Early detection of anastomotic leaks after colorectal surgery by measuring endotoxin in the drainage fluid

BACKGROUND/AIMS: Early detection of anastomotic leaks after colorectal anastomosis is essential for adequate intervention to prevent peritonitis. We investigated whether the measurement of endotoxin (LPS) concentrations in the drainage has any value for the early detection of anastomotic leaks. MATERIALS AND METHODS: Twenty two patients with colorectal anastomosis were enrolled in this study, 3 developed clinically established signs of anastomotic leaks and 19 recovered without complications. LPS concentrations in the drainage, the total daily excreted LPS amounts, leukocyte and thrombocyte counts, plasma urea and creatinine, and body temperature were measured for up to 8 days after surgery and tested for their value to detect anastomotic leaks. RESULTS: LPS concentrations in the drainage fluid and daily excreted LPS amounts of patients with anastomotic leaks were significantly higher compared to the group without anastomotic leaks. On the third postoperative day, LPS concentrations ranged from 5270 to 6750 pg/ml in patients with anastomotic leaks and from 1 to 1848 pg/ml in patients without complications. Total daily excreted LPS amounts were 270-675 ng/day in patients with anastomotic leak and 0-92 ng/day in patients without anastomotic leaks. Both LPS-related parameters allowed reliable detection of anastomotic leaks on day 3 after surgery (Student's t-Test, p < 0.0005), while leukocyte and thrombocyte counts, plasma urea and creatinine, and body temperatures of both patient groups were not significantly different at any time (p > 0.05). CONCLUSION: We found that the measurement of LPS concentrations in the drainage and the daily excreted LPS amount could be valuable parameters for the early detection of anastomotic leaks as early as on the third post-operative day.     

A syntactic approach to scale-space-based corner description

Planar curves are described by information about corners integrated over various levels of resolution. The detection of corners takes place on a digital representation. To compensate for ambiguities arising from sampling problems due to the discreteness, results about the local behavior of curvature extrema in continuous scale-space are employed     

The Nicholas Andry Award-1996. The molecular pathology of osteogenesis imperfecta

A systematic analysis of the molecular pathology of osteogenesis imperfecta was undertaken in 200 cases. The findings indicate that molecular defects of Type I collagen are the major cause of this disease. The mild form of osteogenesis imperfecta is caused by quantitative anomalies of Type I collagen. The other forms of the disease, which are more severe, are caused by quantitative and qualitative anomalies of Type I collagen. The mutant Type I collagen molecules are secreted poorly and are susceptible to intracellular and extracellular degradation with loss of normal and mutant collagen chains. The mutant molecules severely impair the formation of the extracellular matrix causing an abnormal architecture of dermis and bone. The molecular pathology was correlated with the clinical, radiologic, and pathologic features. As a result, the clinical classification was expanded and a new biochemical classification of osteogenesis imperfecta was developed.     

Increased expression of fibroblast growth factors (FGFs) and their receptor by protamine and suramin on Kaposi's sarcoma-derived cells

Growth factors, such as bFGF, have been shown to exert autocrine and paracrine effects on the growth of Kaposi's Sarcoma (KS)-derived cells, which suggested that the inhibitors of angiogenesis may be promising for KS treatment. However, KS lesions have been found to continue to enlarge after patients had been treated with FGF binding antagonists such as suramin. We investigated the effect of protamine and suramine on the growth of KS derived cells in vitro. Although both of these agents which are FGF binding antagonists were found to inhibit the incorporation of 3H thymidine in KS-derived cultured cells, increased expression of bFGF, FGF5 and the FGF receptor was observed after the KS cells were exposed to these substances. These results might explain the clinical observation that FGF binding antagonists such as suramin caused an apparent stimulation of KS tumor growth when administered systemically to patients with AIDS-related KS.