T H E PROBLEM OF SECOND O P E N CARDIOTOMIES James W. Mackenzie, M.D., Herbert Sloan,
M.D.,
Joe D. Morris, M.D., and Aaron Stern, M.D., Ann Arbor,
O
Mich.
operations to repair uncomplicated lesions can be accomplished with a mortality rate of under 1 per cent,13 but little organized informa tion has been published about the problem of second open-heart procedures for patients who have already undergone such operations. 2 ' 7 Reliable perfusion equipment and increased familiarity with intracardiac anatomy and methods of correction have improved the results with most correctable cardiac defects. It seems probable, however, that some patients will still need a second operation. This is a report of our experience with the 22 patients who have undergone a second open-heart procedure at the University of Michigan Medical Center. These patients are our total experience with second operations among the 571 patients operated upon with the aid of extracorporeal circulation through October, 1961. The primary diagnosis of 18 of these patients was some form of ventricular septal defect. Nine patients had an isolated septal defect, 8 a tetralogy of Fallot, and one a single ventricle (Table I ) . Thirteen of the patients with per sistent ventricular septal defects had limitation of activity, but the threat of bacterial endocarditis was the indication for operation in 5 patients with small residual defects.1* One patient, J. M., had a second operation because the first operation was abandoned when a dissecting aneurysm occurred at the site of femoral arterial cannulation during the perfusion.6 It was feared that adhesions between the heart and pericardium might make reoperations unduly hazardous but the adhesions were usually thin and avascular. The heart could be completely freed in most patients, although the dissection was sometimes tedious. In the 3 patients with dense, vascular ad hesions, only enough of the heart was freed to perform the necessary cannulations and incisions. The interval between operations varied from 5 to 30 months, but no correlation was found between this interval and the number and char acter of the adhesions. Early in our experience, Ivalon outflow tract prostheses were inserted to correct outflow narrowing in tetralogy of Fallot. Dissection over these prostheses was particularly troublesome as would be expected from the known tissue response to moderately compressed Ivalon. 3 ' 8 No operation PEN-HEART
Prom the Departments of Surgery and Pediatrics, University of Michigan Medical Center, Ann Arbor, Mich. Received for publication Jan. 4, 1962.
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Vol. 44, No. 4 October, 1962
SECOND O P E N CARDIOTOMIES TABLE
PATIENT
AGE AT F I R S T OPERATION
PRIMARY DIAGNOSIS
I INTERVAL BETWEEN OPERA TIONS (MO.)
T. H.
6 yr.
Tetralogy of Fallot
7
L. B.
8 yr.
Tetralogy of Fallot
6
Tetralogy of Fallot Tetralogy of Fallot Tetralogy of Fallot Tetralogy of Fallot Tetralogy of Fallot Tetralogy of Fallot VSD (hypertensive) t VSD (hypertensive) t VSD VSD (hypertensive) t VSD VSD (hypertensive) t VSD VSD VSD Aorto-pulmonary window; G. a subaortic stenosis Atrial septal defect, secun3 yr. T. F. dum Congenital aortic stenosis 18 yr. J.B. and insufficiency 3 yr. Single ventricle D. B. R. D. 1 yr. Congenital aortic stenosis •Ventricular septal defect tVentricular septal defect with pulmonary arterial systemic pressure. B. R. . D. R. R. A. J. S. J . McD. R.R. F.W. R. B. V.V. S.K. G. D. P . G. D. H. J . M. C.W.
11 9 8 6 8 7 5 4 7 4 4 3 10 14 8 14
yr. yr. yr. yr. yr. yr. yr. yr. yr. yr. yr. mo. yr. yr. yr. yr.
