2218 TRANSPLANTATION 17. Memon MA, Nicholson CM, Clayton-Smith J. Spontaneous aortic rupture in a 22-year-old. Postgrad Med J 1996; 72 (847): 311. 18. Ringe B, Pichlmayr R, Lubbe N, Bornscheuer, Kuse E. Total hepatectomy as temporary approach to acute hepatic or primary graft failure. Transplant Proc 1988; 20 (1): 552. 19. Ringe B, Lubbe N, Kuse E, Frei U, Pichlmayr R. Management of emergencies before and after liver transplantation by early total hepatectomy. Transplant Proc 1993; 25 (1): 1090. 20. Ringe B, Lubbe N, Kuse E, Frei U, Pichlmayr R. Total hepatectomy and the liver transplantation as two-stage procedure. Ann Surg 1993; 218 (1): 3. 21. Ringe B, Pichlmayr R. Total hepatectomy and liver transplantation: a life-saving procedure in patients with severe hepatic trauma. Br J Surg 1995; 82: 837. 22. Rozga J, Podesta L, Lepage E, et al. Control of cerebral edema by total hepatectomy and extracorporeal liver support in fulminant hepatic failure. Lancet 1993; 2: 898. 23. So SKS, Barteau JA, Perdrizet GA, Marsh JW. Successful re- 24. 25. 26. 27. Vol. 69, No. 10 transplantation after a 48-hour anhepatic state. Transplant Proc 1993; 25 (2): 1962. Henderson A, Webb I, Lynch S, Kerlin P, Strong R. Total hepatectomy and liver transplantation as a two-stage procedure in fulminant hepatic failure. Med J Aust 1994; 161: 318. Hammer GB, So SKS, Al-Uzri A, et al. Continuous venovenous hemofiltration with dialysis in combination with total hepatectomy and portocaval shunting. Transplantation 1996; 62 (1): 130. Griffith BP, Shaw Jr BW, Hardesty RL, Iwatsuki S, Bahnson HT, Starzl TE. Venovenous bypass without systemic anticoagulation for transplantation of the human liver. Obstet Gynecol 1985; 160: 271. Lin PJ, Jeng LB, Chen RJ, Kao CL, Chu JL, Chang CH. Femoroarterial bypass using Gott shunt in Liver transplantation following severe hepatic trauma. Int Surg 1993; 78(4): 295. Received 26 April 1999. Accepted 23 October 1999. EMERGENCY PORTACAVAL SHUNT FOR CONTROL OF HEMORRHAGE FROM A PARENCHYMAL FRACTURE AFTER ADULT-TO-ADULT LIVING DONOR LIVER TRANSPLANTATION MITCHELL AMADEO MARCOS,1,2 ROBERT A. FISHER,1 JOHN M. HAM,1 ANN T. OLZINSKI,1 L. SHIFFMAN,3 ARUN J. SANYAL,3 VELIMIR A.C. LUKETIC,3 RICHARD K. STERLING,3 AND MARC P. POSNER1 Division of Transplantation, Department of Surgery, and Section of Hepatology and Liver Transplantation, Division of Gastroenterology, Department of Medicine, Medical College of Virginia, Virginia Commonwealth University, Richmond, Virginia, 23219 As more adults undergo transplantation with partial liver grafts, the unique features of these segments and their clinical significance will become apparent. A patient presented with life-threatening hemorrhage from an iatrogenic laceration to a right lobe graft 11 days after transplantation. The creation of a portacaval shunt effectively controlled the bleeding, allowing more elective replacement of the organ with another right lobe graft. The regeneration process combined with increased portal blood flow and relative outflow limitation may have set the stage for this complication. Any disruption of the liver parenchyma during transplantation should be securely repaired and followed cautiously. Portacaval shunting is an option for controlling hemorrhage from the liver in transplant recipients. The timely availability of a second organ was likely the ultimate determinant of survival for this patient. As the organ shortage becomes more critical, adult-to-adult living donor liver transplantation is emerging as a reasonable alternative to conventional cadaveric transplantation, but there are some considerations unique to partial grafts. 1 Division of Transplantation, Department of Surgery. Address correspondence to: Amadeo Marcos, MD, Division of Transplantation, Medical College of Virginia, P.O. Box 980057, Richmond, Virginia 23298-0057. 3 Section of Hepatology and Liver Transplantation, Division of Gastroenterology, Department of Medicine. 2 These grafts are considerably smaller than the native liver and, as a result, a period of rapid regeneration begins immediately after surgery (1). Regeneration is necessary for the success of this technique, but the implications for management of donors and recipients are not yet fully understood. The assurance of adequate outflow from liver grafts has been recognized as critical for as long as these procedures have been performed. The consequences of limited outflow vary in severity and range from mild graft dysfunction to acute hepatic failure (2). Portal blood flow is higher after liver transplantation, and the relative increase is likely further exaggerated by the comparatively small size of a right lobe graft (3). Outflow limitation may then be of more significance than it would be for a larger graft. Preservation of significant accessory hepatic veins with anastomosis to the inferior vena cava has been recently advocated as a means of augmenting outflow from these grafts (4). Bleeding after whole-organ liver transplantation is a known complication but is generally readily controlled and without serious sequelae. The source is frequently the