[Diagnosis and therapy of large intestine endoscopic perforation].
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On April 15th, 1986, the patient, a 58-year-old man, felt ill because of a stomachache. On April 15, he was referred to our hospital and admitted after having been diagnosed as having pan peritonitis. During surgery, an extraintestinal growth, a small fist-size tumor, was detected in the jejunum. The tumor was partly perforated, and a partial resection of the small intestine was carried out. A histopathological examination led to the diagnosis of a leiomyosarcoma of the small intestine. On June 12, 1987, the patient again returned to our hospital, complaining of a stomachache. A reoperation was performed for perforative peritonitis due to its recurrence but only palliative treatment could be provided.
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Perforated patch-clamp methods for recording ionic currents in the whole-cell configuration were used to test the hypothesis that the ionic mechanisms for the excitatory actions of histamine on enteric neurons include suppression of A-type K(+) current (I(A)). Histamine and the selective histamine H(2) receptor agonist, dimaprit, reduced the amplitude of I(A) without affecting the slope factor for I(A) steady-state inactivation curves. Suppression of I(A) was restricted to after hyperpolarization-type myenteric neurons that were immunoreactive for calbindin. The selective histamine H(2) receptor antagonist cimetidine suppressed the action of histamine and dimaprit. Elevation of intraneuronal cAMP by forskolin, a membrane-permeant analog of cAMP, and treatment with a phosphodiesterase inhibitor suppressed I(A.) The results are consistent with the hypothesis that suppression of I(A) is part of the ionic mechanism responsible for elevation of excitability during both slow synaptic excitation and slow synaptic excitation-like responses evoked by paracrine mediators, such as histamine, in after hyperpolarization-type myenteric neurons.
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Subdiaphragmatic free-air may be indicative of a perforated viscus; however, it is normally present after open abdominal surgery. The objective of this study was to determine the significance and incidence of subdiaphragmatic free air following laparoscopic cholecystectomy (LC). Cases of intestinal perforation following laparoscopic cholecystectomy from 1991 to 1995 at The University of Texas Health Science Center at San Antonio were reviewed and their association with subdiaphragmatic free air was determined. Twenty-five patients undergoing LC and 20 patients undergoing open cholecystectomy (OC) were prospectively evaluated with chest radiographs to determine the incidence and quantity of nonpathologic postoperative free air. Four cases of intestinal perforation resulting from trocar injuries or electrocautery burns occurred among 1603 LCs during this study period, for an incidence of 0.2 per cent. Three of the four patients with perforations were diagnosed postoperatively (2-5 days), and two patients had a moderate volume of subdiaphragmatic free air that aided the diagnosis. The incidence of subdiaphragmatic air following LC was 24 per cent, compared to 60 per cent for OC (P < 0.05). Eighty-three per cent of patients with retained air after LC had a minimal volume, compared to 67 per cent of patients after OC (P < 0.05). Nonpathologic subdiaphragmatic free air may normally be present following laparoscopic cholecystectomy but is uncommon 24 hours after the operation. When present, only a small volume is usually detectable. In the rare situation of intestinal perforation resulting from LC, subdiaphragmatic free air may be an important diagnostic finding.