Infant pediatric liver transplantation results equal those for older pediatric patients.

METHODS: From July 1984 to July 1995, 99 pediatric patients underwent 127 orthotopic liver transplants (OLT) at the University of Wisconsin Children's Hospital. The patients were divided into four groups according to age at time of transplant: group I, 0 to 6 months (n = 20); group II, 6 to 12 months (n = 18); group III, 1 to 2 years (n = 10); and group IV, 2 to 18 years (n = 51). A retrospective analysis was performed to compare these four groups with regard to preoperative indications and demographics, intraoperative technique, complications, and survival. All patients were followed up for 2 to 13 years. RESULTS: Biliary atresia was the most common indication for OLT in all four groups. The average waiting period varied from 19+/-18 days for group I to 44+/-64 days for group IV. Reduced-size liver transplant (I, 41%; II, 52%; III, 28%; IV, 21%), split-liver transplant (I, 0%; II, 7.4%; III, 17%; IV, 2.9%), or whole-liver transplant techniques were used. Although postoperative Intensive Care Unit stay was longer for the 0- to 6-month-old patients (I, 20+/-64; II, 7.6+/-9; III, 13+/-17; IV, 6.8+/-14 days), the total hospital stay (I, 43+/-63; II, 33+/-34; III, 32+/-20; IV, 29+/-31 days) was similar for all patients. The incidence of hepatic artery thrombosis (I, 19%; II, 19%; III, 27%; IV, 16%), biliary tract complications (I, 4.8%; II, 15%; III, 20%; IV, 14%), and retransplantation (I, 9.5%; II, 41%; III, 33%; IV, 14%) were not significantly different between the four groups. Portal vein thrombosis (I, 9.5%; II, 11%; III, 6.6; IV, 0%) and primary nonfunction (I, 9.5%; II, 7.4%; III, 0%; IV, 3.1%) occurred more frequently in the 0- to 6-month and 6- to 12-month groups, however, the 1-, 5-, and 10-year survival rate for patients (I, 85%, 79%, 79%; II, 89%, 74%, 74%; III, 80%, 80%, 80%; IV, 84%, 75%, 75%, respectively) and primary liver allografts (I, 69%, 69%, 69%; II, 72%, 72%, 63%; III, 70%, 70%, 70%; IV, 71%, 57%, 57%, respectively) were not significantly different (P = .98 and P = .83). CONCLUSION: These results demonstrate that OLT can be effectively performed on infants of all ages and that OLT should not be delayed because of age.

Preliminary experience with split liver transplantation.

BACKGROUND: The purpose of split liver transplantation is to alleviate the organ shortage for patients with end-stage liver disease. The procedure, however, has not gained wide acceptance. This is related not only to the complexity of the procedure but also to poorer results and the complications reported to be associated with the technique. STUDY DESIGN: We report 12 split liver transplantation procedures, seven in children and five in adults. Selection criteria were the same as those for whole-size liver transplantation. Patient and graft survival as well as complications were analyzed. Results were analyzed by Wilcoxon life tables. RESULTS: Patient and graft survival rates are 91.6 and 75 percent, respectively. One patient died at 2.5 months after transplantation because of lymphoproliferative disease. Another had acute vanishing bile duct syndrome and required retransplantation at 1.5 months. One patient had retransplantation because of hepatic artery thrombosis. Bile leaks occurred in two patients and hemothorax in one patient. CONCLUSIONS: Our results indicate that split liver transplantation has become a more acceptable method of hepatic transplantation and should be encouraged. Several guidelines can enhance success rates.

100 consecutive liver transplants in infants and children: an 8-year experience.