extrahepatic vasculature and is rarely from the liver itself. Parenchymal injuries can be quite impressive and difficult to manage. Hemorrhage of this type is uncommon after liver transplantation, and its successful management has not been reported. With a partial graft, higher portal venous pressure and flow combined with relative outflow limitation may increase the potential for this type of bleeding. Hepatic artery ligation or embolization and partial liver resection are means 2219 BRIEF COMMUNICATIONS May 27, 2000 of controlling life-threatening parenchymal hemorrhage in trauma victims (5) but are not alternatives after segmental transplantation. The vascular anatomy of a partial graft makes resection almost impossible, and arterial blood flow is critical for transplanted livers (6). Permanent portacaval shunting to control parenchymal bleeding has not previously been reported. Case report: A 49-year-old female with cirrhosis secondary to hepatitis C was listed for liver transplantation as status IIB according to United Network for Organ Sharing criteria. She had known esophageal varices and had a significant bleed requiring banding 1 year before. She underwent living donor liver transplantation using the right lobe from a healthy sibling. The donor evaluation protocol and surgical procedure have been previously reported (4). The mid-hepatic vein was left with the donor, but a significant accessory hepatic vein was preserved and anastomosed to the recipient inferior vena cava. The 690-g lobe rendered a graft-to-recipient body weight ratio of 1.1%. A superficial fracture measuring 3– 4 cm was noted over segment VIII, presumably caused by pressure from a retractor. There was some bleeding after reperfusion that was easily controlled with electrocautery and thrombotic agents. Both donor and recipient recovered uneventfully. Routine ultrasonography of the graft and vasculature on postoperative days 1, 2, 3, and 7 showed patent vessels and normal-appearing parenchyma. Magnetic resonance imaging on postoperative day 7 showed a 95% increase in the size of the transplanted right lobe. There was no hematoma or other obvious abnormality. Laboratory evolution throughout her hospital course was as expected and is shown in Table 1. The patient was discharged home on postoperative day 8 but returned to the emergency room on day 11 complaining of weakness, nausea, and hematemesis. Nasogastric lavage returned a small amount of old blood. Liver ultrasound showed normal parenchyma with patent vessels. There was no free intra-abdominal fluid. Her hemoglobin had dropped from 10 g/dl to 7 g/dl over the preceding 48 hr, and liver function tests were as follows: aspartate aminotransferase 111 U/L, alanine aminotransferase 135 U/L, bilirubin 4.8 mg/dl, and prothrombin time 12.8 sec. Over the next 12 hr, the patient’s hemoglobin dropped precipitously, her abdominal girth increased, and her liver function deteriorated (Table 2). She also became hemodynamically unstable. An emergency laparotomy was performed. A large, ruptured subcapsular hematoma was noted in the area where the laceration had been. The laceration was now a fracture extending all the way to the anterior edge of the liver and was bleeding freely into the abdominal cavity (Fig. 1). It extended deep into the parenchyma and appeared to involve significant vascular structures. Brisk bleeding persisted despite conservative attempts to obtain hemostasis. Continued hemodynamic instability and massive transfusion requirements warranted more aggressive measures. Bleeding decreased significantly with temporary occlusion of the portal vein so an “H” type portacaval shunt was constructed between the native portal vein and the cava using cadaveric iliac vein (Fig. 1). The bleeding promptly stopped and the patient stabilized. The laboratory profile before and after creation of the shunt is summarized in Table 2. Because of the exceptional circumstances, an appeal was made to the regional board, and the patient was relisted as United Network for Organ Sharing status 1 the second day after creation of the shunt. No cadaver organ became available, but several other siblings presented voluntarily for donor evaluation. Her 46-year-old brother was suitable. Over the course of the next 4 days, her liver function improved to some degree, and she remained hemodynamically stable. Magnetic resonance imaging showed a large area of hepatic necrosis (Fig. 2). She and her brother were taken to the operating room 5 days after creation of the portacaval shunt. He underwent right lobectomy for living donation, and she received her second transplant from a living-related liver donor. The second graft gave a graft-to-recipient body weight ratio of 1.2%. The portacaval shunt was taken down. The mass of the failed graft 17 days after transplantation was 1510 g. There was a clot within the main hepatic vein, but all other vessels were patent. Pathologic diagnoses of the explant included early hepatic vein thrombosis (acute), acute infarction, capsular rupture, and congestion. The patient did well after the second transplant, and