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CHANGES IN CEREBROSPINAL FLUID PRESSURE FOLLOWING EXPERIMENTAL SUPERIOR VENA CAVA TO RIGHT PULMONARY ARTERY SHUNT
CHANGES I N CEREBROSPINAL FLUID PRESSURE FOLLOWING EXPERIMENTAL SUPERIOR V E N A CAVA T O RIGHT P U L M O N A R Y ARTERY S H U N T Panagiotis N. Symbas, M.D. (by invitation), (by invitation), (Sponsored
C
Leon P. Woods,
and Harold A. Collins, M.D. (by invitiation),
by H. William
Scott, Jr., M.D., Nashville,
M.D.
Nashville,
Tenn.
Tenn.)
diversion of blood from the superior vena cava into the right pulmonary artery by anastomosis between the two vessels has been used successfully for surgical palliation in several congenital cardiac anomalies 3 ' 7 ' " characterized by impaired pulmonary blood flow. The procedure has special appeal in infants with tricuspid atresia. 2 In such patients a vena cava-pulmonary artery shunt may obviate the frequent occurrence of congestive failure following anastomosis of a systemic artery to a pulmonary artery. If anatomic considerations are excluded, the principal factor influencing function of a vena cava-pulmonary artery shunt is the pulmonary vascular resistance. Even when the pulmonary vascular resistance is assumed to be normal, facial edema and chylothorax are occasionally noted after operation. We recently encountered one infant who manifested a transient cerebral disturbance suggesting cerebral edema following performance of a vena cava-pulmonary artery anastomosis. A study was, therefore, undertaken to observe the changes in cerebrospinal fluid pressure following experimental complete shunting of superior vena caval blood into the right pulmonary artery. OMPLETE
METHOD
Unselected healthy mongrel dogs, weighing from 8 to 16 kilograms, were used for all experiments. Anesthesia was induced by the intravenous administration of pentobarbital (30 mg. per kilogram of body weight). Following the insertion of an endotracheal tube, respiration was maintained by a positive pressure respirator. The chest was opened through the right fifth intercostal space with the use of sterile technique. Side-to-end anastomosis of the superior vena From the Department of Surgery and the S. R. Light Laboratory for Surgical Research, Vanderbilt University School of Medicine, Nashville, Tenn. This investigation was supported in part by Research Grant No. H-5523 from the National Heart Institute, U. S. Public Health Service, and by the Middle Tennessee Heart Association. Read at the Forty-second Annual Meeting of The American Association for Thoracic Surgery a t St. Louis, Mo., April 16-18, 1962. 628
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cava to the right pulmonary artery was accomplished in essentially the manner described by Glenn.6 After completion of the anastomosis, the superior vena cava was ligated centrally. The thoracotomy incision was closed and residual air was aspirated from the thorax. No other special postoperative measures were employed except administration of antibiotics. Venous pressure and cerebrospinal fluid pressure were measured with a saline manometer immediately before operation and at periodic intervals postoperatively. Venous pressure was determined by puneture of the external jugular vein, and cerebrospinal fluid pressure was determined by direct cisternal puncture. Autopsy in all the animals who failed to survive or were sacrificed was performed. Particular attention was devoted to the anastomosis and the appearance of the brain.
VENOUS PRESSURE 1
0
1
5
1
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1
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1
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1
60
PRE-SHUNTTIME
1
90
— I
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-i
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IOH I2H
POST-SHUNT TIME
Fig. 1. RESULTS
Of the 23 animals used, 19 were satisfactory for study. The remaining 4 were excluded because of insufficient data, thrombosis of the anastomosis with signs of severe superior vena caval obstruction, or traumatic cisternal punctures. In the immediate postoperative period there was a consistent rise in spinal fluid and venous pressures (Fig. 1). The average rise of cerebrospinal fluid pressure was 6.0 cm. of saline. At the same time, venous pressure increased an average of 8.6 cm. of saline above the preoperative value. Twenty-four hours after operation the cerebrospinal fluid pressure had risen further, to an average of 8.9 cm. of saline above the preoperative value, while venous pressure had risen 10.3 cm. of saline (Table I ) . TABLE I. AVERAGE POSTOPERATIVE E I S E IN SPINAL FLUID AND JUGULAR VENOUS (CENTIMETERS SALINE ABOVE PREOPERATIVE VALUES)
PRESSURE
POSTOPERATIVE TIME (HOURS)
SPINAL FLUID PRESSURE
JUGULAR VEIN PRESSURE
1 24 72+
6.0 8.9 6.4
8.6 10.3 8.8
J. Thoracic and Cardiovas. Surg.
SYMBAS KT AL.
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In the animals which survived beyond 24 hours, a gradual fall in cerebrospinal fluid and venous pressure was observed, but it remained definitely above the normal preoperative value for as long as 50 days (Fig. 2). Brain swelling, evidenced by an unusually tight fit within the cranial vault and flattening of the cortical gyri, was noted at autopsy in close correlation with the finding of increased spinal fluid pressure. Histologic sections of the brain showed vascular engorgement and petechial hemorrhage (Pig. 3). Pleural effusion was noted in only one animal. The long-term survivors appeared to be as bright and active as they had been preoperatively, and no evidence of cerebral deficiency was apparent.
Pre-Op.
I hr.
24hr.
48hr.
72hr.
96hr.
HOURS POSTOPERATIVE Fig. 2. DISCUSSION
The results of this study indicate that a uniform increase in pressure occurs in the cerebrospinal fluid and superior vena caval system following anastomosis of the superior vena cava to the right pulmonary artery in dogs. The increase in cerebrospinal fluid pressure was roughly proportional to the increase in venous pressure. Despite a tendency to decrease gradually, the cerebrospinal fluid pressure elevation persisted for prolonged periods. Although no cerebral disturbance was apparent, swelling of the brain was noted at autopsy in those animals failing to survive. It was not possible in this study to correlate mortality with the severity of cerebrospinal fluid pressure elevation. Although flow in the superior vena cava was not measured, all pressure determinations were obtained during similar basal conditions. It appears unlikely that significant increments in flow would occur under these circumstances. The increase in venous pressure is, therefore, almost certainly related to the greater resistance of the pulmonary vascular bed as contrasted with that of the right atrium. Under conditions of increased flow the venous pressure could be expected to increase to an even greater degree. Brecht and Matill 1 demonstrated, in acute experiments, that intracranial pressure is primarily dependent upon, and varies with, venous pressure. The deleterious effects of chronically elevated venous pressure were reported by Owens and associates8 who found that occlusion of the dural sinuses or cortical veins in monkeys produced vascular engorgement, cortical swelling, and elevated
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cerebrospinal fluid pressure. A more direct result of increased venous pressure may be the cerebral hemorrhage observed in brain sections in this study. Similar findings were recorded by Darbinyan and Krymskii 5 who found hyperemia and solitary foci of hemorrhage in the brains of 3 dogs in which superior vena cava-pulmonary artery shunt had been performed. The immediate increase in cerebrospinal fluid pressure after superior vena cava-right pulmonary artery shunt must certainly be due to venous distention within the craniospinal space with simple displacement of spinal fluid. If this were the only mechanism involved and if the usual homeostatic action between formation and resorption of cerebrospinal fluid were intact, adjustment of volume would be expected to take place with return of cerebrospinal fluid pressure
Fig. 3.
