Typical signs of acute appendicitis in ultrasonography mimicked by other diseases?

BACKGROUND: The diagnosis of acute appendicitis in pediatric patients is difficult. There are patients with positive ultrasonography without clinical or histological confirmation of acute appendicitis. It is essential to recognise these patients to avoid unnecessary surgery. METHODS: During 1 year, we compared the patients with 'false-positive' ultrasonography with those with 'true-positive' and those with 'true-negative' ultrasonography. RESULTS: Eighty-two patients were admitted to our inpatient ward for suspected appendicitis. Ultrasonography was performed on 68 patients. In sixteen cases, the ultrasonography showed typical signs of acute appendicitis though the patients turned out to be negative for acute appendicitis either by an observation period (n = 13) or by negative histology (n = 3). We could not find any significant differences between the groups in terms of age, gender or laboratory inflammation markers, though the latter tended to be elevated in patients with confirmed appendicitis. CONCLUSIONS: There are patients with clearly visible typical signs of acute appendicitis that do not need surgery and cannot be distinguished from others by age, gender or laboratory values. In conclusion, the clinical presentation still is the determining indicator for need of surgery. The underlying cause of the visible changes of the appendiceal area remains unclear, but there are several presumptions.

Long-term total parenteral nutrition-induced hepatobiliary dysfunction in a rabbit model.

BACKGROUND/PURPOSE: Currently, the reason for hepatobiliary dysfunction associated with long-term total parenteral nutrition (TPN) is much debated and still unclear. No agreement can be achieved about whether bacteriotoxins and sepsis, enteral starvation, consequences of abdominal operations, or the TPN solution itself is the real cause for the disease. Animal models were criticized for their short period of TPN and their failure to demonstrate cholestasis and bile duct proliferation. The aim of this study was to establish an animal model for long-term TPN in which the same alterations of the hepatobiliary system as observed in humans could be produced. METHODS: In this model, rabbits could be kept for the first time under continuous TPN for 4 weeks. Three serial liver biopsy sections were taken operatively from each animal and biochemical analyses were performed four times. A control group of enterally fed rabbits underwent exactly the same procedure in respect to operations and handling, so that differences in macroscopical, biochemical, and histological changes between both groups could be attributed exclusively to TPN. RESULTS: Only in the TPN group gallbladder distension developed in all animals after 1 week. After 3 and 4 weeks, viscous dark bile, sludge and stones, a slight rise in direct bilirubin, and a decline in plasma albumin and alkaline phosphatase was noted. In both groups liver biopsy results showed a similar degree of mild portal inflammation and single-cell necrosis at equivalent time points. These changes could be caused by antiseptics, antibiotics, anesthesia, and operations. Although mild to moderate proliferative changes and no hydropic degeneration developed in the control group during the same time, the TPN group generated marked proliferative and degenerative changes. We noted as early as 1 week after starting TPN a severe hydropic degeneration in 90% of the animals. Fibrosis and bile duct proliferation increased from a slight degree after 1 week up to a moderate to severe degree after 3 and 4 weeks, respectively. CONCLUSIONS: The hepatobiliary alterations associated with TPN in children, which cannot be separated clinically from consequences of multiple other factors, can almost identically be reproduced in our rabbit model as a clear consequence of TPN. Furthermore, the hydropic degeneration of the liver cells begins in zone 3 and is an early predominant feature of hepatobiliary dysfunction in rabbits and infants. It must be rated as a response to a direct cytotoxic effect on the liver cell.

Long-term total parenteral nutrition and cholecystostomy tube in a rabbit model surgical procedure: management and preliminary results.

A rabbit model for long-term total parenteral nutrition (TPN), specially provided with cholecystostomy tube, was designed to investigate further aspects of TPN-associated cholestasis (TPN-AC). Modified surgical procedures concerning vascular access, cholecystostomy tube implantation and authors' original modalities for prolonged infusion management in the rabbit were used. Continuous TPN was performed in 30 young rabbits. Five animals died during the experiment (16.6%) and were excluded from final evaluation. Twenty-five rabbits were successfully maintained on continuous TPN for 28 days without restraint, having a cholecystostomy tube implanted 1 week after initiation of TPN. The collection of blood samples and daily parenteral administration of drugs were simply accomplished via a central venous catheter. At the same time the cholecystostomy tube enabled us to perform daily bile sampling. Saline irrigation of the biliary tree could be carried out in conscious animals maintained on TPN. A 4-week duration of TPN in this rabbit model made it possible for the first time to accomplish serial liver biopsies in order to verify the evolution of histologic changes in TPN-related hepatic dysfunction and possible effects of surgical and medical treatment. A preliminary analysis of operative findings and histology was carried out. An enlarged gallbladder containing hyperviscous bile was found in 80% of the animals 1 week after initiation of TPN. At this time it was possible to observe the first histologic changes consistent with TPN-associated hepatic disease, such as moderate to severe hepatocyte degeneration and portal inflammation. Biliary sludge was seen after 3 weeks of TPN in 70% of the rabbits, as well as a subsequent progression of TPN-associated histologic findings. Portal fibrosis and fatty liver degeneration occurred in 50% of the rabbits and bile duct proliferation in all animals. After 4 weeks of TPN (at autopsy) gallstones were found in 20% of TPN animals, as well as further progression of bile duct proliferation and fibrosis. Our first experiences with this model and preliminary results suggest that this concept offers new possibilities for further elucidation of TPN-associated hepatic dysfunction.