end-to-side to the aorta or to its branches to bypass the site of occlusion; and plastic tubing, FIG. 15.--A, exposure of the massive aneurysm through the bed of the fifth rib and the seventh interspace in a 78-year-old woman. B, cannulation technic of the subclavian artery. C, anastomosis of the woven Dacron graft. (Reprinted with permission, Valiathan, et a/. 196)

d3

which can be temporarily inserted into the aorta proximal and distal to ithe site of occlusion .(Fig. 1:5). The prosthetic grafts may be left to replace the function of the resected aorta or may be removed after the aneurysm has been dealt with and aorticcontinuity re-established. The major advantage of the methods described so far is that heparinization is not required. External shunts made of tubing lined with a coating of graphite, benzalkonium and heparin were designed to prevent clotting within the tubing and have been used clinically with good results,~gG ~ s e of this :material is desirable if it is available, but ordinary Tygon tubing with stainless steel cannulas on the ends has b e e n u s e d in unheparinized patients, without apparent clotting l~rob' lems. ~26 F o r adequate distal flow, large cannulas a n d large tubing should be used, A 7.5 mmr, inner diameteri cannula connected to a~,, inner diameter tubing will pr0vide flows on the order of 2,000 ml./ rain., adequate for most patients. However, :one large man perfused with this size equipment developed paraplegia. For large patients JR" tubing with 9 mm. cannulas should be used. 126 Bypass prosthetic grafts should probably be a minimum o f t2 ram!, indiameter for temporary bypass of the descending thoracic aorta,~.~"or larger if they are to be permanent. The most widely used method for bypass of lesions of the distal arch and descending aorta is some form of partial left-heart bypass. This is usually accomplished by cannulation of the left atrium, with return of blood viathe femoral artery (Fig, 16) With the addition of an oxygenator, blood may be withdrawn from the inferior vena cava via femoral vein cannulation, instead of from the left atrium, and returned to the femoral artery (Fig. 17). In our experience it is sometimes difficult to adjust an inferior caval cannula so as to maintain desired flow rates. By contrast, left atrial cannulation with a large bore catheter provides reliable control of flow and seems preferable except in special circumstances. Arterial return can also be to the distal aorta instead of the femoral artery, if access is convenient. The rate of flow through such a partial bypass is critically important. Distal aortic flow must be at a level sufficient to maintain spinal cord and o ~ a n perfusion so the left heart is allowed to pump enough blood to continue cerebral peffusion without permitting overdistention due to inadequate bypass flow. The m9st widely used figure for calculating the rate of bypass flow has been 20 m l . / k g . / m i n , zs, 73. ~o~ This, obviously, is suitable f o r most situations in view of the successful use of the technic by these authors, However, others have studied flow requirements necessary for maintenance of physiologic pressures in the heart and proximal and distal aorta and suggest that higher flow rates are needed. Austen, e t al. 5 recommended a minimal flow for bypass of the descending aorta of 3 0 / k g . / m i n . , with an ideal flow of 75 m l . / k g . / min. Hug and Taber 116 also found that flows of 60-90 ml./kg./min. were necessary to maintain preocclusion pressures in the left heart 44

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FIo. 16 (lelt). Resection of aneurysm of descending thoracic aorta using extracorporeal circulation. Oxygenated blood is removed from left atrium and pumped into distal aorta through catheter inserted into femoral artery. Pressure is monitored in the right brachial artery. Fro. 17 (right).. -Pump oxygenator and monitor systems with additional inflow lines to be used if necessary for carotid perfusion. (Reprinted with permission, Dillon et aLSO) when the descending thoracic aorta was clamped. Connolly e t al. 48 recommended at least 30 m l . / k g . / m i n , bypass flow, as judged by measurement of renal blood flow, ideally keeping proximal aortic pressure slightly below preocclusion values. Whatever flow rates are used, the proximal and distal aortic pressures should be monitored during bypass. The addition of a catheter for monitoring left atrial pressure, inserted through the left superior pulmonary vein, provides valuable help in avoiding left heart overload and pulmonary congestion. Our own experience using this technic suggests that flows in the range of 30 40 m l . / k g . / m i n , provide a suitable bypass, as reflected by monitoring these pressm'es, together with urine output. Prolonged higher flows s e e m difficult to maintain. The circuit for left-heart bypass, first used clinically by Cooley e t al. 5~ consists simply of tubing run through a roller pump. This continues t o b e a suitable and widelyused method. Connolly e t a/.4Spoint out that higher flows can be obtained and flows can be controlled more easily if a reservoir is placed in the circuit, as was done initially by Cross et aI. G~ F o r b y p a s s from the inferior cava, an oxygenator is required and automatically serves as a reservoir. Since the left lung is 45