to normal in a matter of hours or days. The continued elevation can be explained in at least two ways: (a) increased formation or decreased resorption of cerebrospinal fluid, and (b) increased formation or decreased resorption of extracellular tissue fluid within the brain and cord, producing edema. The latter explanation is the more compatible with our finding of brains which tightly filled the cranial vault, but it may be that both mechanisms are involved. Starling 10 initially explained the conditions regulating the formation and absorption of extracellular tissue fluid. Although the colloid osmotic pressure of the plasma tends to hold water in the capillaries, fluid is forced through the wall of the arterial end of the capillary by the arterial blood pressure. Because venous pressure is lower than plasma osmotic pressure, fluid is drawn into the venous end of the capillary. A decrease in serum osmotic pressure or an in-
632
SYMBAS E T
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crease in venous pressure tends to lessen the gradient which draws fluid into the capillary and produces edema. The clinical significance of this study lies in the recognition of a mechanism by which signs of cerebral dysfunction may occasionally be produced following superior vena cava-right pulmonary artery shunt. Cerebral complications following this operation have rarely been described, but minor degrees of cerebral disturbance may go unrecognized. It is conceivable that a more severe degree of cerebral edema could cause death, particularly during infancy when the pulmonary vascular resistance is at its highest level. Dammann and Perenoz 4 found the ratio of lumen to wall thickness in small muscular arteries of the lungs low at birth with a gradual increase during the first few months of life. Rudolph 9 showed that the calculated pulmonary vascular resistance was high immediately after birth, fell rapidly during the first month of life, and continued in a significant decline until one year of age. It is, thus, possible that performance of a superior vena cava-right pulmonary artery shunt during infancy can result in significant venous hypertension and cerebral symptoms. While other causes are undoubtedly partially responsible for the high mortality in infants following superior vena cava-right pulmonary artery shunt, cerebral edema may be an additional factor. Insufficient data exist to warrant any absolute recommendations concerning the prevention and treatment of cerebral complications following performance of a superior vena cava-right pulmonary artery shunt. It is likely that intracranial pressure increases and cerebral edema will frequently be of insufficient magnitude to need treatment or even be detected. Certainly the suggestion of Glenn regarding the use of a semi-upright position postoperatively is worthwhile. In addition, the maintenance of optimal respiratory ventilation is advantageous since carbon dioxide retention causes increased intracranial pressure. In the presence of obvious cerebral edema an attempt to increase plasma osmotic pressure by the administration of hypertonic substances would probably be of value. A more favorable balance between the production and resorption of tissue fluid might, thus, be accomplished. Although we have had no personal experience with this maneuver, it has been of value in other situations associated with cerebral edema. SUMMARY
1. Side-to-end anastomosis between the superior vena cava and right pulmonary artery was performed in 19 dogs. A definite increase of cerebrospinal fluid and superior vena cava pressure was observed in all the animals. In the immediate postoperative period, the average of cerebrospinal fluid pressure was 6.0 cm. of saline and 24 hours later was 8.9 cm. of saline. The average rise of superior vena cava pressure immediately after operation was 8.6 cm. of saline and 24 hours later was 10.3 cm. of saline. Both cerebrospinal fluid and superior vena cava pressures gradually fell after 24 hours but remained definitely above preoperative values for as long as 50 days.
DISCUSSION
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2. Brain swelling evidenced by an unusually tight fit of the brain within the cranial vault and flattening of the cortical gyri was observed, as well as vascular engorgement and petechial hemorrhages. 3. The semi-upright position, optimal ventilation, and an attempt to increase the plasma osmotic pressure may be beneficial postoperative measures. REFERENCES 1. Brecht, F . C , and Matill, P . M.: Studies on the Cerebrospinal Fluid. VI. A Study of the Effects of Tissue Extracts, Am. J . Physiol. 5 1 : 126, 1920. 2. Bopp, E. K., Larsen, P . B., Caddell, J . L., Patrick, J . E., Hipone, F . A., and Glenn, W. W. L.: Surgical Considerations for Treatment of Congenital Tricuspid Atresia and Stenosis: With Particular Reference to Vena Cava-Pulmonary Artery Anastomosis, J.
THORACIC SURG. 4 3 :
97,
1962.
3. Bakulev, A. N., and Kolesnikov, S. A.: Anastomosis of Superior Vena Cava and Pulmonary Artery in the Surgical Treatment of Certain Congenital Defects of the Heart, J .
THORACIC SURG. 3 7 :
693,
1959.
4. Dammann, J . F., Jr., and Ferenoz, C.: The Significance of the Pulmonary Vascular Bed in Congenital Heart Disease. I. Normal Lungs. I I . Malformations of the Heart in Which There Is Pulmonary Stenosis, Am. H e a r t J . 52: 7, 1956. 5. Darbinyan, T. M., and Krymskii, L. D.: Morphologic Changes in Heart, Lungs, and Brain After Experimental Cavo-Pulmonary Anastomosis, Bull. Exper. Biol. & Med. (USSR) 4 7 : 105, 1959. 6. Glenn, W. W. L., and Patino, J . F . : Circulatory Bypass of the Right Heart. I . Preliminary Observations on the Direct Delivery of Vena Caval Blood Into the Pulmonary Arterial Circulation. Azygos Vein-Pulmonary Artery Shunt, Yale J . Biol. 27: 147, 1954. 7. Nuland, S. B., Glenn, W. W. L., and Guilfoil, P . H . : Circulatory Bypass of the Eight H e a r t . I I I . Some Observations on Long-Term Survivors, Surgery 43: 184, 1958. 8. Owens, G., Stahlman, G., Capps, J . M., and Meirowsky, A. M.: Experimental Occlusion of Dural Sinuses, S. Forum 8: 521, 1957. 9. Eudolph, A. M.: Normal and Abnormal Eespiration in Children. Report of the 37th Boss Conference on Pediatric Research, edited by S. J. Fomon, Ross Laboratories, Columbus p. 65, 1961. 10. Starling: The Fluid of the Body, Chicago, 1909, W. T. Keener Company. 11. Weinberg, M., Jr., Bicoff, J . P., Agustsson, M. H., Steiger, A., Gasul, B . M., Fell, E. H., and Laun, L. L.: Surgical Palliation in Patients With Ebstein's Anomaly and Congenital Hypoplasia of the Right Ventricle, J . THORACIC SURG. 40: 310, 1960.
