Reactive nodular fibrous pseudotumor of the gastrointestinal tract and mesentery.
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Explore the source record for details and available documents.
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Eighteen patients with small intestine or mesenteric injury following blunt abdominal trauma were operated over a 34-month period. Early diagnosis and surgery, less than 6 hours after admission, was achieved in 10 patients (56%), seven of whom had haemorrhagic shock and had positive diagnostic peritoneal lavage or ultrasonography on admission. Three haemodynamically stable patients had a diagnostic abdominal computed tomography. Diagnosis was delayed in eight patients (44%) resulting in a gap between admission and surgery that varied from 20 hours to 46 days. The delay was related to lack of suspicion of injuries in haemodynamically stable patients despite a seat-belt sign, or false negative abdominal computed tomography. Diagnosis was delayed in six of seven patients (86%) where the only injury on admission was an isolated intestinal or mesenteric injury. In 11 patients there were associated abdominal or other system injuries. Late diagnosis was associated with an increased morbidity and longer hospital stay, relating to intestinal and mesenteric injury. In conclusion, a seat belt sign is highly suspicious of intestinal or mesenteric injury. Computed tomography was unreliable in diagnosing blunt intestinal and mesenteric injuries, and if equivocal, should be followed by diagnostic peritoneal lavage if nonoperative management is selected. Delayed diagnosis is often related to isolation of intestinal and mesenteric injury and results in increased morbidity and hospital stay. Every attempt should be made to reach a diagnosis within six hours of admission to the trauma unit. A management algorithm is proposed.
A continuous labelling technique was employed to study the effects of external beta-radiation on the proliferation of endothelial cells and smooth muscle cells in the mesenteric arterioles of mice. Labelled and non-labelled cells of either type were determined by autoradiographic techniques in control animals and at different times (3, 12 and 48 weeks) after single doses of 20 and 45 Gy (2000 and 4500 rads). The fraction of cells labelled, even after 7 days of repeated injections was very low in all instances. Calculations showed very long turnover times for the two cell populations in control animals (greater than 2 years for endothelium and greater than 3 years for smooth muscle). After 20 and 45 Gy, no significant increase in endothelial proliferation was seen except at 3 weeks. No significant increase in labelling was observed in smooth muscle at any time after irradiation. These labelling data have been compared with the pattern of cell depletion of the irradiated endothelium. It was concluded that the depletion was much earlier than expected for a slowly proliferating tissue, if all the cells were cycling very slowly. Such an early depletion is, however, consistent with cell death resulting from a small proportion of the cells having a short cell cycle. The recovery of the endothelial cell numbers between 9 and 12 months was not accompanied by a rise in the fraction of labelled cells. Its is suggested that repopulation may occur from outside the treated area.
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An experimental study was undertaken to evaluate the effect of dose (1 and 2 g/kg b.w.) and molecular weight (40 000, 70 000, 110 000 and 500 000 daltons) of dextran on primary haemostatic plug formation in the rabbit mesenteric microcirculation. All experiments were made 3 h after the infusion of the different substances. Albumin and hydro-oxyethyl starch treatment was used for control plasma volume expansion and did not influence arteriolar and venular haemostasis as compared with saline. Dextran gave a prolonged haemostatic plug formation time with increasing dose and with increasing molecular weights. Clinically relevant doses of dextran 40 and 70 (1 g/kg b.w.) did not influence haemostatic plug formation time.