usuatly retracted during these procedures and since hypoxia is occasionally a problem during operation, the use of an oxygenator in the circuit, even for left atrial-to-femoral bypass, provides both a reservoir and a safeguard against hypoxia, In addition, the apparatus requires no alteration of the equipment used for routine total cardiopfilmonary bypass. The availability of suction to return shed hepafinized blood to the pump is extremely useful. The use of conventional cardiopulmonary bypass need not be described here, exe.ept t o n o t e that additional pumps or arterial line branches may be necessary for the complex perfusions needed for resection of aneurysms of the aortic arch. Peffusion hypothermia to temperatures o f 10 ° C to 20 ° C, with temporary arrest of the circulation permits correction of certain lesions that may hot,otherwise be coiTectable. This !technic remairis somewhat experimental andwill not be dealt with in detail here. It is sufficient to .... 120 o C core temperature (measured in the esophagus and recsay that t u m ) provides about 30 minutes 0fsafe circulatory arrest, and circulatoryarrest for about ! h o u r is feasible at l 0°C. Such technics may be useful for the occasionN:r~ptured aneurys:ri5 and especially for aneurysms that h a v e rupt~r~ii~to the venous system. ~~..~2,35. s3. ~33

SPECIFIC LESIONS SACCULA.R.._ANEURYSMS'----Saccular aneurysms at any site can sometimesbe~removedwitboutinterruption of aortic blood flow, by clamping ttie nectc of the:aneurysm tangential to the aorta (Fig. 1 8). Care. must:be exercised: n o t t o dislodge clot into the aorta. This technic is feasible'becaus6th6aorticwall surroundin2 the aneurysm is often relafi}ely i~n0rmal!iand the neck of:the.aneurysm is sufficiently fibrous to hold{~uture:S:/Well):iAt!times;iaorticocclusion is necessary for treatment of ~ac~tiiaraneUrygmswil~ha:broad base, or when the neck is calcified Rndii~!ifri~biE~!ii~i:i6:this:)cirCumstance an appropriate method of bypass sh6~td:~:b~us6d.i The ianeUrysmalsac is opened and the defect repaired by::dilf~Ct~i~iate?a!:iaOrt6rrhaphy!(Fig. 19). Follow-up confirms that lat~t~i!'{:a6~r}h~hy{~i:!used:in :the ai~propriate circumstance, provides a

~tisfaab~ io~ig-term resi~t:~ig7 ANEuRYSMS:~bF'~THE-'ASCEND1NG.THQRACIC AORTA. - F o r aneurysms hmlted!::toi.theascendm~ aorta,:a median ste~.noton y is the incision of ~hbice:i~i:K~utifie?caval::dannulati0n is c~irried out with arterial return to total bypass. If the size and location of the aneurysm:::rendercavatcannulation difficult, only .one cannula is inserted initiall~y,~and tiie~;Second is.inserted~after partial bypass has begun. The left ventricle is vented and the patient is cooled to 30 ° C. The aorta is clamped: just proximal to the innominate artery and the aneurysm is incised:: The aortic valve is repaired or replaced as necessary, then the proximal e n d o f a woven Dacron graft is sutured to the proximal stump 46