DISCUSSION (PAPERS ANKENEY
BY
HICKMAN
[PAGE 589],
SYMBAS [PAGE 628]
[PAGE
CALLAGHAN
561],
KENNEDY
[PAGE 600],
SHAW
[PAGE
570],
[PAGE 608],
CONNOLLY BILGUTAY
[PAGE
577],
[PAGE
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AND T H E I R ASSOCIATES)
DR. J O H N R. DERRICK, Galveston, Texas.—Thank you for the opportunity to discuss the very interesting paper by Drs. Mortensen and Hickman. I might give you the background of the work we have done in attempting to evaluate clamps. Galveston is 50 miles from Houston. When we got there we had to use the vascular clamps on autopsy material because of the very excellent work being done in Houston. However, we did clamp the aorta of some rabbits and fed them low and high cholesterol diets. The first slide demonstrates the area traumatized by clamping, and within 6 months there was a verj' noticeable change in the intima and subintimal fibrosis. In t r y i n g to evaluate w h a t the clamps would do with varying degrees of arteriosclerosis, we put different types of clamps on in this fashion.
634
DISCUSSION
J. Thoracic and Cardiovas. Surg.
This slide demonstrates the tears one would see in some of the atheromatous material and calcifications with the various types of clamps; this varied with the amount of arterial sclerosis and degeneration of the aorta. At one time, we had a very disastrous hemorrhage occur in a patient when a clamp was applied, so we have since adopted the technique of t i t r a t i n g the patient's blood pressure (those t h a t have high blood pressure) down to a lower level upon applying occlusion clamps, and, in those with severe sclerotic involvement, we use t h e buffer clamp above the sharp-pointed edges of the vascular clamps to prevent the pulsations of the aorta against the vascular clamp from tearing the vessel. DR. A. ROBERT CORDELL, Winston-Salem, N. C — I would like to comment on the excellent paper by Dr. Ankeney and his group, which dealt with t h e aspect of peripheral vascular resistance under varying degrees of perfusion. We have just completed a series on approximately 18 animals wherein we measured t h e total peripheral vascular resistance under conditions of normothermia, having obtained t h e flow r a t e for the perfusion by means of electromagnetic probes placed on the ascending aorta. The average of these figures taken prior to bypass determined our flow rate, and under these conditions we found essentially the same t h i n g Dr. Ankeney has with the measurement of venous How rates. Total peripheral vascular resistance does not change during a period of perfusion of this length with these conditions being set up. I think this is very worth-while work and the group working with Dr. Ankeney should be commended for their approach to this study. DR. J O H N W. K I R K L I N , Rochester, Minn.—I, too, would like to comment briefly on Dr. Ankeney's paper, perhaps on a little different aspect of it. Certainly the d a t a in this paper are so extensive and the implications so profound in some ways t h a t we will all have to study this in the evening a t home before we fully understand it. However, I think the implications, particularly with regard to homologous blood reactions, are extremely important, and I believe Dr. Ankeney has again done us a great service in bringing this important subject to our attention. My own attention was called first to the importance of homologous blood reactions by Dr. Gadboys and Dr. L i t w a k in Miami, Florida; Dr. L i t w a k alluded to this work a bit yesterday. I think on the basis of this very solid foundation of d a t a by Dr. Ankeney concerning t h e response of t h e dog to homologous blood, we have now, somehow, to incorporate this knowledge of homologous blood reactions into our general concepts of the reactions of man to extracorporeal circulation. Perhaps this is one of the most important contributions to such concepts t h a t has emerged in the last few years. After t a l k i n g with Dr. Gadboys and Dr. L i t w a k we began to look at this a little in man, and we have a little information t h a t suggests t h a t , among the other manifestations of this homologous blood reaction, perhaps there is a depression of myocardial function. I think we are all indebted to Dr. Ankeney for his superb d a t a and for bringing this important subject again to our attention. DR. HOWARD L. GADBOYS, Miami, F l a — I would like to t h a n k t h e Association for the privilege of discussing these papers and also Dr. Kirklin for his very kind comments. I think the paper by Dr. Sloan yesterday and those by Drs. Ankeney and Connolly today have touched upon some very exciting facets of extracorporeal circulation in general. We are indebted to Dr. James Dow for pointing out the presence of a syndrome of shock from homologous blood exchange in dogs in 1956. This phenomenon occurs in dogs with simple exchange of homologous blood, without requiring a heart-lung machine or anything other t h a n a reservoir connected to an arteriovenous fistula. As you can see from the slide, when the A-V fistula is opened no appreciable deviations occur until homologous blood is added to the circuit. At this point there soon may
Vol. 44, No. 5 November, 1962
DISCUSSION
635
ensue precipitous changes, characterized by portal hypertension, hepatic engorgement, fall of t h e buffer base, venous oxygen unsaturation, and, frequently, systemic arterial hypotension. Closing the reservoir fistula does not appreciably alter the situation. If one observes the isotopieally obtained circulating blood volumes, even though there have been no external volumetric changes, there may be marked systemic hypovolemia—the volumes on this slide range from 1,438 ml. to 534 ml. If one then gives blood to restore the systemic pressure to normal, the blood balance goes up. The blood volume may not r e t u r n to normal despite t h e fact t h a t there is now a blood balance considerably in excess of the preoperative figure. Consequently t h e weight changes t h a t occur do not reflect the alterations in circulating blood volume. An identical phenomenon is apparent in human beings. This slide is a compilation of d a t a obtained from a number of p a t i e n t s who have undergone extracorporeal circulation. Following perfusion, the patients have lost both plasma and red cells from the isotopieally measurable blood volume. Many of these are patients who "come off the p u m p " in a hypotensive state, even though one known t h a t the blood balance is at, or above, control levels. One can establish the effects of different volumes of homologous blood introduced into the patients by comparing a group of patients undergoing extracorporeal circulation utilizing large priming volumes with those having extracorporeal circulation employing small priming volumes (as exemplified b y left h e a r t bypass). An interesting phenomenon may be observed. When one turns the pump on and simply does a rapid exchange transfusion of a large volume of homologous blood for a brief period, followed by discontinuance of perfusion, the patients may go into shock. In other words, if one turns the pump on and turns the pump off, maintaining extracorporeal volumes constant, one often finds t h a t these patients will develop severe hypovolemia. This does not occur with left heart bypass since only minimal amounts of homologous blood are used. I would like, therefore, to add a word of caution about the use of a reservoir w i t h left h e a r t bypass since this may necessitate increasing the amount of homologous blood utilized. DR. ROBERT J. SCHRAMEL, New Orleans, La.—Last year I reported on prepulmonary bypass with the use of a rotating disk oxygenator and a veno-venous system of perfusion. With this we were able to get p r e t t y good survival in dogs and keep them alive. However, on autopsying surviving dogs the next day, and in all dogs who failed to survive, there were extensive lesions in the lungs. This slide is a low-power magnification and indicates t h a t the major difficulty here is extensive hemorrhage and atelectasis. This slide indicates t h a t the source of this hemorrhage is damage to t h e blood vessel wall. As you can see, this blood vessel wall is disrupted a t this point and is in the process of dissolution here. There is extensive hemorrhage. I n evaluating this further, we have used varying gas mixtures in the oxygenator, and some degree of this sort of thing always occurs but is less as you cut down on the amount of oxygen fed into the oxygenator. However, if the oxygenator and reservoirs are completely removed from the circuit, there are no lesions in the lungs. The animals survive and do very well. These are all standard 6 hour perfusions. This occurs whether the system is primed with dextran or with homologous blood. DR. A R T H U R V I N E B E R G , Montreal, Quebec.—The paper by Drs. Bilgutay and Lillehei is very interesting. I am pleased to see that they use the Ivalon sponge procedure, which we reported a few years ago. I would suggest to them t h a t it would be interesting if they would lower their catheter in t h e aorta a little f a r t h e r down so t h a t it is in t h e descending aorta, and inject
