SURGICAL TREATMENT OF PULMONARY EMBOLISM

SURGICAL TREATMENT OF PULMONARY EMBOLISM

VOLUME 47 JANUARY, 1964 NUMBER 1 Thoracic and Cardiovascular Surgery Original Communications SURGICAL T R E A T M E N T OF P U L M O N A R Y Denni...

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VOLUME 47 JANUARY, 1964 NUMBER 1

Thoracic and Cardiovascular Surgery

Original

Communications

SURGICAL T R E A T M E N T OF P U L M O N A R Y Dennis M. L. Rosenberg, M.D.* and John McNulty,

D

M.D.***

EMBOLISM

Charles Pear ce, M.D.**

(by invitation),

(by

invitation),

New Orleans, La.

the past half century there has been no remarkable change in the fatal prognosis of pulmonary embolism, although it is probably the most thoroughly documented of the serious illnesses. Also, there have been few changes in treatment iintil recently, although attempts at surgical evacuation of pul­ monary embolism are by no means new. Indeed, after Virchow supplied the term for the affliction in 1856, attempts to ameliorate the condition came rapidly. However, more than 100 years later, little has been acquired in the way of de­ tailed knowledge of predisposing conditions and prophylactic measures. It is also true that, in the United States, approximately 3,000 persons die each year from pulmonary embolism,22 and roughly comparable figures are cited from England. 2 Early diagnosis and surgical correction by embolectomy may reduce this appalling fatality. Many of these patients live for sufficiently long periods of time after initial onset of embolism to allow the surgeon to instigate immediate efforts for relief. This thesis has been supported by a study of records of one hundred autopsied cases in which the subjects had died of massive pulmonary embolism at Charity Hospital and Touro Infirmary in New Orleans. 26 In this group of patients, 29 per cent survived for 2 hours or longer, and 10 per cent for at least 10 hours (Table I ) . URING

Prom the Department of Surgery, Tulane University School of Medicine, and Departments of Surgery and Medicine, Touro Infirmary, New Orleans, Da. Read at the Forty-third Annual Meeting of The American Association for Thoracic Sur­ gery at Houston, Texas, April 8-10, 1963. •Associate Professor of Surgery, Department of Surgery, Tulane University School of Medicine. ••Assistant Professor of Surgery, Department of Surgery, Tulane University School of Medicine ; Established Investigator, American Heart Association. •••Instructor of Clinical Medicine, Department of Medicine, Louisiana State University School of Medicine.

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J. Thoracic and

Cardiovas. Surg.

TABLE I . SURVIVAL T I M E I N 92 FATAL CASES OP MASSIVE PULMONARY EMBOLISM (CHARITY H O S P I T A L ) TIME

Less than 10 minutes 10-60 minutes 60 minutes-2 hours 2-12 hours 12-24 hours 2 days or longer

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NO. PATIENTS

38 13 12 17 10 2

It is for selected patients in this group, those who sho\v progressive dete­ rioration, that the more direct approach of pulmonary embolectomy with the aid of extracorporeal circulation is proposed. Experience with 2 patients treated in this manner is outlined, preoperative study and diagnosis are discussed, and details of the surgical approach are presented. INCIDENCE

Waggenspack 39 has stated that in reported series of ' ' sudden ' ' deaths, about 5 per cent are usually attributed to pulmonary emboli. Marcus and Zimmer­ man, 16 in reference to the sequelae of phlebothrombosis, found that postopera­ tive pulmonary embolism developed " i n clinically detectable form is about one out of each 1,000 major cases, with death in about one out of each 5,000 cases." DeTakats and Jesser 0 reported that in the larger hospital services the incidence of pulmonary embolism ranged from 0.1 to 0.2 per cent of all operations, 2 to 4 per cent of all deaths, 6 per cent of postoperative deaths, and approximately 10 per cent of all of the autopsies. At Massachusetts General Hospital, in 10 years, pulmonary embolism was reported in 9 per cent of routine autopsy studies according to Harris, 10 and the findings of Roe and Goldthwait 25 were similar. In 512 patients from Columbus State Hospital, however, the incidence was 25.7 per cent.32 At the Geelong Hospital, Coleman2 computed an approximate inci­ dence of fatal pulmonary embolism as occurring in one of every thousand opera­ tions. De Bakey, 5 in a series collected from the literature, found that 10,497 deaths were caused by pulmonary embolism out of 275,000 autopsy studies, an incidence of 3.8 per cent and that of 3,177,495 operations, death from pulmonary embolism occurred in 4,567-0.11 per cent. It is known that the general incidence increases with age. Of the 100 cases studied from Charity Hospital in New Orleans, 81 patients were 50 years old or older. SIGNS AND S Y M P T O M S

The formation of pulmonary embolism is often insidious, and signs and symptoms may be missing or misleading, even in fatal cases. Although the acute phase may actually simulate other respiratory, cardiovascular, abdominal, or even neurological syndromes, certain manifestations provide important leads to the diagnosis. In a series of 150 cases, studied by Hatch and AYheat27 at the Ochsner Foun-