F~a. 18.- -lntrapericardial aneurysm of the ascending aorta. Multitoothed Potts clamps were applied from either end of the aneurysm and the aneurysm excised. (Reprinted with permission, Bahnson.7)

of the aorta,, preserving the coronary orifices. Coronary perfusion may be used during this time or, if not, aortic root perfusion can be established, and the Patient rewarme-d, while tile distal anastomosis is completed (Fig. 20) Air is carefully evacuated from the heart and aorta before the aortic clamp is removed and bypass discontinued. If aortic regurgitation is present, it may be corrected by replacement of the valve, excision of the noncoronary sinus and leaflet, converting the valve to bicuspid, ''~4. 174 o r b y resuspension of the commissures. 1°' The latter technic is useful mainly for the aortic regurgitation due to dissecting aneurysms. When an aneurysm extensively involves the aortic root below the coronary orifices, it can be excised down to the aortic annulus, saving tongues of aorta containing the coronary orifices. 5z,2°9 In this situation, the method described by Edwards and Kerr 86 might be particularly useful (Fig. 21 ), although we have no experience with it. ANEURYSMS INVOLVING THE AORTIC, ARCH.- .....These aneurysms represent one of the most challenging technical problems in cardiovascular 47

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FIG. 19. -Drawings of aneurysm of the upper thoracic aorta and reconstruction after excision. Eroded vertebral bodies can be seen. These were in contact with the blood stream. (Reprinted with permission, BahnSon.7) surgery, and considerable flexibility must be used in determining the best method of management for each case. Selection of an incision for resection of aneurysms involving the arch is difficult, but generally the chbice lies between bilateral anterior thoracotomy with sternal transection between the left 3d or 4th interspace and the right 3d interspace or median sternotomy with or without an extension into an appropriate left intercostal space. For aneurysms involving mainly the proximal portion of the arch, together 48

possibly with the ascending aorta, sternotomy with an extension is satisfactory. For very large or extensive lesions, bilateral thoracotomy is probably better, especially if the left, chest is elevated somewhat, so that the left side of the incision can be extended as far laterally as possible. In aneurysms of the descending aorta, lesions involving only the distal arch can be satisfactorily approached through a left-lateral thoracotomy. For aneurysms involving only the distal arch, such that the aorta may be clamped betWeen the left carotid and the left subclavian arteries, the bypass is managed the same as for aneurysms of the descending thoracic aorta. However, for those aneurysms involving the entire arch or the proximal arch, provision must be made for avoiding ischemic damage to the brain and heart while the aneurysm is replaced. The shunt graft principle can be used if there is sufficient length of uninvolved ascending aorta to permit end-to-side anastomosis of a Dacron graft, the other end of which is sewed end-to-side to the distal aorta beyond the aneuD'sm. From this prosthesis branches are sutured end-to-side to the innominate and left carotid arteries and to the left subcl~,ian, which may be divided from the aneurysm at the time of anastomosis, if desired (Fig. 22). The branches to the innominate and left carotid should be sewed during partial occlusion of these vessels. If total occlusion is technically necessary, a temporary internal shunt should be used, as for carotid endarterectomy. Thus, with circulation established, the aneurysm may be resected. The shunt grafts should be Fro. 20.-, T e c h n i c for aortic root perfusion.64 aortic~ro~t filled. wi~h l~iood to exctuct~ o i r

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! Fro. 2 1 . . A , technic of Edwards and Kerr for!an :urysms that involve the aortic root below the coronary arteries. B, a woven Teflon graf-c is selected which app r o x i m a t e s the size of the annulus as estimated from outside. A Starr-Edwards valve (size A 11 or A 12) is selected which will!corr.,fortably fit the annulus, again as judged from outside. The valve prosthesis is then sutured inside the Teflon graft with a continuous 2-0 synthetic suture. C, the aortic valve leaflets are excised, and the sewing ring of the prosthetic vatve 'with its attached graft is sutured to the annulus with interrupted sutures. D, the coronary cannulas ar~ then passed through the upper end of the graft, through the side holes, and again out the coronary ostia. E, the holes in the graft are now carefully sutured to the inside of the sac around the coronary ostia with a continuous 4-0 suture. F, the sac of the aneurysm is now wrapped tightly around t h e graft and sutured with an everting 2-0 mattress suture. (Reprinted with permission, Edwards and Kerr.SS)