the remainder of her hospital course was remarkable only for some intermittent bleeding from gastric erosions. She recovered slowly and was ultimately discharged on the 31st day after the second transplant, without permanent sequelae. It is impossible to determine what critical event initiated the rapid expansion of a small hematoma that was undetected on several imaging studies. Several features unique to segmental grafts were probably contributory, however. Subtle outflow limitation caused by even a small hematoma near the hepatic vein could cause progressive engorgement of the graft with expansion of the hematoma and the defect. Increased portal flow would undoubtedly exaggerate any outflow limitation and contribute to blood loss. The tissue sealing a fresh parenchymal defect is undoubtedly weak, and the supporting matrix of a rapidly regenerating liver may be poorly organized and fragile. The growth of the lobe could stress the tissue and vasculature, initiating bleeding and allowing the defect to enlarge. All injuries to the capsule and parenchyma, even if seemingly trivial, should be repaired, and the patient should be followed closely, especially during the period of rapid regeneration (initial 14 days) (1). TABLE 1. Laboratory profile after the first right lobe living donor liver transplant AST (U/L) ALT (U/L) Bilirubin (mg/dl) Ammonia Fibrinogen (mg/dl) Prothrombin time (sec) Day 1 Day 2 Day 3 Day 4 Day 5 602 572 3.2 75 254 13 572 525 3.4 32 198 15 341 335 2.7 30 225 14 152 235 2.5 70 138 2.6 214 12 219 12 2220 TRANSPLANTATION Vol. 69, No. 10 TABLE 2. Laboratory profile immediately before creation of a portacaval shunt through the day of the second right lobe living donor liver transplant AST (U/L) ALT (U/L) Bilirubin (mg/dl) Ammonia (umol/l) Fibrinogen (mg/dl) Prothrombin time (sec) Preshunt Day 1 Day 2 Day 3 Day 4 7848 5999 9.3 49 169 19 2961 1408 10.0 74 206 17 1107 956 13.1 80 214 17 431 537 10.8 54 213 14 140 204 8.6 39 223 13 FIGURE 2. Axial magnetic resonance imaging of the right lobe graft 4 days after creation of the portacaval shunt. A sizable infarct of the superior portion of the graft can be seen. Patent branches of the portal vein are also visualized. FIGURE 1. Schematic representation of the extent of the liver laceration and the H-type portacaval shunt (H). Cadaveric vein was used to construct the communication between the native main portal vein (MPV) and the inferior vena cava. The immediately life-threatening issue facing this patient was hemorrhage from the liver laceration, with failure of conservative management. A portacaval shunt was constructed in an effort to salvage this patient. It was very effective. If the shunt had failed, the only remaining option would have been to remove the graft entirely, leaving the patient anhepatic. Contrary to what might be expected, the patient’s liver function improved after creation of the shunt, suggesting that outflow limitation was contributing to graft dysfunction (7). Experimental studies in animals have shown that portacaval shunts can improve the function and survival of liver grafts and remnants by promoting an appropriate balance between inflow and outflow (8, 9). The main hepatic vein in the explanted right lobe graft was thrombosed. All evidence suggests that this was the result of the hematoma rather than an independent event. The patent vein was visualized by ultrasonography 12 hr before the replacement of the graft, and examination of the explant showed only early hepatic vein thrombosis. Posttraumatic Budd-Chiari syndrome, though rare, has been reported under similar circumstances (10). Graft function improved significantly after the shunt was created, but it is impossible to determine whether it would have reversed completely. The conditions contributing to liver failure (outflow limitation and hemodynamic instability) were largely reversed, and the trend may well have continued. Retransplantation was mandated by the large area of necrotic tissue that almost certainly would have become an abscess. Though there was a large area of devitalized tissue, a significant portion of the liver, corresponding to the area drained by the accessory hepatic vein, was preserved. This patient’s liver function stabilized enough to sustain life, and the graft was replaced more electively. The need for adequate venous outflow from partial grafts cannot be overemphasized. We have routinely preserved accessory hepatic veins 2221 BRIEF COMMUNICATIONS May 27, 2000 greater than 5 mm. Little ischemic time is added by anastomosis of these vessels (4). The supply of cadaveric organs in our region has become very unreliable, and living donors may represent the only means of survival for patients with crises such as this. Though critically ill initially, patients battling only acutely reversible problems can do very well if they receive a timely transplant (11), and appropriate timing may well have been the ultimate determinant of survival and good outcome for this patient. Transplantation in the face of hemodynamic instability could have been fatal or resulted in irreversible complications. Infection was inevitable with inappropriate delay and would have at least caused further decompensation and may have ultimately been fatal. Regrettably, this complication was iatrogenic, and the liver lost in this case came from a living donor. 