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dation Hospital in New Orleans, 73 per cent had a presenting complaint of dyspnea, the most common symptom. Other signs and symptoms were pleuritic chest pain in 72 per cent, cough in 45 per cent, and hemoptysis in 27 per cent. Feelings of apprehension or of impending doom were part of the subjective manifestations in 15 per cent. Seventeen per cent of the patients complained of pain referable to the abdomen, an often overlooked symptom of primary pul­ monary embolism. Major signs were limited to the thorax in most, and few extrathoracic mani­ festations could be characterized as prominent findings. Thoracic examination was recorded either at the time or shortly after onset of symptoms; the most frequent sign, present in 54 per cent of patients, was that of râles. The next most frequent findings were decreased breath sounds and pleural friction rub. The outstanding cardiac abnormality was arrhythmia. Ventricular or auricu­ lar premature sounds, gallop rhythm, atrial fibrillation, and different types of supraventricular tachycardia were noted in 21 per cent of the patients. In 10 patients in whom the pulmonic sounds were recorded, an increase was noted in each, a change from the findings on the previous physical examination. Other physical findings included rib tenderness and hypotension. The most prominent extrathoracic finding was a positive Homan's sign in 29 per cent of patients and in more than half of this group unilateral edema was a concomitant manifestation. Fever was noted in most cases. Comparable observations were documented in the Charity Hospital study. In the 100 cases reviewed, pulmonary embolism was the cause or a major con­ tributing factor of death. In only 46 cases, or less than half, was the clinical diagnosis of pulmonary emboli or venous thrombosis made. Leg or calf pain, respiratory distress, chest pain, sweating, pallor, cyanosis, rapid pulse, desire to defecate, and apprehension were reported in some combination in 34 of these 46 patients. Furthermore, in 23 of these patients, pain in the calf or leg was the only presenting symptom. In an additional 2 patients, convulsions which preceded rapid death were the only clinical signs noted. The significance of calf and leg pain should be emphasized, as it was initially the only indication of thromboembolic disease in nearly one fourth of these cases. Other investigators have shown that even with well-organized thrombophlebitis, which is not likely to cause emboli per se, one half to one third of the patients have associated phlebothrombosis in the same or contralateral venous systems which can cause fatality. 21 Cough, "precordial oppression," and nausea and vomiting are not infre­ quent findings. Besides pleuritic chest pain, pain in the shoulder may be present, and distention of the veins in the neck in the later stages of illness is common. Associated neurological signs and symptoms may occasionally cloud the diagnostic view in patients with pulmonary embolism. Israel and Goldstein12 reported the cases of 2 patients whose symptoms were indicative of cerebrovascular insufficiency. Hussey 11 had one patient whose only sign was that of syncope. The sites of origin of emboli are variable, but the pelvic veins and those of the lower extremities are justifiably to be suspected. In many instances the

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J. Thoracic and

Cardiovas. Surg.

origins are never discovered. In the Charity Hospital series, 39 per cent were still unknown after autopsy study. Surprisingly, in only 2 per cent were the deep pelvic veins the source of disease. The veins of the leg were most often involved. The sites of origin in order of frequency were : legs, 34 ; right heart, 10; femoral veins, 6; iliac veins, 5; vena cava, 2; from liver tumor, 1; and right subclavian vein, 1 (Table I I ) . TABLE I I .

S I T E S OP ORIGIN o r

Undetermined Calf veins Right atrium Femoral veins Hypogastrie veins Inferior vena cava Deep pelvic pains Subclavian vein Liver tumor embolus

PULMONARY E M B O L I *

39 34 10 6 5 1

•Autopsy study of 100 cases.

DIAGNOSIS

Diagnosis of acute pulmonary embolism may be difficult, especially if the signs and symptoms are obscure. Conversely, when the symptomatology is ob­ vious, diagnosis of a typical case may present no problems at all and the litera­ ture abounds with descriptions. In a classic example, the patient develops retrosternal constriction and is oppressed by feelings of impending disaster. Cold sweat, pallor, and tachypnea will be manifest. The patient will have hypoten­ sion, weak and rapid pulse, and distention of the veins in the neck. The major problem in differentiation is acute myocardial infarction. Here the serial electrocardiographic findings are of great help and may indicate changes that characterize acute cor pulmonale. In instances of concomitant car­ diac disease or anomaly, however, the difficulty of interpretation will be increased. In the severely ill patient with diverse complications, the classical diagnostic features may be obscured. Although many useful diagnostic aids are available, all too often use of these measures is limited by the time factor, which is crucial in many or most cases. As suggested by Wacker and Snodgrass, 38 three laboratory examinations may be utilized. The serum lactic dehydrogenase may be elevated, hyperbilirubinemia may occur while the serum concentration of glutamic oxaloacetic acid transaminase may be only slightly elevated or normal. A physiologic approach to diagnosis was recommended by Robin and associates,24 based on a significant difference between the alveolar and arterial carbon dioxide tensions which re­ sult from prolonged ventilation of nonperfused portions of the lung tissue. Al­ though Cooley and associates,3 in their report of a successful embolectomy, point out that the method is not a particularly sensitive one, these investigators found the difference of 7 mm. Hg between the arterial and alveolar carbon dioxide tensions in their patient to be diagnostically meaningful. Roentgenographic examination can provide immediate supportive evidence,

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especially if one is aware of the possibility of pulmonary infarction and em­ bolism and is alert for their detection. In many of the cases reviewed, chest roentgenograms were available in the immediate period after the first episode of embolism and in about one third of these the radiologist had reported that there were findings suggestive of embolus. A roentgenological diagnosis of pneu­ monia was oeeasionally made. The majority of x-ray films taken in the immediate postembolus period showed no change from previous films. Angiocardiographic examination, proved experimentally to demonstrate pulmonary emboli in animals, has been used successfully for this purpose clini­ cally. Although angiocardiographic examination of the acutely ill patient is admittedly hazardous, the attendant dangers have proved to be minimal to date. Certainly, if its use precludes the risk of a needless and much more hazardous thoracotomy, angiocardiography is a warranted procedure. In both patients in whom pulmonary emboleetomy was performed, angiocardiographic examination produced no untoward effects and gave indispensable evidence of the embolie process.