Fro. 22. Use of bypass grafts and reconstruction measures in management of arch aneurysms. (Reprinted with permission, Shumacker.178)

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FIG. 23. The previous technic for resection and replacement of aneurysm of ascending aorta extending into transverse aortic arch. A, during cardiopulmonary bypass, catheters for cerebral perfusion were threaded through graft and inserted through opened aneurysm into.ostia of innominate and left carotid arteries. Occlusion of left subclavian artery may permit "subclavian steal." B, after completioi,Jof distal anastomosis, the catheters were removed, the aortic clamp was advanced onto the graft, and the cerebral circulation restored through the descending aorta during proximal anastomosis and valve replacement. The peiiod of selective cerebral perfusion was reduced by this technic. (Reprinted with permission, Bloodwell e t al.30) left in place, if possible, as the permanent reconstruction but may be replaced, if necessary. Aneurysms which involve the entire arch plus the ascending aorta cannot be handled in this fashion, as there is no place to connect the proximal end of the aortic shunt graft without interrupting the circulation. Thus, cardiopulmonary bypass is required. In one method, illustrated in Figure 23, the innominate and carotid arteries are perfused directly during total cardiopulmona .ry bypass, while the arch is replaced. The left subclavian artery is simply clamped. Evidence of postoperative neurologic damage in some of the patients, however, is attributed to "subclavian steal," causing ischemia during perfusion. This is corrected by retrograde perfusion of the left axillary artery. By this method the entire cerebral circulation is well perfused. The results with regard to reduction in neurologic damage remain unclear. 30 Although the cannulation is complex, an uncluttered operative field is provided and direct attack upon the aneurysm is facilitated. The same type of cannulation has been successfully used without an individual p u m p for each arterial line, allowing local vascular resistance to determine flow (Fig. 24). Using these methods, time can be saved if the brachiocephalic vessels can be reimplanted as a unit (Fig. 25). Waldhausen 2°° has suggested an approach which combines the shunt graft technic with the use of cardiopulmonary bypass. This method seems reasonable, if 51

P I G . 24. Simplified exlracorporeal circuitand cannulations for excision of aneurysm of aortic arch and prosthetic replacement. Separate•pumps for perfusion of cerebral vessels are not used, and corormry ariery perfusion is omitted. Cerebral blood flow through each catheter is regulated by cerebral vascular resistance. (Reprinted with permission, Pearce, e t al.~63)

suitable. Exposure of the brachiocephalic vessels may be a problem, however, as exposure of long segments of these vessels may be difficult before the aneurysm is decompressed. All methods involving cardiopulmonary bypass provide the usual access for coronary perfusion, which should be used if the aorta is clamped for long periods of time. ANEURYSMS OF THE DESCENDING THORACIC A O R T A . ~ A left lateral thoracotomy is the incision of choice for aneurysms of the descending FIG. 25. A, prostlaehc replacement after aneurysm excision is facilitated by preserving a cuff of aortic wall at the origin of the innominate, carotid, and subclavian arteries. B, only three anastomoses are then required: proximal aortic, distal aortic, and brachiocephalic cuff to prosthesis. (Reprinted with permission, Pearce, et a/.163)