545
30 5 9 16 26 11 12 13 15 6 10 30 26 12 15 18 5
REASON FOR SECOND OPERATION
VSD*; residual infundibu lar stenosis V S D ; intractable cardiac failure VSD VSD VSD VSD VSD VSD VSD VSD VSD V S D ; tricuspid insufficiency VSD VSD VSD VSD VSD Persistent aorto-pulmonary window Mitral insufficiency
14
Aortic insufficiency
6 6
VSD Mitral insufficiency
pressure 75 per cent or more of
was abandoned because dissection was too difficult, nor were technical problems related to this dissection responsible for a fatality. The common femoral artery or the superficial femoral artery was used for insertion of the arterial cannula at the original operation, and the correspond ing vessel of the other side was used for insertion of a pressure recording catheter. Eight of these 22 patients were 5 years of age or less at the time of the original procedure. Bilateral femoral arterial occlusion occurred in one child who was 3 years old at the time of the original operation. The other occlusion was at the insertion site of the arterial cannula in a 7-year-old child. The cardiotomy incisions appeared well healed. In 3 of the patients in whom a compressed Ivalon outflow tract gusset had been placed, there was bulging adjacent to the right patch. This was not a false aneurysm, as described by Payne and Kirklin, 9 but may have been a precursor of such an aneurysm. There was no evident thinning of the myocardium adjacent to the incision in other patients to suggest significant interference with coronary arterial supply. On occasion the coronary arterial arrangement was obscured by scarring over the surface of the heart. When scarring hid the previous incision, its exact position could be identified by palpation. Four causes of persistence or recurrence of ventricular septal defects were found at operation. In patients with large ventricular defects, such as are found
546
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AL.
J. Thoracic and Cardiovas. Surg.
in tetralogy of Fallot, either the posterior margin of the defect had not been closed satisfactorily at the first operation, or the sutures had pulled out of the muscular superior rim. Later experience has suggested that the sutures were not placed well enough into the tough fibrous base of the aortic valve. The third cause of failure was due to small defects around sutures placed through the thin membranous ventricular septum. The least common cause of failure was the result of attempts to close small, low, muscular ventricular defects obscured by the trabeculae carneae in the apex of the right ventricle. In only one of the original operations for these persistent ventricular septal defects did the surgeon think that an excellent closure had been obtained. Persistence of the defects was suspected early in the postoperative period. None of these pa tients had a history or operative findings to suggest that disruption of the repair was caused by endocarditis. The repair carried out at the second operation has been varied according to the findings. In patients in whom a septal prosthesis had been used originally the margin of the defect was sutured to the original patch, using deeply placed sutures in the muscular area, well away from the conduction bundle of His. The presence of persistent defects even after reoperation suggests that it might be better to remove the original patch and to insert a new one. Ventricular septal defects closed by direct suture at the first operation were reinforced with figure-of-eight sutures. In most of these patients the need for adequate exposure required extensive dissection of adhesions between the tricuspid valve insertions and the interventricular septum. In re-exploration of patients with recurrent defects in the muscular part of the septum near the apex of the right ventricle, it was helpful to use a small separate ventricular incision directly over the defect. The extracorporeal circulation system in use at the University of Michigan consists of a rotating disc oxygenator, roller pump for arterial perfusion, and gravity venous return. 1 * Flow rates of approximately 2.4 L. per square meter of body surface per minute are used to maintain a mixed venous oxygen satura tion of 70 per cent at normothermic levels. Since September, 1959, this basic system has been supplemented in most open-heart operations by blood stream cooling to an esophageal temperature of about 29° C. The routine use of Fluothane in the oxygenator and the sternal splitting incision were adopted about this time, but it seemed worth while to compare the acid-base studies of the few patients operated upon with the aid of the two different perfusion techniques. Acid-base studies were obtained from 8 patients whose first operation was at near normothermic levels and whose second operation was at hypothermic levels (Table I I ) . Direct control of the acid-base status by addition of such chemicals as hydrochloric acid or sodium bicarbonate was not attempted, al though a 2 per cent carbon dioxide-98 per cent oxygen gas mixture wTas used in the oxygenator. Methods of determination and calculation are given in Table II. We have omitted the data of bicarbonate, pC0 2 , and buffer base for hypothermic levels because of disagreement as to the proper reference temperature and physiologic significance of these determinations. 1 ' *•5- "> 15 The important
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acid-base data are those of the postperfusion period when the results of inade quate perfusion become readily apparent. Comparison of these data show no significant differences in acid-base balance despite our impression that the addition of hypothermia to extracorporeal circulation has improved the post operative course. Certainly hypothermia at these levels has not been accom panied by increased metabolic acidosis and the operation has been easier technically. TABLE IT. COMPARISON OF ACID-BASE STATUS o r P A T I E N T S PERFUSED W I T H AND W I T H O U T ADJUVANT MODERATE BLOOD STREAM COOLING (AVERAGES—RANGE IN P A R E N T H E S I S ) HCOat SAMPLE
pH*
Extracorporeal
(mEq./L.)