Fig·. 1.—Clots removed by emboleetomy from right and left pulmonary arteries. CASE HISTORIES CASE I was previously published in detail. 2 « This 39-year-old man had sustained multiple injuries to the trunk and extremities. Ten days later he developed a swelling of the right calf and thigh, followed by low mid-sternal discomfort and tachycardia and sharp pain in the right shoulder. When seen in consultation the patient was alert, although obviously acutely ill. The neck veins were somewhat distended. A loud systolic murmur was audible over the precordium. A gallop rhythm could be discerned, and the second pulmonary sound was accentuated. Abnormal electrocardiographic findings included sinus tachycardia (140 per minute), general flattening of T waves, and right axis deviation. On roentgenographic study, the right pulmonary artery apparently terminated abruptly.

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EOSENBERG,

PEARCE,

McNULTY

J. Thoracic and Cardiovas. burg.

As deterioration was progressive, arrangements were made at once for angiocardiographic study. This revealed conspicuous pooling of dye in the right side of the heart with only minimal dye entering the left upper lobe. The femoral arterial oxygen saturation was 83 per cent and the pC0 2 34 mm. Hg. Pulmonary embolectomy was performed April 17, 1961, with the use of extracorporeal circulation with a disc oxygenator. No clots were visible when the main pulmonary artery was opened longitudinally, but when long grasping forceps and the suction tip were introduced, large multiple thrombi were removed from the right and left pulmonary arteries (Fig. 1 ) . After bypass was dis­ continued the inferior vena cava and the right axillary veins were ligated. Initially, the patient progressed satisfactorily. On the second postoperative day, hypoxia became evident, progressed, and resulted in death 60 hours after operation. At postmortem study, many small thrombi were found in the peripheral arteries of both lungs.

Fis. 2.—Roentgenogram which shows bilateral basal lobe infarction. CASE II.—A man, 31 years of age, entered Touro Infirmary on Aug. 30, 1962, with a provisional diagnosis of right lower lobe pneumonia or pulmonary infarction. In 2 days it was clear that the latter condition prevailed. Two weeks later the patient had further episodes of infarction in both the lower left and right lobes (Fig. 2 ) . Clinically, he deteriorated rapidly, and customary medical management brought about no improvement in his con­ dition. The blood pressure was 110 over 80 mm. Hg, and an increasing tachycardia of between 120 and 140 was reported. The temperature ranged between 100° and 103° F . No tenderness was detectable along the course of the deep veins of the lower extremities and there had been no edema.

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On Sept. 13, 19C2, when the patient was seen in consultation, lie was obviously in a state of advanced illness. He was anxious, conspicuously dyspneic, and somewhat cyanotic. Respiration was shallow; tliere was some evidence of circulatory collapse; and the pulse was 120 per minute. On roentgenographic study, bilateral infarction of the lower lobes seemed to exist. Tliere was a decrease in the vascular markings to the left lung. Angiocardiographic ex­ amination showed the entire left lung to contain no opacifying medium, and the dye was,

Fig. 3.—Angiocardiogram shows hold-up of dye in right side of heart. No dye is seen in pul­ monary arterial tree, except in vessels to right lower lobe.

Fig. 4.—Embolus removed from left pulmonary artery.

ROSENBERG, PEARCE, McNULTY

J. Thoracic and

Cardiovas. Surg.

«BSS Fig. 5.—Photograph shows massive swelling" from thrombophlebitis aggravated by inferior vena cava ligation. seemingly, arrested in the right side of the heart and in the main pulmonary artery. I n the arteries to the right lower lobe only, a minimal amount of the dye could be visualized (Fig. 3 ) . Femoral arterial oxygen saturation was 83 per cent and carbon dioxide tension was 39.5 mm. Hg. Massive pulmonary embolism was diagnosed and surgical extirpation was planned with the use of extraeorporeal circulation. Thoracotomy was performed Sept. 14, 1962. A transverse incision was used to enter both pleural cavities in the fourth intercostal space and divided the sternum. The pulmonary artery pressure was 25 mm. H g systolic. A Kay-Cross disc-type pump oxygenator was used for complete temporary cardiopulmonary bypass. The vessel was not noticeably tense and no clot was visible when it was first opened. On digital exploration, a large thrombus was palpable in the left pulmonary artery, which was removed with a gallbladder stone-holding forceps. The clot, which contained semi-organized caste-like projections from the pulmonary artery branches, was 5 cm. long and 3 cm. in diameter (Fig. 4 ) . I n the right pulmonary artery no clots could be palpated at first, but with the forceps and by suction small pieces were obtained from the branches. Repeated manual compression of the lungs from the periphery toward the hilum failed to dislodge any peripherally-situated emboli. The arteriotomy wound was sutured and use of the oxygenator was discontinued after 9 minutes of total cardiopulmonary bypass. The inferior vena cava λvas then ligated through a right flank muscle splitting incision. Oxygénation improved noticeably after operation. Studies on the day after embolectomy showed arterial oxygen saturation to be 95.3 per cent and carbon dioxide tension 33.4 mm. Hg. On the third postoperative day, the patient developed massive bilateral thrombophlebitis of the lower extremities (Fig. 5 ) . Anticoagulants, fibrinolysin, and ilio-femoral vein thrombectomy were necessary for control. He improved rapidly but recovery was further delayed by an infection of the femoral arteriotomy, which necessitated ligation of the artery. H e was discharged Oct. 30, 1962, and has remained well, returning to his previous occupation as a carpenter (Fig. 6 ) . DISCUSSION