636
DISCUSSION
J. Thoracic and Cardiovas. Surg.
their dye in this region. By so doing, they will get a much b e t t e r filling of the sponge. We have done this in animals, but, as yet, not in man. Radiopaque dye injected into the descending aorta in t h e animal shows many mediastinal vessels going toward the heart. In addition, the Ivalon sponge appears to become opacified. The outline, shown by cineangiography in the case reported by the authors after an Ivalon sponge operation, was most interesting because it is very similar to t h a t which we have seen in angiographic studies made in our animals. I t would be worthwhile if studies could be carried out to t r y and show rilling of the myocardium from the left ventricular lumen. This has been done by us in animals, and we have found evidence which indicates t h a t the Ivalon sponge procedure tends to make the heart siphon blood from the left ventricular lumen into the myocardium, as well as from the pericardial vessels. This technique of angiocardiography appears to be very interesting, and I congratulate the speakers. DR. J A M E S D. HARDY, Jackson, Miss.-—The careful work j u s t presented has important clinical and physiological implications. The incidence of verying degrees of increased superior caval pressure, following the Glenn operation, is probably greater t h a n is commonly suspected. We have several times recognized this complication and have treated the cerebral manifestations in our patients with intravenously administered urea, at times with apparent benefit. We, also, use the upright position and we t r y to lower the severely elevated hematocrit readings preoperatively. However, I wish particularly to comment upon a death t h a t occurred. The patient was a boy who was temporarily improved after operation but, thereafter, his condition deteriorated and he died about 36 hours postoperatively. Autopsy disclosed a p a t e n t anastomosis where the rather small r i g h t pulmonary a r t e r y had been joined to the superior vena cava, b u t there was virtually total thrombosis of the smaller branches of the pulmonary artery, throughout the lung. This was especially well observed on the cut surface. I t appeared t h a t several rheologic factors might have contributed to the extensive thrombosis: (1) the unusually small size of the right pulmonary a r t e r y and its branches, providing poor run-off; (2) the relatively large volume of blood delivered by the superior vena cava, and (3) the increased blood viscosity due to polycythemia. Venous shunts are low pressure shunts a t best, and almost twice the usual pressure may be required to produce a given volume of flow with polycythemic blood as compared with normal or moderately anemic blood. One wonders to what extent occlusion occurs in the lung vascular bed in patients who nonetheless survive. Taking this problem to the experimental laboratory, Dr. Russell Cannon, of our resident staff, has found the incidence of thrombosis, in otherwise normal dogs, to be reduced b y either heparinization or t h e infusion of low molecular weight dextran, following the Glenn procedure. DR. W I L L I A M W. L. G L E N N , New Haven, Conn.—I certainly have enjoyed and appreciated the studies t h a t have been done by the Vanderbilt group, and I thoroughly agree with their main thesis that cerebral edema (following anastomosis of the superior vena cava to the right pulmonary artery) can and does occur in some animals and in some patients. I n experiments we did some time ago on animals we measured the venous pressures immediately after anastomosing t h e superior vena c a v a to t h e right pulmonary a r t e r y and found the average mean venous pressure in the superior vena cava in 55 animals to be 172 mm. of saline. This fell in the early postoperative period but, and as also stated by the authors, it never fell to normal. This has been our experience in patients also, although we have hesitated—as a m a t t e r of fact have avoided—measuring venous pressures in the superior vena cava immediately postoperatively. I n fact we do not do this for one month after operation for fear of precipitating thrombosis.
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DISCUSSION
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However, in general, the findings are similar: t h a t is, there is a persistent, though moderate, elevation in venous pressure. The factors t h a t may cause cerebral edema after superior vena cava-pulmonary artery anastomosis should be considered in all of these cases: (1) operative total occlusion of the superior vena cava during performance of the anastomosis (we believe t h a t total occlusion should be strictly avoided), (2) an increase in pulmonary vascular resistance due to long-standing pulmonary hypertension or persistent fetal characteristics of the pulmonary arterioles, and (3) a too small anastomosis of the superior vena cava to the right pulmonary artery, which is usually due to a small pulmonary artery. Although it may not be clear to you on this slide—here, for example, is a pulmonary artery of about 8 mm. in diameter. The lumen has been cut down to about 4 mm. by sutures; then the vessel has been anastomosed to the side of the ascending aorta. This is in a 4-year-old child with tricuspid atresia whose pulmonary artery was considered too small for a primary anastomosis to the superior vena cava. This is the same pulmonary a r t e r y 18 months later, now very much larger (2 cm. in diameter). The pressure in the right pulmonary artery is now 60 mm. H g versus 80 mm. Hg in the aorta. We separated the right pulmonary artery from the aorta and anastomosed it to the superior vena cava which lay just below. Fortunately, the pulmonary hypertension did not persist and the child made an uneventful recovery. (The venous pressure in the superior vena cava 2 months after operation was 160 mm. of saline.) This would appear to be a satisfactory method of managing the difficult problem of a small pulmonary a r t e r y in patients requiring a caval-pulmonary artery shunt. The third reason for a possible increase in pressure in the superior vena cava after anastomosis to the pulmonary artery is compression of the pulmonary vessels due either to atelectasis, or presence of fluid or air in the right pleural space. As an example, this slide shows the chest roentgenograms of a 7-month-old infant with tricuspid atresia, immediately postoperatively, after he developed atelectasis of the right upper lobe and a chylothorax. For a time he appeared to be in critical condition, with edema of the face and suffusion of the upper part of the body, but fortunately he recovered and the signs of obstruction to flow through the superior vena cava disappeared. This slide shows an angiocardiogram made in the same child 21 months postoperatively. He is now 28 months old. The anastomosis is widely patent and the flow of dye is into all parts of the lung. Incidentally, in this case there is no evident dilatation of the superior vena cava or constriction of the anastomosis. This has also been our experience in other patients undergoing this operation and suggests t h a t the anastomosis grows as the child grows.
