LIVER TRANSPLANTATION 20:512–513, 2014
EDITORIAL
Late Hepatic Artery Thrombosis in Pediatric Liver Transplantation: An Incomplete Story Amy Gallo and Carlos O. Esquivel Division of Abdominal Transplantation, Stanford University School of Medicine, Stanford, CA Received March 31, 2014; accepted April 1, 2014.
See Article on Page 591 It has now been 50 years since the first pediatric liver transplant, and the success of these transplants— patient and graft survival—still largely depends on our ability to maintain artery patency. Although many interventions, medical and technical, have been implemented, the truth remains that a high percentage of arteries continue to become occluded and thus compromise patient outcomes.1 Early thrombosis often leads to graft compromise and failure, and this requires reoperation and retransplantation. The prevalence and clinical relevance of late hepatic artery thrombosis (HAT) remain unclear. € et al.2 In this issue of Liver Transplantation, Kivela present a cross-sectional study of 34 liver transplant patients less than 18 years old over a 10-year period (starting in 1987) with a median follow-up of 9.5 years (interquartile range 5 4.0-16.4 years). Ninety-nine pediatric patients originally underwent transplantation in that time frame. Thirty-two percent of these patients were deceased. Thirty-four of the surviving 66 patients were available to undergo magnetic resonance imaging (MRI) with contrast for an evaluation of HAT. Interestingly, they report that 44% of these 34 patients had evidence of late arterial thrombosis, with late thrombosis defined as thrombosis 1 month after the date of transplantation; this was much higher than the previously reported rates (1.2%-2.7%).3-6 As the discussion makes clear, this could represent 23% of patients in the best case scenario and 71% in the worst case scenario because only 52% of the whole population underwent imaging. By comparing the MRI findings with ultrasonography, laboratory, biopsy, and clinical data, the authors have done a compre-
hensive job of analyzing these patients at time points surrounding MRI. They bring attention to the possibility that late HAT is wildly underdiagnosed during the standard follow-up of pediatric patients. Our 2 most pressing concerns regarding these data are (1) whether the late HAT rate of 44% is accurate for longterm pediatric transplant survivors and (2) what the clinical application of this knowledge should be as we go forward. One of the biggest concerns in accepting this high percentage for late thrombosis is that the MRI technique described in the article’s methodology was not consistently angiographic. Without angiography, it may be hard to draw convincing conclusions about HAT, especially without any indication of flow issues on a similarly timed ultrasound examination. It is well known that ultrasound is not the gold standard for the detection of HAT; however, changes in flow can suggest a need for a closer investigation.7 It is surprising that there was no suggestion of intrahepatic changes in flow on ultrasound for these patients. In addition, if we agree that ultrasound accuracy is as poor as suggested at this institution (40% sensitivity), it is possible that a percentage of these patients had unrecognized early HAT if ultrasound was the only imaging performed in the early posttransplant period. For comparison, in the year 2008 at our institution, Lucile Packard Children’s Hospital at Stanford, 40 transplants were performed in children less than 18 years of age (43% were
EDITORIAL
Late Hepatic Artery Thrombosis in Pediatric Liver Transplantation: An Incomplete Story Amy Gallo and Carlos O. Esquivel Division of Abdominal Transplantation, Stanford University School of Medicine, Stanford, CA Received March 31, 2014; accepted April 1, 2014.
See Article on Page 591 It has now been 50 years since the first pediatric liver transplant, and the success of these transplants— patient and graft survival—still largely depends on our ability to maintain artery patency. Although many interventions, medical and technical, have been implemented, the truth remains that a high percentage of arteries continue to become occluded and thus compromise patient outcomes.1 Early thrombosis often leads to graft compromise and failure, and this requires reoperation and retransplantation. The prevalence and clinical relevance of late hepatic artery thrombosis (HAT) remain unclear. € et al.2 In this issue of Liver Transplantation, Kivela present a cross-sectional study of 34 liver transplant patients less than 18 years old over a 10-year period (starting in 1987) with a median follow-up of 9.5 years (interquartile range 5 4.0-16.4 years). Ninety-nine pediatric patients originally underwent transplantation in that time frame. Thirty-two percent of these patients were deceased. Thirty-four of the surviving 66 patients were available to undergo magnetic resonance imaging (MRI) with contrast for an evaluation of HAT. Interestingly, they report that 44% of these 34 patients had evidence of late arterial thrombosis, with late thrombosis defined as thrombosis 1 month after the date of transplantation; this was much higher than the previously reported rates (1.2%-2.7%).3-6 As the discussion makes clear, this could represent 23% of patients in the best case scenario and 71% in the worst case scenario because only 52% of the whole population underwent imaging. By comparing the MRI findings with ultrasonography, laboratory, biopsy, and clinical data, the authors have done a compre-
hensive job of analyzing these patients at time points surrounding MRI. They bring attention to the possibility that late HAT is wildly underdiagnosed during the standard follow-up of pediatric patients. Our 2 most pressing concerns regarding these data are (1) whether the late HAT rate of 44% is accurate for longterm pediatric transplant survivors and (2) what the clinical application of this knowledge should be as we go forward. One of the biggest concerns in accepting this high percentage for late thrombosis is that the MRI technique described in the article’s methodology was not consistently angiographic. Without angiography, it may be hard to draw convincing conclusions about HAT, especially without any indication of flow issues on a similarly timed ultrasound examination. It is well known that ultrasound is not the gold standard for the detection of HAT; however, changes in flow can suggest a need for a closer investigation.7 It is surprising that there was no suggestion of intrahepatic changes in flow on ultrasound for these patients. In addition, if we agree that ultrasound accuracy is as poor as suggested at this institution (40% sensitivity), it is possible that a percentage of these patients had unrecognized early HAT if ultrasound was the only imaging performed in the early posttransplant period. For comparison, in the year 2008 at our institution, Lucile Packard Children’s Hospital at Stanford, 40 transplants were performed in children less than 18 years of age (43% were