Medical management of patients with massive pulmonary embolism Avili often be the only therapeutic measure necessary because clinical improvement is evident. Infusion of vasopressor drugs, venous ligation, and anticoagulant therapy may be used, depending upon the individual circumstance. In contrast,

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Pig. 6.—Photograph of patient made 2 months after pulmonary embolectomy.

embolectomy utilizing extracorporeal circulation should be considered if rapid improvement does not follow conservative treatment. Trendelenburg 34 ' 35 proposed pulmonary embolectomy in 1908. Of his 3 original patients, none survived. He wrote of the problem in 1912, " A l l new and difficult problems required much work, favorable conditions and unfaltering confidence and perseverance. This holds good also in the operation for pulmonary embolism. Twelve times we have done it at the clinic, my assistants oftener than myself, and not once with success. And yet I would continue trying. This much we have learned from our cases, that the diagnosis in all surgical cases is easy; invariably did we find the emboli." 33 The first successful operation of this sort came in 1924 and was done by Kirschner. 13 In 1958, the first successful pulmonary embolectomy in this country was performed by Steenburg and associates.29 Cooley, Beall, and Alexander 3 were first to report success with pulmonary embolectomy done with extracor­ poreal circulation. However, Sharp 44 had performed one using the same tech­ nique a short while prior to this.* Allison and co-workers1 used general body hypothermia and cardiac inflow occlusion. The surgical success are tabulated in Table III. •This sentence and Reference 44, as well as mention in Table III, were added to this text as a result of the information given by Dr. Bahnson in his discussion of this paper.

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1 4 2 2 1 1 1 2 1* 1 1 1 1 1 1 1 1 1 *Not massive embolism.

YEAR OP REPORT

1924 1927-31 1928 1930 1936 1939 1947 1953-56 1955 1958 1960 1960 1961 1960 1961 1962 1962 1963

MCNULTY

J. Thoracic and Cardiovas. Surg.

III.

1

REPORTED BY

Kirschneris Meyer". i» Crafoord & Giertz 4 , s Nystrom 2 3 Valdonise Lewis 1 5 Lehneri* Marion et al.**, n, si Vandecasteele et al. 3 7 Warren et al.29 Dubost & J o u a s s e f Wieberdink 4 1 Sharp 4 * Allison et al.i Cooley et al. 3 Rosenberg et al. Couves et al. 4 2 Donaldson et al. 4 3

The decision for pulmonary emboleetomy or conservative management is a difficult one to make. Continuing deterioration with progressive hypotension and tachycardia, failure of the right side of the heart, increasingly rapid respira­ tion, and progressive electrocardiographic changes are signs which favor a de­ cision for emboleetomy. If emboleetomy is chosen, certain considerations are extremely important. First, diagnosis must be assured. Second, supportive measures should be con­ tinued, including oxygen inhalation and intravenous administration of vasopressor substances. Third, preparations should be made for extracorporeal circulation during the period required to remove the embolus or emboli from the pulmonary arterial tree. There is all too little time to be expended in obtaining fresh heparinized blood and in sterilization and assemblage of a standard pump oxygenator system. Portable pumps with pre-sterilized disposable plastic bubble oxygenators may be a solution in that they can be primed and ready for operation quickly. Partial bypass can be effected prior to induction of general anesthetic and the same disposable oxygenators can be used for extracorporeal bypass for the perfor­ mance of emboleetomy. Available units have a maximum oxygenating capacity of approximately 3,500 ml. of blood per minute. This is wholly adequate for an adult patient for the brief period needed for pulmonary emboleetomy (10 to 20 minutes), and the plan seems more practical than attempts to maintain an as­ sembled sterilized rotating disc or other type of oxygenator in constant readiness. Banked ACD blood that is less than 5 days old or hemodilution techniques using 5 per cent glucose and water, or saline, or dextran, can be used to prime the bubble oxygenator systems. A transverse intercostal incision about the level of the third or fourth rib with division of the sternum affords quick and satisfactory surgical exposure. A longitudinal incision is made in the main pulmonary artery and the cardio-

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pulmonary bypass is established. The artery and its branches are carefully ex­ plored and emboli extracted. The embolus is, of course, not always in the main artery, and, if it has gone out into the small branches, manual compression of the lungs may be used to dislodge peripheral portions for extraction. The lung is squeezed from the periphery inward, toward the hilum, so that the clot is "milked" out of the vessel. After closure of the chest, the inferior vena cava should be ligated to pre­ clude further embolization. This step is particularly important since anticoagu­ lant therapy cannot safely be re-instituted for 24 to 48 hours after thoracotomy. SUMMARY