C
Leon P. Woods,
and Harold A. Collins, M.D. (by invitiation),
by H. William
Scott, Jr., M.D., Nashville,
M.D.
Nashville,
Tenn.
Tenn.)
diversion of blood from the superior vena cava into the right pulmonary artery by anastomosis between the two vessels has been used successfully for surgical palliation in several congenital cardiac anomalies 3 ' 7 ' " characterized by impaired pulmonary blood flow. The procedure has special appeal in infants with tricuspid atresia. 2 In such patients a vena cava-pulmonary artery shunt may obviate the frequent occurrence of congestive failure following anastomosis of a systemic artery to a pulmonary artery. If anatomic considerations are excluded, the principal factor influencing function of a vena cava-pulmonary artery shunt is the pulmonary vascular resistance. Even when the pulmonary vascular resistance is assumed to be normal, facial edema and chylothorax are occasionally noted after operation. We recently encountered one infant who manifested a transient cerebral disturbance suggesting cerebral edema following performance of a vena cava-pulmonary artery anastomosis. A study was, therefore, undertaken to observe the changes in cerebrospinal fluid pressure following experimental complete shunting of superior vena caval blood into the right pulmonary artery. OMPLETE
METHOD
Unselected healthy mongrel dogs, weighing from 8 to 16 kilograms, were used for all experiments. Anesthesia was induced by the intravenous administration of pentobarbital (30 mg. per kilogram of body weight). Following the insertion of an endotracheal tube, respiration was maintained by a positive pressure respirator. The chest was opened through the right fifth intercostal space with the use of sterile technique. Side-to-end anastomosis of the superior vena From the Department of Surgery and the S. R. Light Laboratory for Surgical Research, Vanderbilt University School of Medicine, Nashville, Tenn. This investigation was supported in part by Research Grant No. H-5523 from the National Heart Institute, U. S. Public Health Service, and by the Middle Tennessee Heart Association. Read at the Forty-second Annual Meeting of The American Association for Thoracic Surgery a t St. Louis, Mo., April 16-18, 1962. 628
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cava to the right pulmonary artery was accomplished in essentially the manner described by Glenn.6 After completion of the anastomosis, the superior vena cava was ligated centrally. The thoracotomy incision was closed and residual air was aspirated from the thorax. No other special postoperative measures were employed except administration of antibiotics. Venous pressure and cerebrospinal fluid pressure were measured with a saline manometer immediately before operation and at periodic intervals postoperatively. Venous pressure was determined by puneture of the external jugular vein, and cerebrospinal fluid pressure was determined by direct cisternal puncture. Autopsy in all the animals who failed to survive or were sacrificed was performed. Particular attention was devoted to the anastomosis and the appearance of the brain.
VENOUS PRESSURE 1
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1
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PRE-SHUNTTIME
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— I
2H
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3H
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8H
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IOH I2H
POST-SHUNT TIME
Fig. 1. RESULTS
Of the 23 animals used, 19 were satisfactory for study. The remaining 4 were excluded because of insufficient data, thrombosis of the anastomosis with signs of severe superior vena caval obstruction, or traumatic cisternal punctures. In the immediate postoperative period there was a consistent rise in spinal fluid and venous pressures (Fig. 1). The average rise of cerebrospinal fluid pressure was 6.0 cm. of saline. At the same time, venous pressure increased an average of 8.6 cm. of saline above the preoperative value. Twenty-four hours after operation the cerebrospinal fluid pressure had risen further, to an average of 8.9 cm. of saline above the preoperative value, while venous pressure had risen 10.3 cm. of saline (Table I ) . TABLE I. AVERAGE POSTOPERATIVE E I S E IN SPINAL FLUID AND JUGULAR VENOUS (CENTIMETERS SALINE ABOVE PREOPERATIVE VALUES)
PRESSURE
POSTOPERATIVE TIME (HOURS)
SPINAL FLUID PRESSURE
JUGULAR VEIN PRESSURE
1 24 72+
6.0 8.9 6.4
8.6 10.3 8.8
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In the animals which survived beyond 24 hours, a gradual fall in cerebrospinal fluid and venous pressure was observed, but it remained definitely above the normal preoperative value for as long as 50 days (Fig. 2). Brain swelling, evidenced by an unusually tight fit within the cranial vault and flattening of the cortical gyri, was noted at autopsy in close correlation with the finding of increased spinal fluid pressure. Histologic sections of the brain showed vascular engorgement and petechial hemorrhage (Pig. 3). Pleural effusion was noted in only one animal. The long-term survivors appeared to be as bright and active as they had been preoperatively, and no evidence of cerebral deficiency was apparent.
Pre-Op.
I hr.
24hr.
48hr.
72hr.
96hr.
HOURS POSTOPERATIVE Fig. 2. DISCUSSION
The results of this study indicate that a uniform increase in pressure occurs in the cerebrospinal fluid and superior vena caval system following anastomosis of the superior vena cava to the right pulmonary artery in dogs. The increase in cerebrospinal fluid pressure was roughly proportional to the increase in venous pressure. Despite a tendency to decrease gradually, the cerebrospinal fluid pressure elevation persisted for prolonged periods. Although no cerebral disturbance was apparent, swelling of the brain was noted at autopsy in those animals failing to survive. It was not possible in this study to correlate mortality with the severity of cerebrospinal fluid pressure elevation. Although flow in the superior vena cava was not measured, all pressure determinations were obtained during similar basal conditions. It appears unlikely that significant increments in flow would occur under these circumstances. The increase in venous pressure is, therefore, almost certainly related to the greater resistance of the pulmonary vascular bed as contrasted with that of the right atrium. Under conditions of increased flow the venous pressure could be expected to increase to an even greater degree. Brecht and Matill 1 demonstrated, in acute experiments, that intracranial pressure is primarily dependent upon, and varies with, venous pressure. The deleterious effects of chronically elevated venous pressure were reported by Owens and associates8 who found that occlusion of the dural sinuses or cortical veins in monkeys produced vascular engorgement, cortical swelling, and elevated
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cerebrospinal fluid pressure. A more direct result of increased venous pressure may be the cerebral hemorrhage observed in brain sections in this study. Similar findings were recorded by Darbinyan and Krymskii 5 who found hyperemia and solitary foci of hemorrhage in the brains of 3 dogs in which superior vena cava-pulmonary artery shunt had been performed. The immediate increase in cerebrospinal fluid pressure after superior vena cava-right pulmonary artery shunt must certainly be due to venous distention within the craniospinal space with simple displacement of spinal fluid. If this were the only mechanism involved and if the usual homeostatic action between formation and resorption of cerebrospinal fluid were intact, adjustment of volume would be expected to take place with return of cerebrospinal fluid pressure
Fig. 3.