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thoracic aorta. The patient's hips should be rotated to provide access to the left femoral artery. Usually a rib is removed to provide the widest possible exposure. The proximal margin of most descending thoracic aneurysms is at or near the left subclavian artery, and removal of the fifth rib provides adequate proximal and distal exposure. If the aneurysm is more distal, removal of the sixth rib may be preferable. Access to the distal end of large aneurysms can be difficult. Occasionally it is necessary to make a second incision in a lower intercostal space to provide safe exposure, utilizing the same soft tissue incision. After exposing the aneurysm, a choice must be made regarding control of the circulation during aortic cross clamping. As discussed earlier, simple cross clamping at normothermia risks ischemic damage to the spinal cord as well as overdistention of the heart. Basically, the choice lies between the use of an external shunt or some form of partial left-heart bypass. The latter has been more widely used. The use of an external shunt has the advantage of avoiding heparinization. The size of the aneurysm is not often a limiting factor in its use. Distal cannulation can be either to the aorta or to the femoral artery, while .proximal cannulation can be to the aorta or to the left subclavian artery. However, there is no way to return shed blood, so this technic is not appropriate in situations where return of blood may be necessary. Our experience has largely been with left atrial-to-femoral bypass, but a wider trial of temporary shunt bypass seems reasonable. After opening the aneurysm, the aorta is reconstructed in the usual manner with a Dacron prosthesis. With traumatic aneurysms, end-toend reapproximation is occasionally feasible, s. ls5 as is patch graft repair of a partial aortic wall defect. As with abdominal aneurysms, the entire sac need not be removed so long as only viable aneurysm wall is left. If the sac is removed, this can usually be deferred until the prosthesis is in place and the heparin has been neutralized. A maio/- concern following resection of the descending thoracic aorta, even with good distal perfusion, is the risk of postoperative spinal cord damage and paraplegia. This results from interruption of the arteria m a g n a which arises variably from the lower thoracic or upper lumbar portion of the aorta and supplies the anterior spinal artery.I, ss We know of no reliable way to locate this vessel preoperatively. One must simply keep interruption of intercostal vessels to the minimum, compatible with treatment of the aneury, sm, and make a special effort to preserve any unusually large intercostal arteries found in the distal thoracic aorta. Postoperative aorticopulmonary fistulas occasionally develop. TM The causes are thought to be similar to those leading to the development of a false aneurysm at any suture line. Covering suture lines with viable tissue, or if that is unavailable, wrapping with Teflon felt, should provide prophylaxis against this complication. 1~4 53

THORACOABDOMINAL AN.EURYSMS Thoracoabdomina! aneurysms are apparentty not rare. Fomon, e t at. 9z found 7 among 249 aneurysms of the aorta and its major branches on review of 7 , 6 4 2 autopsy records. However, reported surgical experience is limited. The first successful resection of such an aneurysm was reported by Ethredge, e t al. 9° in 1955. Since then occasional cases have been described, TM ~la but the major experience has been that of De Bakey and h~s group, 99 who-reported 42 cases. Arteriosclerosis was the cause of these lesions in 62% of their patients, with syphilis the cause in 2 6 % . Males predominated 8 to 1. An anterolateral thoracotomy with a separate midline abdominal incision was used at normothermia. Others?Z~have favored a thoracoabdominal approach combined with mild kypothermia. The technic of resection is illustrated in Figure 26, utilizing the shunt graft principle to prevent ischemia. Rob zT~ in his series of approximately 20 cases, found 3 in which the ~eliac axis and superior mesenteric artery were totally occluded prior to surgery. Blood was supplied to the viscera via a greatly enlarged inferior mesenteric artery.. Inability to reconstruct Fro. 26.. D r a w i n g of steps of operative technicin resection and graft replacement of thoracoabdominat aortic aneurysms. (Reprinted with permission, Garrett, et al.g9 )