Orthotopic liver transplantation has become the treatment of choice for most children and infants with end-stage liver disease. The purpose of this retrospective study was to examine the results of 100 consecutive liver transplants performed in infants and children at a single institution. During an 8-year study period (July 1984 to December 1992), 100 pediatric liver transplants were performed in 76 patients. Thirty-four patients (44.7%) were infants (mean age, 7.0 months; mean weight, 6.1 kg), and 42 (55.3%) were children (mean age, 8.2 years; mean weight, 30.6 kg). There were 36 reduced-size liver transplants (RLT) and 64 whole-size transplants (WLT). Eight infants (23.5%) and 10 children (20.7%) required retransplantation. After transplantation, 71% of the patients had one or more rejection episodes, 66% had one or more infections, 17.1% had biliary complications, and 39.4% required one or more reoperations. There were 17 deaths. The actuarial 8-year survival rate for the patients with biliary atresia was 82.3%; for all infants in this series, it was 77.6%. No difference in patient survival was noted when RLT was compared with WLT. The overall 8-year actuarial patient survival rate for infants and children was 77.3%.

Helicobacter pylori, gastritis, and ulcers in pediatrics.

Hp now appears to be more than a simple commensal organism in patients with gastritis or peptic ulcer disease. Microbiologic, serologic, and epidemiologic studies all confirm that Hp has an important role in children with abdominal pain. Hp is found in the gastric mucosa of children with histologically proven gastritis or peptic ulcer. The organism can be transmitted from human to human with evidence of colonization, appearance of gastritis, and serum antibody response. Antimicrobial therapy directed at Hp eradicates colonization and resolves symptoms. Hp antibodies appear more frequently in familial clusters and the frequency of antibody positivity increases with age. Children are more likely to have symptomatic disease associated with elevated antibody titers. Recurrence of disease is associated with reappearance of the organism. At the present time, colonization can be detected only by gastric biopsy; however, it may be possible eventually to diagnose or follow infections by obtaining serum antibody titers or urea breath-testing. The natural history of Hp infection is unclear. Although it can cause an acute gastritis, it generally is found in association with chronic gastritis. The increase in seropositivity with age may mean that slow changes evolve over decades or that age cohorts have been infected differentially. How does antral colonization with Hp cause duodenal ulceration? The organism is not found in the duodenum and most patients with gastritis do not develop ulcers. This may be related to changes in acid production and mucosal protection associated with Hp colonization, but few studies have been done. What factors initiate Hp infection? Both volunteers who became colonized first suppressed acid secretion with H2-antagonists. Hypochlorhydria also seems to follow Hp infection in these same studies. The role of diet and drugs, or other environmental and genetic factors, in initiating infection is largely unexplored. An effective means of therapy needs to be developed. Although Hp appears sensitive in vitro to many compounds, it is difficult to eradicate in vivo, especially with monotherapy. Single-drug therapy suppresses the organism, but recurrence rates are high. It is difficult to deliver effective doses of drugs to the mucous niche the organism has selected and concerns about long-term therapy and its side effects persist. Current data suggest no ready solution to the initial case presentation. A child with primary gastritis or duodenal ulcer should be treated first with standard antacid and H2-receptor antagonist therapy. If endoscopy is performed, biopsies of normal-appearing areas of gastric antrum should be stained for Hp and a biopsy urease test should be performed.(ABSTRACT TRUNCATED AT 400 WORDS)

Human plasma lipoproteins and total parenteral nutrition with intravenous fat emulsion.

Lipoprotein concentration and composition before and after Intralipid infusion were investigated in seven adult surgical patients receiving continuous total parenteral nutrition. Plasma samples were obtained prior to parenteral alimentation, after 7 days of glucose/amino acid solution without Intralipid, and again following 5 days of daily Intralipid. Cholesterol, triglyceride, protein, and phospholipid concentrations were determined on very low-, low-, and high-density lipoprotein from each specimen. After Intralipid very low-density lipoprotein concentration fell to 29% (p less than 0.015) of pre-Intralipid levels. There was no substantial increase in low-density lipoprotein phospholipid post-Intralipid to suggest the presence of lipoprotein-X. Plasma total triglyceride levels declined by 33% after Intralipid (p less than 0.01) and plasma total cholesterol levels rose by 40% (p less than 0.02). In our patients, in whom metabolic mechanisms were not saturated, it would appear that Intralipid was metabolized by activated lipoprotein lipase pathways, without the appearance of hyperlipidemia or abnormal lipoproteins.