to normal in a matter of hours or days. The continued elevation can be explained in at least two ways: (a) increased formation or decreased resorption of cerebrospinal fluid, and (b) increased formation or decreased resorption of extracellular tissue fluid within the brain and cord, producing edema. The latter explanation is the more compatible with our finding of brains which tightly filled the cranial vault, but it may be that both mechanisms are involved. Starling 10 initially explained the conditions regulating the formation and absorption of extracellular tissue fluid. Although the colloid osmotic pressure of the plasma tends to hold water in the capillaries, fluid is forced through the wall of the arterial end of the capillary by the arterial blood pressure. Because venous pressure is lower than plasma osmotic pressure, fluid is drawn into the venous end of the capillary. A decrease in serum osmotic pressure or an in-
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crease in venous pressure tends to lessen the gradient which draws fluid into the capillary and produces edema. The clinical significance of this study lies in the recognition of a mechanism by which signs of cerebral dysfunction may occasionally be produced following superior vena cava-right pulmonary artery shunt. Cerebral complications following this operation have rarely been described, but minor degrees of cerebral disturbance may go unrecognized. It is conceivable that a more severe degree of cerebral edema could cause death, particularly during infancy when the pulmonary vascular resistance is at its highest level. Dammann and Perenoz 4 found the ratio of lumen to wall thickness in small muscular arteries of the lungs low at birth with a gradual increase during the first few months of life. Rudolph 9 showed that the calculated pulmonary vascular resistance was high immediately after birth, fell rapidly during the first month of life, and continued in a significant decline until one year of age. It is, thus, possible that performance of a superior vena cava-right pulmonary artery shunt during infancy can result in significant venous hypertension and cerebral symptoms. While other causes are undoubtedly partially responsible for the high mortality in infants following superior vena cava-right pulmonary artery shunt, cerebral edema may be an additional factor. Insufficient data exist to warrant any absolute recommendations concerning the prevention and treatment of cerebral complications following performance of a superior vena cava-right pulmonary artery shunt. It is likely that intracranial pressure increases and cerebral edema will frequently be of insufficient magnitude to need treatment or even be detected. Certainly the suggestion of Glenn regarding the use of a semi-upright position postoperatively is worthwhile. In addition, the maintenance of optimal respiratory ventilation is advantageous since carbon dioxide retention causes increased intracranial pressure. In the presence of obvious cerebral edema an attempt to increase plasma osmotic pressure by the administration of hypertonic substances would probably be of value. A more favorable balance between the production and resorption of tissue fluid might, thus, be accomplished. Although we have had no personal experience with this maneuver, it has been of value in other situations associated with cerebral edema. SUMMARY
1. Side-to-end anastomosis between the superior vena cava and right pulmonary artery was performed in 19 dogs. A definite increase of cerebrospinal fluid and superior vena cava pressure was observed in all the animals. In the immediate postoperative period, the average of cerebrospinal fluid pressure was 6.0 cm. of saline and 24 hours later was 8.9 cm. of saline. The average rise of superior vena cava pressure immediately after operation was 8.6 cm. of saline and 24 hours later was 10.3 cm. of saline. Both cerebrospinal fluid and superior vena cava pressures gradually fell after 24 hours but remained definitely above preoperative values for as long as 50 days.
DISCUSSION
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2. Brain swelling evidenced by an unusually tight fit of the brain within the cranial vault and flattening of the cortical gyri was observed, as well as vascular engorgement and petechial hemorrhages. 3. The semi-upright position, optimal ventilation, and an attempt to increase the plasma osmotic pressure may be beneficial postoperative measures. REFERENCES 1. Brecht, F . C , and Matill, P . M.: Studies on the Cerebrospinal Fluid. VI. A Study of the Effects of Tissue Extracts, Am. J . Physiol. 5 1 : 126, 1920. 2. Bopp, E. K., Larsen, P . B., Caddell, J . L., Patrick, J . E., Hipone, F . A., and Glenn, W. W. L.: Surgical Considerations for Treatment of Congenital Tricuspid Atresia and Stenosis: With Particular Reference to Vena Cava-Pulmonary Artery Anastomosis, J.
THORACIC SURG. 4 3 :
97,
1962.
3. Bakulev, A. N., and Kolesnikov, S. A.: Anastomosis of Superior Vena Cava and Pulmonary Artery in the Surgical Treatment of Certain Congenital Defects of the Heart, J .
THORACIC SURG. 3 7 :
693,
1959.
4. Dammann, J . F., Jr., and Ferenoz, C.: The Significance of the Pulmonary Vascular Bed in Congenital Heart Disease. I. Normal Lungs. I I . Malformations of the Heart in Which There Is Pulmonary Stenosis, Am. H e a r t J . 52: 7, 1956. 5. Darbinyan, T. M., and Krymskii, L. D.: Morphologic Changes in Heart, Lungs, and Brain After Experimental Cavo-Pulmonary Anastomosis, Bull. Exper. Biol. & Med. (USSR) 4 7 : 105, 1959. 6. Glenn, W. W. L., and Patino, J . F . : Circulatory Bypass of the Right Heart. I . Preliminary Observations on the Direct Delivery of Vena Caval Blood Into the Pulmonary Arterial Circulation. Azygos Vein-Pulmonary Artery Shunt, Yale J . Biol. 27: 147, 1954. 7. Nuland, S. B., Glenn, W. W. L., and Guilfoil, P . H . : Circulatory Bypass of the Eight H e a r t . I I I . Some Observations on Long-Term Survivors, Surgery 43: 184, 1958. 8. Owens, G., Stahlman, G., Capps, J . M., and Meirowsky, A. M.: Experimental Occlusion of Dural Sinuses, S. Forum 8: 521, 1957. 9. Eudolph, A. M.: Normal and Abnormal Eespiration in Children. Report of the 37th Boss Conference on Pediatric Research, edited by S. J. Fomon, Ross Laboratories, Columbus p. 65, 1961. 10. Starling: The Fluid of the Body, Chicago, 1909, W. T. Keener Company. 11. Weinberg, M., Jr., Bicoff, J . P., Agustsson, M. H., Steiger, A., Gasul, B . M., Fell, E. H., and Laun, L. L.: Surgical Palliation in Patients With Ebstein's Anomaly and Congenital Hypoplasia of the Right Ventricle, J . THORACIC SURG. 40: 310, 1960.