Surgical therapy now actually affords hope for some patients with pul­ monary embolism. With advances in cardiovascular surgery, the operation of pulmonary embolectomy is being performed more frequently and successfully, at least 5 such cases being reported in the past 2 years. The fact that approximately 30 per cent of patients may survive a massive pulmonary embolus for 2 hours or longer lends support to the belief that planned surgical intervention with the aid of extracorporeal circulation not only is fea­ sible but could be successful in a fair proportion of these patients. A successful pulmonary embolectomy is described. REFERENCES 1. Allison, P. R., Dunnill, M. S., and Marshall, R. : Pulmonary Embolism, Thorax 15: 273, 1960. 2. Coleman, K. J . : Prophylaxis in Pulmonary Embolism, M. J . Australia 2 : 285, 1962. 3. Cooley, D. A., Beall, A. C , Jr., and Alexander, J . K. : Acute Massive Pulmonary Em­ bolism, J . A. M. A. 177: 283, 1961. 4. Crafoord, C.: Two Cases of Obstructive Pulmonary Embolism Successfully Operated Upon, Acta chir. scandinav. 64: 172, 1928. 5. De Bakey, M. E. : Critical Evaluation of the Problem of Thromboembolism, Surg. Gynec. & Obst. 98: 1, 1954. 6. Γ/eTakats, G., and Jesser, J . H . : Pulmonary Embolism: Suggestions for its Diagnosis, Prevention and Management, J . A. M. A. 114: 1415, 1940. 7. Dubost, C , and Jouasset, D . : Operation de Trendelenburg: Documents sur embolie pulmonaire massive, Ann. chir. 14: 1067, 1960. 8. Francillon, J., Marion, P., Tartulier, M., and Rautenberg, J . : Embolie pulmonarie, Lyon chir. 5 1 : 304, 1956. 9. Giertz, K. H., and Crafoord, C. : On the Thrombo-embolic Disease and its Surgical Treat­ ment, Acta chir. scandinav. 64: 121, 1928. 10. Harris, H. W. : Pulmonary Embolism and Infarction, M. Clin. North America 4 3 : 69, 1959. 11. Hussey, H. H. : Recognition of Pulmonary Embolism, North Carolina M. J . 17: 56, 1956. 12. Israel, H. L., and Goldstein, F . : The Varied Clinical Management of Pulmonary Em­ bolism, Ann. Int. Med. 47: 202, 1957. 13. Kirschner, M.: Ein durch die Trendelenburgsche Operation geheilter Fall von Embolie der Art. pulmonalis, Arch. Klin. Chir. 133: 312, 1924. 14. Lehner, A. : Eine erfalgreiche Trendelenburgsche Embolie-operation, Schweiz, med. Wchnschr. 77: 127, 1947. 15. Lewis, I . : Trendelenburg's Operation for Pulmonary Embolism; Successful Case, Lancet 1: 1037, 1930. 16. Marcus, E., and Zimmerman, L. M. : Principles of Surgical Practice, New York, 1960, The Blakiston Division of McGraw-Hill Book Company, Inc. 17. Marion, P . : Coeur pulmonaire aigu. Arteriotomie pulmonaire gauche. Embolectomie rétrograde partielle, Guerison, Mém. Acad. chir. 79: 239, 1953. 18. Meyer, A. W. : Eine weitere erfalgreiche Trendelenburgsche Lungenembolieoperation, Arch. Klin. Chir. 167: 136, 1931.

