Groth, CG

Halgrimson, CG

Martineau, GL

Palmer, WM

Pappas, G

Penn, I

Starzl, TE

PubMed

Name not available

Hemodynamic alterations caused during orthotopic liver transplantation in humans

D-Scholarship@Pitt

Reprinted from SCRGEllY, St. Louis Vol. 70, No.6, Pages 872-875, December, 1971 (Printed in the ll. S. A.) (Copyright ® 1971 b>' The C. V. ?[osby Company) Hemodynamic alterations orthotopic liver transplantation tn humans DU<ing mthotopic livcc t<ao'pl=taLion in normal dogs, it is necessary, at the time that the portal vein and inferior vena cava are cross-clamped, to shunt the venous return from these systems back to the heart in order to prevent cardiovascular collapse.!' 4 In man, who is probably naturally endowed with a richer collateral circulation and who has additional venous pathways secondary to liver disease, this has not been necessary,3 and our clinical impression has been that the interruption of venous return has been rea-sonably well tolerated. The present study was done to quantitate the changes in hemodynamics in six patients during orthotopic liver transplantation. To our knowledge, this kind of information has not been previously reported. METHODS Hemodynamic measurements were per-formed on six patients (Table I) who under-went hepatic transplantation. Two were chil-Aided by research grants from the Veterans Adminis-tration, by Grants No. RR·()()()51 and RR-00069 from the General Clinical Research Centers Program of the Division of Research Resources, National Institutes of Health, and by Grants No. AI-10176-01, AI-AM-OSn9S, AM-07772, and HE-09110 of the United States Public Health Service. Presented at the Twenty.fifth Annual Meeting of the Society for Va:-;cular Surgery, Philadelphia, Pa" June 18-19, 1971. 872 SURGERY December, 1971 caused during GEORGE PAPPAS, M.D. WILLIAM M. PALMER, M.D. GERARD L. MARTINEAU, M.D. ISRAEL PENN, M.D. CHARLES G. HALGRIMSON, M.D. CARL G. GROTH, M.D. THOMAS E. ST ARZL, M.D. DENVER, COLO. From the Department of Surgery, University of Colorado School of Medicine, and the Denver Veterans Administration Hospital dren, both aged 312 years, with biliary atre-sia. Two were adolescents (aged 15Y2 and 16 years), of whom one had Wilson's disease and end-stage cirrhosis and the other had chronic aggressive hepatitis with hepatic failure. The other two patients were adults, both 47 years old, with Laennec's cirrhosis (Table I). Following induction of anesthesia, catheters were inserted into a radial artery and superior vena cava via a peripheral vein to monitor arterial and central venous pressures and to perform cardiac output studies. Serial hemo-dynamic measurements were made before, during, and following hepatic transplanta-tion. Cardiac outputs were determined with the use of the dye-dilution technique (cardio-green) and an output computer.* Other hemodynamics studies included mean arterial blood pressure, central venous pressure, heart rate, stroke volume, and peripheral vascular resistance. These observations were made se-quentially (Fig. 1) as follows: (1) before or during laparotomy; (2) during dissection of the recipient's liver; (3) shortly after cross-clamping the inferior vena cava, portal vein, and hepatic artery (early anhepatic phase); (4) just before revascularization of the new liver (late an hepatic phase); (5) approximately one hour later; and (6) sev--::Lcxington Instruments Corp., Waltham, Mass. Vol. 70, No.6, pp. 872-875 Volume 70 Number 6 Table I. Liver recipients Age Date of Orthotopic liver transplantation 873 Blood Replace. Fluid re-Ascites Loss ment placement Patient (yr.) Disease operation (c. c.) (c. c.) (c. c.) (c. c.) E. S. 47 Laennec's cirrhosis 1/16/70 5,000 6,700 7,500 1,500 S.N. 30: Biliary atresia 9/19/70 Little 3,750 4,000 5,700 K. p. 3y~ Biliary atresia 9/22/70 Little 1,500 1,750 2,750 P.P. 47 Laennec's cirrhosis 10/ 8/70 13,000 6,500 6,500 13,700 C.E. 16 Chronic aggressive hepa- 2/27/71 10,000 8,600 10,000 15,900 titis (cirrhosis) G.W. 150: Wilson's disease (cirrhosis) 3/23/71 Little 4,000 3,800 4,800 eral hours after transplantation with the pa-tient awake. During the operation, fluid and blood losses and changes in electrolytes, acid-base profile, and blood sugar levels were ap-propriately managed. RESULTS Hemodynamic changes before, during, and following hepatic transplantation are shown in Figs. 1 through 4. Alterations in hemo-dynamics became apparent before any of the vessels were clamped; these occurred while the host liver was being mobilized. At times, marked displacement of the organ was neces-sary with resultant interference with venous return. During the anhepatic phase (with clamping of the portal vein and inferior vena cava), the cardiac index, stroke volume in-dex, and mean arterial' pressure fell. The maximum mean fall in cardiac index and stroke volume amounted to 43 and 39 