DISCUSSION (PAPERS ANKENEY
BY
HICKMAN
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KENNEDY
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SHAW
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CONNOLLY BILGUTAY
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AND T H E I R ASSOCIATES)
DR. J O H N R. DERRICK, Galveston, Texas.—Thank you for the opportunity to discuss the very interesting paper by Drs. Mortensen and Hickman. I might give you the background of the work we have done in attempting to evaluate clamps. Galveston is 50 miles from Houston. When we got there we had to use the vascular clamps on autopsy material because of the very excellent work being done in Houston. However, we did clamp the aorta of some rabbits and fed them low and high cholesterol diets. The first slide demonstrates the area traumatized by clamping, and within 6 months there was a verj' noticeable change in the intima and subintimal fibrosis. In t r y i n g to evaluate w h a t the clamps would do with varying degrees of arteriosclerosis, we put different types of clamps on in this fashion.
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This slide demonstrates the tears one would see in some of the atheromatous material and calcifications with the various types of clamps; this varied with the amount of arterial sclerosis and degeneration of the aorta. At one time, we had a very disastrous hemorrhage occur in a patient when a clamp was applied, so we have since adopted the technique of t i t r a t i n g the patient's blood pressure (those t h a t have high blood pressure) down to a lower level upon applying occlusion clamps, and, in those with severe sclerotic involvement, we use t h e buffer clamp above the sharp-pointed edges of the vascular clamps to prevent the pulsations of the aorta against the vascular clamp from tearing the vessel. DR. A. ROBERT CORDELL, Winston-Salem, N. C — I would like to comment on the excellent paper by Dr. Ankeney and his group, which dealt with t h e aspect of peripheral vascular resistance under varying degrees of perfusion. We have just completed a series on approximately 18 animals wherein we measured t h e total peripheral vascular resistance under conditions of normothermia, having obtained t h e flow r a t e for the perfusion by means of electromagnetic probes placed on the ascending aorta. The average of these figures taken prior to bypass determined our flow rate, and under these conditions we found essentially the same t h i n g Dr. Ankeney has with the measurement of venous How rates. Total peripheral vascular resistance does not change during a period of perfusion of this length with these conditions being set up. I think this is very worth-while work and the group working with Dr. Ankeney should be commended for their approach to this study. DR. J O H N W. K I R K L I N , Rochester, Minn.—I, too, would like to comment briefly on Dr. Ankeney's paper, perhaps on a little different aspect of it. Certainly the d a t a in this paper are so extensive and the implications so profound in some ways t h a t we will all have to study this in the evening a t home before we fully understand it. However, I think the implications, particularly with regard to homologous blood reactions, are extremely important, and I believe Dr. Ankeney has again done us a great service in bringing this important subject to our attention. My own attention was called first to the importance of homologous blood reactions by Dr. Gadboys and Dr. L i t w a k in Miami, Florida; Dr. L i t w a k alluded to this work a bit yesterday. I think on the basis of this very solid foundation of d a t a by Dr. Ankeney concerning t h e response of t h e dog to homologous blood, we have now, somehow, to incorporate this knowledge of homologous blood reactions into our general concepts of the reactions of man to extracorporeal circulation. Perhaps this is one of the most important contributions to such concepts t h a t has emerged in the last few years. After t a l k i n g with Dr. Gadboys and Dr. L i t w a k we began to look at this a little in man, and we have a little information t h a t suggests t h a t , among the other manifestations of this homologous blood reaction, perhaps there is a depression of myocardial function. I think we are all indebted to Dr. Ankeney for his superb d a t a and for bringing this important subject again to our attention. DR. HOWARD L. GADBOYS, Miami, F l a — I would like to t h a n k t h e Association for the privilege of discussing these papers and also Dr. Kirklin for his very kind comments. I think the paper by Dr. Sloan yesterday and those by Drs. Ankeney and Connolly today have touched upon some very exciting facets of extracorporeal circulation in general. We are indebted to Dr. James Dow for pointing out the presence of a syndrome of shock from homologous blood exchange in dogs in 1956. This phenomenon occurs in dogs with simple exchange of homologous blood, without requiring a heart-lung machine or anything other t h a n a reservoir connected to an arteriovenous fistula. As you can see from the slide, when the A-V fistula is opened no appreciable deviations occur until homologous blood is added to the circuit. At this point there soon may
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ensue precipitous changes, characterized by portal hypertension, hepatic engorgement, fall of t h e buffer base, venous oxygen unsaturation, and, frequently, systemic arterial hypotension. Closing the reservoir fistula does not appreciably alter the situation. If one observes the isotopieally obtained circulating blood volumes, even though there have been no external volumetric changes, there may be marked systemic hypovolemia—the volumes on this slide range from 1,438 ml. to 534 ml. If one then gives blood to restore the systemic pressure to normal, the blood balance goes up. The blood volume may not r e t u r n to normal despite t h e fact t h a t there is now a blood balance considerably in excess of the preoperative figure. Consequently t h e weight changes t h a t occur do not reflect the alterations in circulating blood volume. An identical phenomenon is apparent in human beings. This slide is a compilation of d a t a obtained from a number of p a t i e n t s who have undergone extracorporeal circulation. Following perfusion, the patients have lost both plasma and red cells from the isotopieally measurable blood volume. Many of these are patients who "come off the p u m p " in a hypotensive state, even though one known t h a t the blood balance is at, or above, control levels. One can establish the effects of different volumes of homologous blood introduced into the patients by comparing a group of patients undergoing extracorporeal circulation utilizing large priming volumes with those having extracorporeal circulation employing small priming volumes (as exemplified b y left h e a r t bypass). An interesting phenomenon may be observed. When one turns the pump on and simply does a rapid exchange transfusion of a large volume of homologous blood for a brief period, followed by discontinuance of perfusion, the patients may go into shock. In other words, if one turns the pump on and turns the pump off, maintaining extracorporeal volumes constant, one often finds t h a t these patients will develop severe hypovolemia. This does not occur with left heart bypass since only minimal amounts of homologous blood are used. I would like, therefore, to add a word of caution about the use of a reservoir w i t h left h e a r t bypass since this may necessitate increasing the amount of homologous blood utilized. DR. ROBERT J. SCHRAMEL, New Orleans, La.—Last year I reported on prepulmonary bypass with the use of a rotating disk oxygenator and a veno-venous system of perfusion. With this we were able to get p r e t t y good survival in dogs and keep them alive. However, on autopsying surviving dogs the next day, and in all dogs who failed to survive, there were extensive lesions in the lungs. This slide is a low-power magnification and indicates t h a t the major difficulty here is extensive hemorrhage and atelectasis. This slide indicates t h a t the source of this hemorrhage is damage to t h e blood vessel wall. As you can see, this blood vessel wall is disrupted a t this point and is in the process of dissolution here. There is extensive hemorrhage. I n evaluating this further, we have used varying gas mixtures in the oxygenator, and some degree of this sort of thing always occurs but is less as you cut down on the amount of oxygen fed into the oxygenator. However, if the oxygenator and reservoirs are completely removed from the circuit, there are no lesions in the lungs. The animals survive and do very well. These are all standard 6 hour perfusions. This occurs whether the system is primed with dextran or with homologous blood. DR. A R T H U R V I N E B E R G , Montreal, Quebec.—The paper by Drs. Bilgutay and Lillehei is very interesting. I am pleased to see that they use the Ivalon sponge procedure, which we reported a few years ago. I would suggest to them t h a t it would be interesting if they would lower their catheter in t h e aorta a little f a r t h e r down so t h a t it is in t h e descending aorta, and inject