4. 5. 6. 7. 8. 9. REFERENCES 1. Marcos A, Fisher R, Ham J, et al. Liver regeneration and function in donors and recipients after adult to adult right lobe living donor liver transplantation. Transplantation 2000; 69: 1375. 2. Hesse U, Defreyne L, Pattyn P, Kerremans I, Berrevoet F, de Hemptinne B. Hepato-venous outflow complications following orthotopic liver transplantation with various techniques for hepato-venous reconstruction in adults and children. Transpl Int 1996; 9 (suppl 1): S182. 3. Paulsen A, Klintmalm G. Direct measurement of hepatic blood 10. 11. flow in native and transplanted organs, with accompanying systemic hemodynamics. Hepatology 1992; 16: 100. Marcos A, Fisher R, Ham J, et al. Right lobe living donor liver transplantation. Transplantation 1999; 68(6): 798. Feliciano D. Surgery for liver trauma. Surg Clin North Am 1989; 69: 273. Tzakis A, Gordon R, Shaw B, Iwatsiki S, Starzl T. Clinical presentation of hepatic artery thrombosis after liver transplantation in the cyclosporine era. Transplantation 1985; 40: 667. Capussotti L, Vergara V, Polastri R, Marucci M, Bouzari H, Fava C. A critical appraisal of the small-diameter portacaval Hgraft. Am J Surg 1996; 170: 10. Ueno S, Kobayashi Y, Kurita K, Tanabe G, Aikou T. Effect of prior portosystemic shunt on early hepatic hemodynamics and sinusoids following 84% hepatectomy in dogs. Res Exp Med 1995; 195; 1. Ku Y, Fukomoto T, Nishida T, et al. Evidence that portal vein decompression improves survival of canine quarter orthotopic liver transplantation. Transplantation 1995; 59: 1388. Markert D, Shanmuganathan K, Mirvis S, Nakajima Y, Hayakawa M. Budd-Chiari syndrome resulting from intrahepatic IVC compression secondary to blunt hepatic trauma. Clin Radiol 1997; 52: 384. Rosen H, Madden J, Martin P. A model to predict survival following liver retransplantation. Hepatology 1999; 29: 365. Received 15 September 1999. Accepted 2 November 1999. CHOLESTEROL EMBOLIZATION IN RENAL ALLOGRAFTS MARY G. RIPPLE, DOUGLAS CHARNEY, AND TIBOR NADASDY1 Department of Pathology, The Johns Hopkins Hospital, Baltimore, Maryland 21287 Renal cholesterol embolization (RCE) in native kidneys has a dismal outcome and frequently leads to irreversible renal failure. RCE may rarely occur in renal allografts as well, particularly if the recipient or the donor has prominent atherosclerosis. The natural history of RCE in renal transplants is unknown. We have reviewed the surgical pathology files of The Johns Hopkins Hospital in the 14-year period between 1984 and early 1999 and found 7 RCE cases among 1500 renal transplant biopsies (0.47%). One of the seven cases had three biopsies showing cholesterol emboli, the first of which was a postreperfusion (immediate posttransplant) biopsy. The probable source of the cholesterol emboli was the recipient in six cases and the donor in one case. Five donors were cadaveric and two were living donors. Six biopsies were taken within the first 4 months posttransplant (four were postreperfusion biopsies). One recent patient had the inciting event of arteriography and stent placement 2 years posttransplant and is currently doing well. One kidney failed due to posttransplant lymphoproliferative disorder (PTLD), another kidney failed with complicating opportunistic infections, and the other five 1 Current affiliation and address correspondence to: Tibor Nadasdy, MD, Department of Pathology, University of Rochester Medical Center, Box 626, 601 Elmwood Avenue, Rochester, NY 14642. View publication stats were functioning 2 to 6 years posttransplant. A literature review revealed additional 14 RCE cases in renal transplants. Combining our cases with those in the literature (21 cases), reveals that the origin of the RCE was probably the recipient in 11 cases (seven cadaveric, two living-related, and two unknown), and the donor in 10 cases (eight cadaveric and two unknown). Graft failure occurred in two of the 11 cases, where RCE was of probable recipient origin. Seven of the 10 kidneys, where the RCE was probably of donor origin, failed due to allograft dysfunction; one of them also developed superimposed rejection and cytomegalovirus infection. We conclude that if RCE is originating in the recipient, graft survival is usually good. In contrast, if RCE is of donor origin, graft dysfunction and subsequent graft loss are common. The reason for this difference may be the more extensive RCE developing in an atherosclerotic cadaveric donor during organ procurement or severe trauma leading to death. Renal cholesterol embolization (RCE) in native kidneys is an uncommon, but well-known complication of severe atherosclerosis. RCE frequently leads to renal failure and the outcome is dismal. It has been reported to occur after inciting events, such as aortic surgery and angiography; however, it may also occur spontaneously, particularly in association