fibrin and Enterocolitis--Pseudomembranous

E. coli O157:H7 may cause hemorrhagic colitis resembling ischemic colitis. Diagnosis is usually made by finding sorbitol-negative colonies on MacConkey agar that react with O157 and H7 antisera. Most ischemic colitis is idiopathic, but some may be caused by E. coli O157:H7, inasmuch as this organism can produce fibrin thrombi in colon vasculature. The objectives of this study were to determine whether E. coli O157:H7 infection can be diagnosed retrospectively from paraffin blocks of colon sections and whether an association exists between E. coli O157:H7 infection and colonic ischemia.. Paraffin-embedded sections of normal colon (n = 2) and various colitides [ischemic (n = 11), E. coli O157:H7 (n = 2), IBD (n = 8) and pseudomembranous (n = 3)] were used. Sections were deparaffinized, rehydrated, incubated with 3% peroxide in methanol, rinsed, and incubated with peroxidase-labeled antibody isolated from goats immunized with whole E. coli O157:H7. Sections were stained with peroxidase chromagen reagent and counterstained with hematoxylin. Coarse, granular, orange-brown staining was considered positive. To determine the localization of the chromagen deposits, three cases that stained positive, including one of the culture-proved E. coli O157:H7 colitis and two of colonic ischemia, were processed for electron microscopy.. Both cases (100%) of E. coli O157:H7 colitis and three of 11 (27.3%) cases of ischemic colitis stained positive by light microscopy. In one culture-proved case, electron microscopy demonstrated staining of bacillary structures; in two cases of colonic ischemia, extensive deposits of chromagen material were present that were associated neither with inflammatory cells nor with bacterial forms.. Immunoperoxidase staining of archival sections may be used to diagnose E. coli O157:H7 infection. An etiological role for this organism is possible in some cases of colonic ischemia.

Topics: Aged; Antibodies, Bacterial; Chromogenic Compounds; Colitis; Colitis, Ischemic; Colon; Coloring Agents; Enterocolitis, Pseudomembranous; Escherichia coli Infections; Escherichia coli O157; Female; Fibrin; Gastrointestinal Hemorrhage; Hematoxylin; Humans; Immunoenzyme Techniques; Inflammatory Bowel Diseases; Male; Microscopy, Electron; Middle Aged; Paraffin Embedding; Retrospective Studies; Thrombosis

To explore the pathophysiology of the necrotizing enterocolitis caused by polycythemia in the newborn dog, the effect of acute polycythemia on fibrinogen disappearance rate was studied in 38 puppies (3-14 days). All pups received an exchange transfusion removing 65 ml/kg of blood and transfusing 85 ml/kg of either whole blood (control, resulting hematocrit = 37), or packed red blood cells (polycythemia, resulting hematocrit = 68). Necrotizing enterocolitis was found in 15 of 19 polycythemic and four of 19 control pups (p less than 0.01). 125I fibrinogen and Evan's blue (an albumin marker) were injected 2 h after transfusion and the concentration of clottable labeled fibrinogen and albumin tracer were measured at 1/2 and 2 h after injection. The fraction of the tracer that disappeared over the 1 1/2-h period was calculated. In the polycythemic group 45 +/- 18 SD% of the clottable fibrinogen disappeared versus only 28 +/- 15% in the control group (p less than 0.01). In the polycythemic group 36 +/- 21% of the albumin tracer disappeared versus 31 +/- 12% in the control group (NS). Thus polycythemia in the newborn dog is associated with an increased disappearance rate of clottable fibrinogen not associated with a general increase in protein disappearance rate. Thus an intravascular coagulopathy is evident in the polycythemic animals. Whether this coagulopathy is the cause of the necrotizing enterocolitis or is secondary to the necrotizing enterocolitis seen in this animal model cannot be determined from this experiment.

Topics: Animals; Animals, Newborn; Blood Coagulation Disorders; Blood Viscosity; Disease Models, Animal; Dogs; Enterocolitis, Pseudomembranous; Female; Fibrin; Fibrin Fibrinogen Degradation Products; Fibrinogen; Iodine Radioisotopes; Lactates; Male; Polycythemia; Time Factors

Ninety-three postoperative patients 1 day to 13 years of age had blood cultures, limulus lysate assay, determination of fibrin degradation products, white blood cell and platelet counts. Seven groups were studied. The limulus lysate assay was often positive (64%) in the presence of gram negative septicemia but there were false positives and negatives. The tests for fibrin degradation products were inconsistent. The white blood cell count was low in babies with gram negative septicemia. One hundred per cent of the infants with gram negative septicemia had a platelet count below 150,000; 71% below 100,000 (average 67,000 septic babies, 257,000 non-septic babies). The drop in platelet count with gram negative septicemia was abrupt---as much as 222,000 in 24 hours. Platelets increased when therapy was effective. Two children with gram negative septicemia had platelet counts of 50,000 and 20,000. The platelet count for patients with gram positive septicemia was 299,000, and above 150,000 in all children with ruptured and non-ruptured appendicitis and major surgery without gram negative septicemia. It was concluded that serial measurements of platelet count in the postoperative infant and child was a rapid and reliable method for early detection of gram negative septicemia and changes in platelet count in response to treatment was an indicator of the effectiveness of therapy.

Topics: Abdominal Muscles; Adolescent; Appendicitis; Bacteria; Bacterial Infections; Blood Cell Count; Blood Platelets; Child; Child, Preschool; Enterocolitis, Pseudomembranous; Escherichia coli Infections; Fibrin; Gangrene; Humans; Infant; Infant, Newborn; Intestinal Obstruction; Klebsiella Infections; Leukocyte Count; Liver Neoplasms; Platelet Aggregation; Postoperative Complications; Pseudomonas Infections; Sepsis; Time Factors