636
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their dye in this region. By so doing, they will get a much b e t t e r filling of the sponge. We have done this in animals, but, as yet, not in man. Radiopaque dye injected into the descending aorta in t h e animal shows many mediastinal vessels going toward the heart. In addition, the Ivalon sponge appears to become opacified. The outline, shown by cineangiography in the case reported by the authors after an Ivalon sponge operation, was most interesting because it is very similar to t h a t which we have seen in angiographic studies made in our animals. I t would be worthwhile if studies could be carried out to t r y and show rilling of the myocardium from the left ventricular lumen. This has been done by us in animals, and we have found evidence which indicates t h a t the Ivalon sponge procedure tends to make the heart siphon blood from the left ventricular lumen into the myocardium, as well as from the pericardial vessels. This technique of angiocardiography appears to be very interesting, and I congratulate the speakers. DR. J A M E S D. HARDY, Jackson, Miss.-—The careful work j u s t presented has important clinical and physiological implications. The incidence of verying degrees of increased superior caval pressure, following the Glenn operation, is probably greater t h a n is commonly suspected. We have several times recognized this complication and have treated the cerebral manifestations in our patients with intravenously administered urea, at times with apparent benefit. We, also, use the upright position and we t r y to lower the severely elevated hematocrit readings preoperatively. However, I wish particularly to comment upon a death t h a t occurred. The patient was a boy who was temporarily improved after operation but, thereafter, his condition deteriorated and he died about 36 hours postoperatively. Autopsy disclosed a p a t e n t anastomosis where the rather small r i g h t pulmonary a r t e r y had been joined to the superior vena cava, b u t there was virtually total thrombosis of the smaller branches of the pulmonary artery, throughout the lung. This was especially well observed on the cut surface. I t appeared t h a t several rheologic factors might have contributed to the extensive thrombosis: (1) the unusually small size of the right pulmonary a r t e r y and its branches, providing poor run-off; (2) the relatively large volume of blood delivered by the superior vena cava, and (3) the increased blood viscosity due to polycythemia. Venous shunts are low pressure shunts a t best, and almost twice the usual pressure may be required to produce a given volume of flow with polycythemic blood as compared with normal or moderately anemic blood. One wonders to what extent occlusion occurs in the lung vascular bed in patients who nonetheless survive. Taking this problem to the experimental laboratory, Dr. Russell Cannon, of our resident staff, has found the incidence of thrombosis, in otherwise normal dogs, to be reduced b y either heparinization or t h e infusion of low molecular weight dextran, following the Glenn procedure. DR. W I L L I A M W. L. G L E N N , New Haven, Conn.—I certainly have enjoyed and appreciated the studies t h a t have been done by the Vanderbilt group, and I thoroughly agree with their main thesis that cerebral edema (following anastomosis of the superior vena cava to the right pulmonary artery) can and does occur in some animals and in some patients. I n experiments we did some time ago on animals we measured the venous pressures immediately after anastomosing t h e superior vena c a v a to t h e right pulmonary a r t e r y and found the average mean venous pressure in the superior vena cava in 55 animals to be 172 mm. of saline. This fell in the early postoperative period but, and as also stated by the authors, it never fell to normal. This has been our experience in patients also, although we have hesitated—as a m a t t e r of fact have avoided—measuring venous pressures in the superior vena cava immediately postoperatively. I n fact we do not do this for one month after operation for fear of precipitating thrombosis.
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However, in general, the findings are similar: t h a t is, there is a persistent, though moderate, elevation in venous pressure. The factors t h a t may cause cerebral edema after superior vena cava-pulmonary artery anastomosis should be considered in all of these cases: (1) operative total occlusion of the superior vena cava during performance of the anastomosis (we believe t h a t total occlusion should be strictly avoided), (2) an increase in pulmonary vascular resistance due to long-standing pulmonary hypertension or persistent fetal characteristics of the pulmonary arterioles, and (3) a too small anastomosis of the superior vena cava to the right pulmonary artery, which is usually due to a small pulmonary artery. Although it may not be clear to you on this slide—here, for example, is a pulmonary artery of about 8 mm. in diameter. The lumen has been cut down to about 4 mm. by sutures; then the vessel has been anastomosed to the side of the ascending aorta. This is in a 4-year-old child with tricuspid atresia whose pulmonary artery was considered too small for a primary anastomosis to the superior vena cava. This is the same pulmonary a r t e r y 18 months later, now very much larger (2 cm. in diameter). The pressure in the right pulmonary artery is now 60 mm. H g versus 80 mm. Hg in the aorta. We separated the right pulmonary artery from the aorta and anastomosed it to the superior vena cava which lay just below. Fortunately, the pulmonary hypertension did not persist and the child made an uneventful recovery. (The venous pressure in the superior vena cava 2 months after operation was 160 mm. of saline.) This would appear to be a satisfactory method of managing the difficult problem of a small pulmonary a r t e r y in patients requiring a caval-pulmonary artery shunt. The third reason for a possible increase in pressure in the superior vena cava after anastomosis to the pulmonary artery is compression of the pulmonary vessels due either to atelectasis, or presence of fluid or air in the right pleural space. As an example, this slide shows the chest roentgenograms of a 7-month-old infant with tricuspid atresia, immediately postoperatively, after he developed atelectasis of the right upper lobe and a chylothorax. For a time he appeared to be in critical condition, with edema of the face and suffusion of the upper part of the body, but fortunately he recovered and the signs of obstruction to flow through the superior vena cava disappeared. This slide shows an angiocardiogram made in the same child 21 months postoperatively. He is now 28 months old. The anastomosis is widely patent and the flow of dye is into all parts of the lung. Incidentally, in this case there is no evident dilatation of the superior vena cava or constriction of the anastomosis. This has also been our experience in other patients undergoing this operation and suggests t h a t the anastomosis grows as the child grows.