Circulation Without Adjuvant (8 patients) 1. Pre-perfusion (arterial) 7.42 18.3 2. At end of perfusion (arterial) 7.41 15.8 3. Postperfusion 3.2 hr. (4.5-2.5) (arterial) 7.31 18.7 Extracorporeal
pco2t (mm./Hg)
A (Bb+) bt (mEq./L.)
Hypothermia 30 26
-4.7 -6.7
38
-6.6
Circulation
With Adjuvant Hypothermia to 30° C, Esophageal (Same 8 patients) 1. Pre-perfusion (arterial) 7.38 20.2 37 -4.5 2. At end of perfusion (arterial) 7.39 3. PostperfusionJ 3.5 hr. (6-2.5) (arterial) 7JU 2JL0 43 -4.8 ♦Plasma pH determinations were done on whole blood in a Cambridge model R pH meter using water-jacketed glass electrode at a constant temperature of 37.5°C. and corrected to patient's temperature, using a factor of 0.014 pH units per l^C.10 Esophageal temperature used for correction of samples taken during operation and rectal temperature used for samples taken after operation. fWhole blood total carbon dioxide content was determined by method of Van Slyke and Neill.16 Plasma bicarbonate, CO2 pressure, and12 change in whole blood buffer base were calcu lated from nomogram of Singer and Hastings. JSeven patients. RESULTS
No effort has been made to perform routine postoperative cardiac catheterization in these patients. Therefore, it is difficult to be sure of their exact hemodynamic status. Seven of these patients are without an organic murmur, are asymptomatic, and are presumed to be free of residual defects. Ten still have murmurs of unknown significance. Depending upon their functional status, it may be necessary to consider cardiac catheterization and even a third operation for some of them. In this series of 22 patients there were three opera tive and two late deaths. Operative Deaths.— B. B. was a 4-year-old boy with a hypertensive ventricular septal defect closed in September, 1956. Although the procedure was complicated by aortic insufficiency, an Ivalon prosthesis was inserted. Persistence or recurrence of the defect was suspected soon postoperatively and confirmed by cardiac catheterization. Eeoperation was performed 13 months after the first operation. The second operation was complicated by operating room power failure soon after completion of the cardiotomy. The incision was quickly resutured, the heart resuscitated, and after correction of the power failure the operation was completed with the aid of potassium cardioplegia. Closure of the residual septal defect was accom plished without further difficulty but the patient died in the recovery room. At postmortem examination the defect was closed but there was a 3 mm. fenestration and wrinkling of the
MACKENZIE E T AL.
548
J. Thoracic and Cardiovas. Surg.
posterior cusp of the aortic valve. I t was not evident whether this was an iatrogenic defect or a congenital one, although the severe aortic insufficiency encountered at the first operation suggested the possibility of a congenital basis. D. B., a 3-year-old boy, had partitioning of a single ventricle with an Ivalon prosthesis in June, 1959. Postoperatively he developed congestive failure characterized by recurrent pleural effusions, and cardiac catheterization demonstrated a ventricular septal defect. Reoperation was attempted in December, 1959, because of intractable cardiac failure. Several small defects were seen but exposure was difficult and they were poorly closed. He died in the operating room. Examination of the heart showed that a contributing cause of death was pulmonary outflow tract obstruction from encroachment by the large Ivalon septal prosthesis. R. D. was a 2-year-old boy who had correction of congenital aortic stenosis in January, 1961. I n the postoperative period he developed congestive heart failure. Beoperation was undertaken through a right lateral thoracotomy in June, 1961, to correct mitral insufficiency. Adhesions made the aorta difficult to free for clamping and there was troublesome aortic insufficiency while on perfusion, but anterior and posterior annuloplasty of the mitral valve was carried out. There was marked foaming in the left atrium during the procedure. The patient died 36 hours after the operation, presumably of air embolism.