per-cent, respectively, whereas the average fall in mean arterial pressure was 18 percent (Figs. 1 through 3). Simultaneously, the peripheral vascular resistance rose by 71 per-cent (Fig. 4), but the pulse rate rose only slightly (four percent) . Following revascularization of the new liver and during the immediate postoperative period, hemodynamic alterations reverted toward pretransplantation levels. Central venous pressure did not change significantly during the operation. One patient, an extremely ill child (Patient S. N.) had an initial cardiac index of 1.3 L. per minute per square meter, which fell to 0.7 L. per minute per square meter during 4 N ~ " 3 Z ~ " 2 (J) 0:: W I--.J ---- ANHEPATIC PHASE ~ E.S. ~::. ~'Ke ~ ~~~~!-r ...-C.E. :~~------ ~ ----::::----- '\ S.N. ~------O~~--r---~--~--~~~ o 234 HOURS 13-15 Fig. 1. Cardiac indices measured before, during, and following orthotopic liver transplantation in six patients. Note the reduction during the an-hepatic phase when the inferior vena cava and portal vein were cross-clamped. The indices re-turned to prehepatectomy levels following revas-cularization of the new liver. the anhepatic phase. During revascularization of the new liver, cardiac arrest occurred. This was immediately corrected by external car-diac massage, blood replacement, and ad-ministration of inotropic agents. DISCUSSION During orthotopic liver transplantation in the dog, interruption of portal venous and inferior caval return to the heart produces cardiovascular collapse. To obviate this com-plication, it is necessary to shunt blood from both venous systems back to the heart. This can be accomplished with two separate bypass catheters.1 Alternatively, a side-to-side anas-tomosis may be constructed between the in-ferior vena cava and superior mesenteric vein, 874 Pappas et al. 60 50 C\J ~ 40 ~ <! 30 W £l) 20 ....... u u 10 ---- ANHEPATIC PHASE IE' ~~:: _________ S.N ~--~--~--~--~~~ o 2 3 4 13-15 HOURS Fig. 2. The changes in stroke volume index in the same six patients paralleled the changes in cardiac index seen in Fig. 1. ---- ANHEPATIC PHASE 110 100 90 80 en 70 I 60 E 50 E 40 30 20 10 0 ~~--~---r--~--~~~ o 2 3 4 13-15 HOURS Fig. 3. In four patients, the mean arterial pressure fell during the anhepatic phase, whereas it rose in two (G. W. and C. E.). There was an average fall in mean arterial pressure of 18 percent during the anhepatic phase. and then a single external Silastic shunt is placed between the external iliac and jugular veins to decompress both venous systems dur-ing the anhepatic phase.4 The absolute necessity for effective venous decompression in the dog was erroneously extrapolated to be a mandatory technical condition in the first trials of orthotopic liver transplantation in man, and, in our initial clinical experience, similar shunts to those used in the dog were employed. The bypasses were cumbersome and may have contributed to an unacceptably high incidence of post-operative thromboembolism.3 In all later cases, the portal vein and inferior vena cava were cross-clamped without the aid of any N ~ I U"l I E u I U W (f) I W Z >-Cl 5500 5000 4500 4000 3500 3000 2500 2000 1500 1000 500 Surgery December 1971 ---- ANHEPATIC PHASE '-r--""""--'--"'T""""-,..--j I--r-o 2 3 4 13-15 HOURS Fig. 4. The peripheral vascular resistance rose during the anhepatic period but returned to pre-existing levels following the transplantation. shunts.3 It was found that the procedure was reasonably well tolerated, probably because man has inherently richer collateral veins in the venous system. In addition, patients with chronic liver disease have an even greater anastomotic capability, presumably as a re-sult of an increase in size and number of such collateral veins, a concept that has been shown by Picache and associates2 to pertain in dogs as well. In the patients during vena caval and portal cross-clamping, a slight duskiness of the intestine has been noted, more so when liver replacement was for hepatoma than when it was for cirrhosis.3 At the same time, a fall in blood pressure was usually noted, which returned to pre-existing levels after the clamps were released. In one particularly interesting case, a child had liver replace-ment for biliary atresia with essentially no hemodynamic changes. He required a second orthotopic transplant 68 days later. At the second operation, there was very severe hypo-tension during the anhepatic phase, pre-sumably because of involution of pre-existing collaterals in the intervening two months.3 In all the presently reported patients, portal hypertension and extensive collateral veins were present. Nevertheless, alterations in he-modynamics occurred before the cross-clamp-ing of the venous return from the lower half of the body. At that time, the recipient's liver was being prepared for excision, and marked displacement of