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19. Meyer, A. W.: Operative Treatment of Embolism of the Lungs, Surg. Gynec. & Obst. 50: 891, 1930. 20. Meyer, W.: The Surgery of the Pulmonary Artery, Ann. Surg. 58: 188, 1913. 21. Moran, I . J . : Pulmonary Embolism in Non-Salvagable Patients With Venous Thrombosis, Am. J . Clin. Path. 17: 205, 1947. 22. Neuhof, H. : Venous Thrombosis and Pulmonary Embolism, New York, 1948, Grune & Stratton, Inc. 23. Nystrom, G. : Experiences With the Trendelenburg Operation for Pulmonary Embolism, Ann. Surg. 92: 498, 1930. 24. Robin, E. D., Julian, D. G., Travis, D. M., and Crump, C. H. : A Physiologic Approach to the Diagnosis of Acute Pulmonary Embolism, New England J . Med. 260: 586, 1959. 25. Roe, B. B., and Goldthwait, J . G. : Pulmonary Embolism. Statistical Study of Post Mortem Material at Massachusetts General Hospital, New England J . Med. 241: 679, 1949. 26. Rosenberg, D. M. L., and Digiglia, J . : Unpublished materials. 27. Hatch, H., and Wheat, J . : Personal communication. 28. Rosenberg, D. M. L., Eckman, P . J., and Pearce, C. W. : Surgical Treatment of Massive Pulmonary Embolism With the Use of Extracorporeal Circulation, J . Cardiovas. Surg. 3 : 128, 1962. 29. Steenburg, R. W., Warren, R., Wilson, R. E., and Rudolf, L. E . : A New Look at Pul­ monary Embolectomy, Surg. Gynec. & Obst. 107: 214, 1958. 30. Stoney, W. S., and Adams, J . E.: The Diagnosis of Acute Pulmonary Embolism by Arteriography, Am. Rev. Resp. Dis. 83: 26, 1961. 31. Tournaire, A., Tartulier, M., Deyrieux, F., Blum, J., and Marion, P . : Le coeur pulmonaire aigu dans l'embolie pulmonaire, in L'Expansion Scientifique Française, Paris, 1956. 32. Towbin, A . : Pulmonary Embolism: Incidence and Significance, J . A. M. A. 156: 209, 1954. 33. Trendelenburg, F . : Cited by Meyer.20 34. Trendelenburg, F . : Ueber die Operative Behandlung der Embolie der Lungenarterie, Arch. Klin. Chir. 86: 686, 1908. 35. Trendelenburg, F.: ZUT Operation der Embolie der Lungenarteries, Deutsche med. Wchnschr. 34: 1172, 1908. 36. Valdoni, P . : Un caso di embolia dell'arteria polmonaire guarite con 1'embolectomia, Policlin. 4 3 : 911, 1936. 37. Vandecasteele, J., Linquette, M., and Desruelles, J . : Embolies pulmonaires récidivantes. Embolectomie pulmonaire et ligature de la veine cave inférieure dans le même temps opératoire, Arch. mal. coeur. 48: 872, 1955. 38. Wacker, W. E. C , and Snodgrass, P . J . : Serum L D H Activity in Pulmonary Embolism Diagnosis, J . A. M. A. 174: 2145, 1960. 39. Waggenspack, C. A., J r . : Pulmonary Embolism: Obvious and Obscure, J . Louisiana State M. Soc. 114: 319, 1962. 40. Wessler, S., and Thomas, D. P . : The Treatment of Venous Thrombosis and Pulmonary Embolism, M. Clin. North America 46: 1277, 1962. 41. Wieberdink, J . : Trendelenburg's Operation for Pulmonary Embolism With Modified Technic. Report of a Case of Successful Intervention, J . Internat. Coll. Surgeons 34: 380, 1960. 42. Couves, C. M., Sproule, B. J., and Frazer, B. S.: Acute Pulmonary Embolism: Successful Embolectomy Using Cardiopulmonary Bypass, Canad. M. A. J . 86: 1056, 1962. 43. Donaldson, G. N., Williams, L., Scannell, G., and Shaw, R. : A Reappraisal of the Ap­ plication of the Trendelenberg Operation to Massive F a t a l Embolism, New England J . Med. 268: 171, 1963. 44. Sharp, E. H . : Pulmonary Embolectomy: Successful Removal of a Massive Pulmonary Embolus With the Support of Cardiopulmonary Bypass. Case Report. Ann. Surg. 156: 1-4, 1962. DISCUSSION MR. P H I L I P ALLISON, Oxford, England.—I would like to support Dr. Rosenberg's contention of a more aggressive attitude by surgeons to this disease. I t is important for us to realize, however, that the subject which we have been discussing so far would be better termed ' ' terminal pulmonary embolus. ' ' By the time these patients are really ill and require treatment, they have suffered many episodes of pulmonary emboli. Postmortem examinations of any patient who has died of pulmonary embolus and a careful histological study of the lung will show multiple emboli of all different ages. I t is my belief that these

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emboli start either on the operating table or very shortly after. I am sure we would agree ultimately t h a t the ideal approach to this condition is prevention. I would like to stress that we have no satisfactory way of forecasting this severe terminal situation of pulmonary emboli. As has been pointed out this morning, the electroeardiographic changes are unsatisfactory in the early stages. X-ray examination is negative. All these things, of course, change in the terminal stages. I think one of the most important indications of embolus in any postoperative patient is a continual slight fever with attacks of shortness of breath. I t is very easy to go around the wards and hear a patient complaining that he is a little short of breath, and we p a t him on the back and say, " W e l l , you are bound to b e ; you have had your chest open or your abdomen opened. ' ' I think these little attacks of shortness of breath are of great clinical significance and should not be ignored. There is one other factor, and it does not detract in any way from my belief t h a t we should be aggressive about this condition. We want to know, if a patient gets over his pulmonary embolus, what residual respiratory deficiency he may have. [Slide] Here is a radiopaque pulmonary embolus put into a dog. I t is completely filling the right pulmonary artery. There is a bronchospirometer in place. [Slide] Here it is on the lateral view. [Slide] The bronchospirometrie tracing shows that the oxygen uptake of this lung was nil at the time of impaction of the embolus. [Slide] Here you see the bronchospirometrie tracing, the left lung above continuing and increasing the oxygen uptake, and the oxygen uptake of the right lung stopping al­ together. We found as a result of these experiments that, within 2 weeks, 80 per cent of lung function had returned. The radiological follow-up of these patients, together with histologie pictures at various times, shows that the clots have been reduced to little fibrous plaques within 3 weeks, and there is no evidence at all in the pulmonary vascular tree of where the clot had been after 28 days. So, we do know that if patients recover from a severe attack of pulmonary embolus their vascular tree will return to normal. [Slide] This is the same dog. This slide was taken one week after impaction of the embolus, and you see it has disappeared. So, the outlook from the point of view of respiratory function in these patients is good if they get over the severe effects of large pulmonary emboli. DE. F R E D E R I C K S. CROSS, Cleveland, Ohio.—Dr. Albert Mowlem and I had the opportunity to operate on a patient with a massive pulmonary embolus in August, 1962. There are certain aspects of this case that are important and should be emphasized. As far as establishing the diagnosis of a massive pulmonary embolus is concerned, we are faced with the same problems as were discussed earlier in this meeting concerning dissecting aneurysms. For the most part, it will be a clinical diagnosis. We will have to make our minds up from the clinical findings, and succeed or fail on this basis. We were fortunate to have a patient who exhibited classical signs and symptoms of a massive pul­ monary embolus along with good laboratory evidence. [Slide] This x-ray film was taken about 5 hours after the onset of symptoms and shows the large shadow in the base of the left lung, suggestrve of a pulmonary infarct. There is also a diminution of the peripheral vascular markings and an accentuation of the hilar vascular markings. These changes were not present in earlier x-ray films. I n addition, a switch to right axis deviation was demonstrated by electrocardiography. These findings, accompanied by the fact that the patient continued in shock with a rapid pulse and respira­ tions for a sufficiently long period to convince us that he was not going to get better, made the decision to proceed with surgery an easy one. I would like to comment a bit on circulatory support as an important part of this procedure. Although circulatory support can be started in the patient's room, it was not necessary with our patient. We did cannulate the femoral artery and vein under local anesthesia and hooked the patient up to the pump oxygenator in the operating room prior