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the o c c l u d e d vessels in 2 of these p a t i e n t s did n o t p r e v e n t a successful l o n g - t e r m result. T h e o p e r a t i v e m o r t a l i t y in D e B a k e y ' s series was 2 6 % , with 4 late d e a t h s a m o n g the survivors. In the 19 patients free of a s s o c i a t e d card i o v a s c u l a r disease at the time of resection, the o p e r a t i v e m o r t a l i t y was o n l y I 1 % . E x p e r i e n c e is insufficient to p r o v i d e m e a n i n g f u l statistical d a t a reg a r d i n g i n d i c a t i o n s f o r resection of t h o r a c o a b d o m i n a l a n e u r y s m s . H o w e v e r , this is a f o r m i d a b l e o p e r a t i o n a n d p r o b a b l y s h o u l d be p e r f o r m e d o n l y for e n l a r g i n g o r s y m p t o m a t i c lesions. REFERENCES I. Adams, H. D., and Van Geertruyden, H. H.: Neurologic complications of aortic surgery, Ann. Surg. 144:574, 1956. 2. Alexander, J., and Byron, F.: Aortectomy for thoracic aneurysms, J.A.M.A. 126:1139, 1944. 3. Alley, R. D. (In discussion of paper by Spencer, F. C., Guerin, P. F., Blake, H. A.. and Bahnson, H. T.): Report of 15 patients with traumatic rupture of the thoracic aorta, J. Thoraclc & Cardiovas. Surg. 41 : 1, 1961. 4. Atik, M. (In discussion of paper by Fry, et al.) : Infection complicating the use of plasticarterial implants, Arch. Surg. 94:600, 1967. 5. Austen, W. G., and Shaw, R. S.: Experimental studies with extracorporeal circuits as a method to enable surgical attack on thoracic aneurysms, J. Thoracic & Cardiovas. Surg. 39:337, 1960. 6. Bahnson, H. T.: Considerations in the excision of aortic aneurysms, Ann. Surg. 138:377, 1953. 7. Bahnson, H. T.: Definitive treatment of saccuiar aneurysms of the aorta with excision of sac and aortic suture, Surg., Gynec. & Obst. 96:382, 1953. 8. Bahnson, H. T.: Excision of aortic aneurysms, Maryland M. J. 2:537, I963. 9. Bahnson, H. T., and Nelson, A. R.: Cystic medial necrosis as a cause of localized aortic aneurysm amenable to surgical treatment, Ann. Surg. 144: 519, 1956. 10. Baird, R. J., Tutassaura, HI, and Miyagishima, R. T.: Use of the left renal vein for portal decompression, Ann. Surg. 173:551, 1971. 11. Barker, A. G., Jr., Roberts, B., Berkowitz, H., and Barker, C.: Risk of excision of abdominal aortic aneurysms- a happy trend. Presented at the Society for Vascular Surgery, 24th Annual Meeting, June, 1970. 12, Barratt-Boyes, B. G.: Symptomatology and prognosis of abdominal aortic aneurysm, Lancet 2:716, 1957. 13. Barry, K. G., Mazze, R. I., and Schwartz, F. D.: Prevention of surgical oliguria in renal hemodynamic suporession by sustained hydration, New England J. Med. 270:1371, I964. 14. Baumler, R. A.: Arteriosclerotic abdominal aortic aneurysm rupturing into the intestine, J.A.M.A. 176:!46, 1961. 15. BealI, A. C., Jr., Cooley, D. A., Morris, G. C., and De Bakey, M. E.: Perforation of arteriosclerotic aneurysms into the inferior vena cava, Arch. Surg. 86:137, 1963. I6, Beall, A. C., Jr., Holman, M. R., Morris, G. C., and De Bakey, M. E.: Mannitol induced osmotic diuresis during vascular surgery. Renal hemodynamic effect, Arch. Surg. 86:48, 1963. 17. Belsey, R. H., Dowlatshahi, K., Keen, G., and Skinner, D. B.: Profound hypothermia in cardiac surgery, J. Thoracic & Cardiovas. Surg. 56:497, 1968. 55