the organ was often required. The altered hemodynamics were probably Volume 70 Number 6 related to partial interruption of venous re-turn during liver retraction. Moreover, the cardiac output, stroke volume, and mean ar-terial blood pressure fell even more during occlusion of the portal vein and inferior vena cava; there was a concomitant increase in peripheral vascular resistance. Following re-vascularization, these potentially serious changes returned to prehepatectomy levels. During the anhepatic phase, fluid and blood replacement were given in excess of loss in anticipation of volume depletion incurred '.vith revascularization of the new liver. This may be responsible for less noticeable changes in hemodynamics during the late anhepatic phase. Cardiac arrest in one patient occurred during revascularization of the new liver, but with successful resuscitation. The incident could probably have been avoided if sufficient blood replacement had been furnished prior to revascularization. The findings of this study indicate that significant hemodynamic alterations occur in clinical orthotopic transplantation during in-terruption of venous return from the portal vein and lower half of the body. However, no permanent harmful effects are produced if this period is kept short. I t need not be a particularly dangerous part of the opera-tion, provided that there is careful monitor-ing and appropriate treatment. SUMMARY In clinical orthotopic transplantation of the liver, alterations in cardiohemodynamics occUlTed during interruption of the portal vein and inferior vena cava. The cardiac output, stroke volume, and mean arterial pressure fell by 43, 39, and 18 percent, re-spectively, with a concomitant rise in periph-eral vascular resistance (71 percent) and only a slight increase in heart rate (four percent) during the anhepatic phase. These changes returned to prehepatectomy levels following revascularization of the new liver. Although hemodynamic alterations occur during liver transplantation, with careful monitoring and appropriate therapy, no permanent harmful effects are produced. Orthotopic liver transplantation 875 REFERENCES I. Moore, F. D., Wheeler, H. B., Demissianos, H. V., Smith, L. L., Balankura, 0., Abel, K., Greenberg, J. B., and Dammin, G. J.: Experi-mental whole-organ transplantation of the liver and of the spleen, Ann. Surg. 152: 374, 1960. 2. Picache, R. S., Kapur, B. M. L., and Starzl, T. E.: The effect of liver disease on the need for venous decompression during the anhepatic phase of canine orthotopic liver transplanta-tion, SURGERY 67: 319, 1970. 3. Starzl, T. E. (with the assistance of Putnam, C. W.): Experience in hepatic transplantation, Philadelphia, Pa., 1969, W. B. Saunders Com-pany. 4. Starzl, T. E., Kaupp, H. A., Brock, D. R., Lazarus, R. E., and Johnson, R. V.: Recon-structive problems in canine liver homotrans-plantation with special reference to the post-operative role of hepatic venous flow, Surg. Gynecol. Obstet. 111: 733,1960. DISCUSSION Dr. Robert West Hopkins (Providence, R. 1.). I have just one quick question. Looking at the slides, it occurred to me that the major fall in cardiac output occurred prior to the anhepatic phase. It was not entirely clear to me whether the fall of 40 percent during the anhepatic phase referred to the comparison with the initial measure-ments or with the measurements immediately prior to clamping the various veins. In other words, are we sure that the fall in cardiac output was due to the crooo-cJamping or was it perhaps related also to anesthesia and the operative procedure itself? Dr. Worthington G. Schenk, Jr. (Buffalo, N. Y.). The same sort of question occurred to me. It looked as though this drop might be due to manipulation, and, if so, those of us who manipu-late the liver for reasons other than transplantation would like to know how to prevent a 50 percent drop of the cardiac output during manipulation. Dr. George Pappas (closing). The drop in car-diac output during the early an hepatic phase was compared with control levels, that is, those mea-sured immediately following the induction of anesthesia. Hemodynamic determinations during mobilization of the liver were intentionally made while marked displacement of the liver was present and probable partial interruption of venous return. Anesthesia can well alter the cardiohemodynamics. We believe that the changes noted are real in that, following revascularization of the new organ, the hemodynamics returned to control levels with-out adjusting, to any appreciable degree, the anesthetic agents used. 

Hemodynamic alterations caused during orthotopic liver transplantation in humans.

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Hemodynamic alterations caused during orthotopic liver transplantation in humans.

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