14

ROSENBERG, PEARCE, McNULTY

J. Thoracic and Cardiovas. Surg.

to starting anesthesia. During the induction of anesthesia his blood pressure which had been 90 mm. H g systolic suddenly became unobtainable. We immediately started circulatory support and were then able to carry the patient with a systolic blood pressure of about 100 mm. H g until we were able to get him on full cardiopulmonary bypass. From this point on the operation is relatively easy and is comparable to a pulmonary valvulotomy. [Slide] This is a picture of the clot that was removed. The clot extended into the right ventricle, and this indentation was caused by the pressure of the pulmonary valve. I t is pretty much a complete cast of both pulmonary arteries. As has been suggested previously, we also massaged the lungs to remove distal clots, and, in addition, inserted forceps and the suction tip as far distally as possible to remove clots. I think the Trendelenburg operation failed in many instances because there was in­ sufficient time to remove these distal clots. We did the operation with a Kay-Cross oxygenator primed with bank blood which was easily obtainable, some 5 per cent dextrose, and a little fresh blood. The patient had not been properly anticoagulated prior to his pulmonary embolus and, on the basis of our previous indications for caval ligation (namely, repeated emboli in the face of adequate anticoagulation), we did not ligate the vena cava, but rather continued the anticoagulation started just prior to operation. He has not had recurrent emboli, and we possibly avoided the complications of vena caval ligation. The very rapid return of this man's vital signs to normal, as well as the marked improvement in his general condition following the pulmonary embolectomy, was certainly a gratifying experience. DR. ARTHUR C. BEALL JR., Houston, Texas.—I would like to congratulate Dr. Rosen­ berg and his associates on their fine presentation, and briefly to bring our series in Houston up to date. [Slide] First, I would like to stress the importance of manual compression of the lungs. Without such a technique, embolectomy in our patients would have been incomplete; some patients require as much as 15 minutes to remove all of the emboli. [Slide] The first patient was operated upon 2 years ago this month. [Slide] All of these clots were removed. Only by manual compression of the lung was complete embolectomy possible. This patient continues to do well. [Slide] Likewise, this 74-year-old man, who had a pulmonary embolus following prosta­ tectomy, has done well following embolectomy. [Slide] Three months ago, we had the opportunity to see a patient on the medical service in whom there had been a previous embolus some 10 days before. He then developed chest pain and went into shock with rather typical signs of pulmonary embolism. [Slide] He was in shock approximately 6 hours prior to our seeing him, and there was some temporary difficulty with renal function following surgery. [Slide] The clots removed from this man are seen here, and, again, without manual compression of the lungs it would not have been possible to get out many of these peripheral emboli. [Slide] Summarizing our experience, the first patient was operated upon in April, 1961, with fresh heparinized blood to prime the pump oxygenator. The second was operated on in June, 1961, with fresh heparinized blood. The most recent patient was operated on in Jan­ uary, 1963, with the use of 5 per cent dextrose in water to prime the pump oxygenator. We believe this is a significant advantage. In the first 2 patients it required 2 to 3 hours to make preparations for bypass. I n the latter patient only 15 minutes was required. [Slide] This was accomplished by using a disposable oxygenator primed with dextrose in water. With rapid preparation this patient was salvaged. I d o n ' t believe he would have survived long enough for us to have obtained fresh heparinized blood. DR. H E N R Y T. BAHNSON, Pittsburgh, Pa.—Ordinarily I decry efforts to establish priority, but on seeing the long list, such as that presented by Dr. Rosenberg, I am prompted to state that there was at least one successful case of treatment with the bypass in this country prior to those listed by Dr. Cooley.