Late Deaths.— S. K. was a 4-year-old boy with hypertensive ventricular septal defect. Closure was performed in 1959 but he soon developed refractory congestive failure. Cardiac catheteriza tion revealed a small persistent ventricular defect, and right atrial pressure curves suggested concomitant tricuspid valve disease. At reoperation three small ventricular defects were closed and the annulus of the tricuspid valve plicated. H e continued to have apparent con gestive failure and died 9 months after the second operation. The cause of this boy's con gestive failure puzzled us. The findings a t the second operation seemed inadequate to explain his continuing severe difficulty. When the heart was examined following death the septal defects were closed. There was glomerular enlargement, diffuse acute and chronic mem branous glomerulonephritis, and degenerative fatty infiltration of proximal renal tubules in the kidneys. Although detailed kidney function tests were not performed, numerous urinalyses showed persistent albuminuria with occasional hyaline and coarse granular casts. Urea clearance 6 weeks after his second operation was 58 per cent of normal, but he was edematous at that time and the significance of this test is uncertain. B. R., an 11-year-old girl, had tetralogy of Fallot. I n December, 1957, an Ivalon prosthesis was used to close a large ventricular septal defect. An Ivalon patch was placed in the outflow tract. Because of continued difficulty and cardiac catheterization confirmation of a persistent ventricular septal defect, reoperation was performed in June, 1960. The septal prosthesis was unattached to the superior rim of the defect. This area was closed satisfactorily. She died suddenly at home 14 months after the second operation. When the heart was examined at the University of Michigan Medical Center, there was no residual septal defect. A contributing cause of death appeared to be subaortic stenosis resulting from projection of the Ivalon septal patch into the left ventricle. SUMMARY AND CONCLUSIONS
1. Twenty-two patients underwent second open-heart operations for re sidual or persistent defects. 2. If necessary, second operations can be carried out with an acceptable mortality rate. 3. Secondary closure of the residual defects is difficult and may require extensive revision of the original closure.
SECOND O P E N CARDIOTOMIES
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REFERENCES 1. Bernhard, W. F., Carroll, S. E., Schwarz, H. F., and Gross, R. E . : Metabolic Alterations Associated With Profound Hypothermia and Extracorporeal Circulation in the Dog and
Man,
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793,
1961.
2. Callaghan, J . C , Dvorkin, J., and Buchanan, D.: Reoperation for Disruption of Repair of Interventricular Septal Defect, A. M. A. Arch. Surg. 78: 755, 1959. 3. Dobell, A. R. C , Sanchez, F . R., and Murphy, D. R.: Experimental Evaluation of Ivalon as Replacement for Right Ventricular Myocardium, A. M. A. Arch. Surg. 8 1 : 118, 4. Edmark, K. W.: Continuous Blood p H Measurement With Extracorporeal Cooling, Surg. Gynee. & Obst. 109: 743, 1959. 5. Fairley, H. B . : Metabolism in Hypothermia, Brit. M. Bull. 17: 52, 1961. 6. Jones, T. W., Vetto, R. R., Winterscheid, L. C , Dillard, D. H., and Merendino, K. A.: Arterial Complications Incident to Cannulation in Open-Heart Surgery: With Special Reference to the Femoral Artery, Ann. Surg. 152: 969, 1960. 7. March, H. W., Gerbode, F., and Hultgren, H. N . : The Reopened Ventricular Septal Defect: A Syndrome Following Unsuccessful Closure of Interventricular Septal Defects Particularly in Association With Infundibular Stenosis, Circulation 24: 250, 1961. 8. Blumberg, J . B., Griffith, P . O., and Merendino, K. A . : The Effect of Specific Compres sion on Soft-Tissue Response to Formalinized Polyvinyl Alcohol (Ivalon) Sponge: A Critical Evaluation, Ann. Surg. 151: 409, 1960. 9. Payne, W. S., and Kirklin, J . W.: Late Complications After Plastic Reconstruction of Outflow Tract in Tetralogy of Fallot, Ann. Surg. 154: 53, 1961. 10. Rosenthal, T. B . : The Effect of Temperature on the p H of Blood and Plasma In Vitro, J . Biol. Chem. 173: 25, 1948. 11. Severinghaus, J . W.: Respiration and Hypothermia, Ann. New York Acad. Sc. 80: 384, 1959. 12. Singer, R. B., and Hastings, A. B . : An Improved Clinical Method for the Estimation of Disturbances of the Acid-Base Balance of Human Blood, Medicine 27: 223, 1948. 13. Sloan, H . : Unpublished data. 14. Sloan, H., Mackenzie, J., Stern, A., and Sigmann, J . : Open Heart Surgery: Experience With 360 Patients, J . Michigan M. Soc. 59: 1659, 1960. 15. Trede, M., Foote, A. V., and Maloney, J . V., J r . : Pathophysiologic Aspects of Profound Hypothermia With Extracorporeal Circulation, Ann. Surg. 154: 210, 1961. 16. Van Slyke, D. D., and Neill, J . M.: The Determination of Gases in Blood and Other Solutions by Vacuum Extraction and Manometric Measurement. I., J . Biol. Chem. 6 1 : 523, 1924.