18. Bennett, D. E., and Cherry, J. K.: The natural history of traumatic aneurysms of lhe aorta, Surgery 61:516, 1967. 19. Bernstein, E. F., Fisher, J. C., and Varco, R. L.: Is excision the optimum treatment for all abdominal aortic aneurysms, Surgery 61:83, 1967. 20. Bicks, R. O., Bale, G. F., Howard, H., and McBurney, R. F.: Acute and delayed colon ischemia after aortic aneurysm surgery, Arch. Int. Med. 122: 249, 1968. 21. Blaisdell, F. W., DeMattei, G. A., and Gauder, P. J.: Extraperitoneal thoracic aorta to femoral bypass graft as replacement for an infected aortic bifurcation prosthesis, Am. J. Surg. 102:583, 1961. 22. Blaisdell, •F. 'W., and Hall, A. D.: Axillo-femoral artery bypass for lower "k • extremity lschemla, Surgery 54: 563, 1963. 23. Blaisdell, F. W., Lim, R. C., Jr., Amberg, J. R., Choy, S. H., Hall, A. D., and Thomas, A. N.: Pulmonary micro-embo!ism. A cause of morbidity and death after major vascular surgery, Arch. Surg. 93:776, 1966. 24. Blakemore, A. H., and King, B.: Electrothermic coagulation of aortic aneurysms, J.A.M.A. 111 18~!, ~' 1938. 25. Blakemore, A. H., and Voorhees, A. B.: Aneurysm of the aorta. A review of 365 cases, Angiology 5:209, 1954. 26. Blakemore, A. H., and Voorhees, A. B.: The use of tubes constructed from vinyon-N. Cloth in bridging arterial defects, experimental and clinical, Ann. Surg. 140:324, 11954. 27. Blickenstaff, D. E., and Nice, C. M., Jr.: Aortic aneurysms secondary to mediastinal abscess. Report of two cases, Dis. Chest 48:534, 1965. 28. Bloodwell, R. D., Hallman, G. L., BealI, A. C., Cooley, D. A., and De Bakey, M. E.: Aneurysms of the descending thoracic aorta. Surgical considerations, Surg. Clin. North America 46:901, 1966. 29. Bloodwell, R. D., Hallman, G. L., and Cooley, D. A.: Aneurysms of the ascending aorta with aortic valvular insufficiency, Arch. Surg. 92:588, 1966. 30. Bloodwell, R. D., Hallman, G. L., and Cooley, D. A.: Total replacement of the aortic arch and the "subclavian steal" phenomenon, Ann. Thoracic Surg. 3:236, 1968. 31. Blum, L.: Ruptured aneurysm of abdominal aorta, New York J. Med. 68: 2061, 1968. 32. Borst, H. C., Schaudig, A., and Rudolph, W." Arterio-venous fistula of the aortic arch: Repaired during deep hypothermia and circulatory arrest, J. Thoracic & Cardiovas. Surg. 48:443, 1964. 33. Boyd, L. J.: A study of four thousarid reported cases of aneurysm of the thoracic aorta, Am. J. M. Sc. 168: 654, 1924. 34. Brant, B., Armstrong, R. P., and Vetto, R. M.: Vaso depressor factor" in declamping shock production, Surgery 67: 650, 1970. 35. Brickman, R. D., Yates, A. J., Crisler, C., Schwentker, E., Bron, K., and Bahnson, H. T.: Circulatory arrest during profound hypoth~rmia for treatment of complicated disease of major vessels, Arch. Surg. 103:259, 1971. 36. Bryant, L. R., Bowlin, J., Malette, W., and Danielson, G. K.: Thoracic aneurysms with aorto-bronchial fistula, Ann. Surg. 168:79, 1968. 37. Campbell, G. S.: Physiologic and technical htctors in the surgical treatment of abdominal aortic aneurysms, Surgery 62:789, 1967. 38. Cannon, J. A., Van DeWaler, J., and Barker, W. F.: Experience with the surgical management of I00 consecutive cases of abdominal aortic aneurysm, Am. J. Surg. 106: 128, 1963. 39. Ching, C. C., and Hughes, R. K.: Arteriosclerotic aneurysrns of the thoracic a o r t a - l a t e stage of a diffuse disease, Am. J. Surg. 114:853, 1967. 40. Clowes, G. H. (In discussion of paper by Conn, et al.): Infected arterial grafls: Experience in 22 cases with emphasis on unusual bacteria and techniques, Ann. Surg. 171:704, 1970. 56

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