Vol. 47, No. 1 January, 1964

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Based on the work of Mr. Allison, Dr. Edwin Sharp successfully treated such a patient on Feb. 17, 1961, at Johns Hopkins Hospital with extracorporeal bypass. The patient was presented soon after that, at a meeting of the alumni of that institution in Baltimore. This presentation was known to Dr. Cooley and his associates before their report, and referred to in one of their later reports. Dr. Sharp's patient has subsequently done quite satisfactorily. DR. ALTON OCHSNER, JR., New Orleans, La.—Dr. Rosenberg has demonstrated that even in New Orleans, a successful embolectomy can be done, so I can talk about an unsuc­ cessful case. If I adopt what Sterling Edwards calls ' ' positive thinking, ' ' I can tell you about a successful case of a patient who survived as long as 48 hours. The point is that this patient, we thought, had a successful embolectomy. The patient persisted with cor pulmonale and died. At autopsy, when we examined the lungs, the pul­ monary arterial tree was filled with clots, in spite of the fact that we had done a very careful milking of the lungs as described by Cooley. When one looked at this situation—and none of the cases that were presented today by Dr. Beall actually had these small clots that filled the arterioles of this patient— two thoughts came to mind that I wish to pass on to you: First, this patient had been in shock for a prolonged period. One of Dr. Beall's patients was in shock for 6 hours. Perhaps this destroyed my thesis, but I just wonder if it is going to be possible ever to do successful emboleetomies in patients who have been in prolonged shock, assuming they have not had good enough bronchial flow to maintain patency of the distal pulmonary vascular bed while there is occlusion of the proximal bed. The other thought i s : Is there any place for retrograde perfusion of these lungs through the pulmonary veins? DR. BRUCE PATON, Denver, Colo.—We have had three experiences in Denver using a disposable oxygenator filled with dextrose and saline. A 31-year-old lady, 3 weeks after an orthopedic operation, collapsed suddenly at noon with a typical clinical picture of pul­ monary embolus. There was considerable procrastination about the decision for operation. She then collapsed again and became moribund about 4:30 P.M. and was rushed to the operating room, where perfusion was started, circulation restored, and the emboli removed, but she later died. In the second case, in January, a lady who had had a fractured ankle early in De­ cember, followed by a thrombophlebitis after 6 weeks, definite infarction of the left lower lobe, and massive pulmonary embolus a few days later, collapsed in her room while prepa­ rations were being made for embolectomy. She was rushed to the operating room, the emboli were removed, and she survived 5 days but had cerebral damage because of hypertension, and died after 5 days. After having learned from these two experiences, we had a better experience in April. At the Veterans Administration Hospital a patient under the care of Dr. Marchioro had intestinal obstruction 5 weeks after a successful renal homotransplant. One week after the intestinal obstruction he had a massive pulmonary embolism at 2:30 P.M. At 3:15 P.M., he was removed to the operating room. [Slide] This slide shows the emboli from the second lady. [Slide] This slide shows the emboli from the man Operated in April, the longest of which is 8 inches. Three days after the pulmonary embolectomy, the patient underwent a filter operation of the inferior vena cava; he later made a complete recovery. DR. CONRAD LAM, Detroit, Mich.—Dr. Rosenberg mentioned that, at the conclusion of his operation, he ligated the vena cava. My remarks are related to this terminal part of his operation. I n our institution we have been opposed to the ligation of the vena cava, and I believe his one patient had a pretty bad leg for a while, and his final photograph showed the patient only from the waist up.



R O S E N B E R O , P E A R C E , McNTJLTY

J. Thoracic and Cardiovas. Surg.

If one does not wish to ligate the vena cava, he might use a little nylon clip which we have placed in a large number of dogs and which has always prevented embolism in them. [Slide] Dr. Zikria from our group and Dr. Taber developed this clip. I t is another way of channelizing or making partitions in the vena cava which will prevent an embolus of any size from reaching the heart. A good recommendation for the clip is t h a t Dr. Cooley has used it a number of times (more times than we have), and, judging from the number of reorders we have had, it must be a very satisfactory way of preventing subsequent pulmonary embolism. DR. ROSENBERG (Closing).—I.appreciate the remarks of the discussers. As is always true with the Houston group, they have a series, and we congratulate them on their suc­ cesses. I n regard to vigorous squeezing of the lung, I am not absolutely as convinced as Dr. Beall is about the efficacy of this maneuver. Surely one must produce more edema, and there are enough problems in the postoperative period. We did, however, squeeze the lungs in one case but did not get out any more peripheral emboli. I must apologize to Dr. Bahnson for not knowing about his case. We certainly will review the total series so that he will have proper priority. To Dr. Ochsner's question of whether this can be done after prolonged shock, I believe so. I d o n ' t know how long shock has to be present to be prolonged, but I do think we demonstrated, in the second patient who was in hypotensive shock for 12 hours, that it can be done. The question of retrograde perfusion: I think this possibly is an approach. I would like to see perfusion with the flbrinolytic drugs, for what they are worth. We did not know about Dr. P a t o n ' s 3 cases; of course they are recent, and the last one being successful. Dr. Lam, I am sorry about the picture. He d i d n ' t have any clothes on, so I did not think it necessary to show more than I did. However, he has no edema at all at this stage. I do like your clamps and I would like you to send me a few. I want to show one final slide that belongs to Dr. Soutter of Wisconsin, who did this pulmonary embolectomy. [Slide] This shows a preoperative angiocardiogram, in which we see a block in the pul­ monary arteries. [Slide] This is the postoperative study which demonstrates a successful embolectomy. If we have any more cases, we will certainly do postoperative angiocardiographic studies.