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J. P. is a 20-month-old Portuguese male patient who presented with a diagnosis of biliary atresia. Approximately 10 months previously the patient had undergone a laparotomy and cholecystectomy for unexplained jaundice. At the time of surgery the diagnosis of biliary atresia was established, and the patient was later transferred for liver transplantation evaluation.
The physical examination showed a deeply jaundiced infant male patient in no apparent distress. Systolic blood pressure was 94, heart rate 102, respiratory rate 28, temperature 35.9°C, and the weight was 8.9 kg. The sclera were icteric, neck supple, lung fields were clear bilaterally, heart was regular and without murmurs. Abdominal girth was 52 cm with obvious superficial venous collaterals. The liver and spleen were enlarged and easily palpable.
Laboratory studies included: Hct 32%, WBC 9.0, Plt 249K, total bilirubin 16.2, GGTP 194, SGOT 268, SGPT 93, and AP 856. Blood urea nitrogen, creatinine, amylase, and albumin were all within normal limits.
Ultrasonography revealed a cirrhotic liver with patent hepatic vessels and no bile-duct dilatation.
The patient was transplanted on 7/15/87 without complications. The arterial anastomosis was performed between the donor abdominal aorta and the celiac axis of the recipient (after ligation of the donor left gastric and splenic arteries). On the 1st postoperative day the patient had an ultrasound that showed no pulsation in the hepatic artery. Arterial thrombosis was confirmed by angiography.
The patient was retransplanted the following day (7/17/87) with a liver that was slightly smaller than ideal. During the harvesting of the liver, it was noted that the donor (a 12-month-old child) had significant pericardial and right pleural adhesions. During the final stages of harvesting the liver, a large artery was found entering the right lower lobe of the lung from the diaphragm, an obvious pulmonary sequestration. The artery was preserved and was later found to be emanating from the celiac axis. In addition, the liver had a triple arterial supply: an hepatic artery from the celiac, a left hepatic branch from the left gastric artery, and a right hepatic branch from the superior mesenteric artery. A modification of the fold-over technique (1) was done, but because of the size of the liver there was not adequate length to comfortably anastomose this complex to the recipient celiac axis. For this reason, the pulmonary artery originating from the donor celiac axis was used to make the anastomosis (Fig. 1).
The patient recovered from this 2nd transplantation uneventfully and was discharged from the hospital on 8/23/87 with normal liver function. The patency of his arterial complex was established 4 times postoperatively by ultrasound. On his last out-patient visit, he was doing well with a bilirubin of 0.4, PT 11.7 sec, SGOT 19, SGPT 10, and a GTP 16.
The celiac axis as the origin of a pulmonary arterial sequestration is present 1% of the time (2). As symptoms of pulmonary sequestration almost always present early in life with complications leading to corrective surgery, this anomaly as a harvesting enigma will probably be found only in children. As was shown here arterial anomalies do not preclude the use of the hepatic graft and can often be used advantageously.
Donor organs should not be discarded secondary to vascular anomalies. A thorough understanding of reconstructing the hepatic arterial supply can be both organ- and life-saving.
1This work was supported by Research Grants from the Veterans Administration and Project Grant No. AM 29961 from the National Institutes of Health, Bethesda, MD.