Journal of gastrointestinal surgery : official journal of the Society for Surgery of the Alimentary Tract
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J. Gastrointest. Surg. · Jan 1999
Role of angiography and embolization for massive gastroduodenal hemorrhage.
The role of mesenteric angiography and embolization for massive gastroduodenal bleeding is unclear. We reviewed the records of patients who underwent angiography for acute, nonmalignant, and nonvariceal gastric or duodenal hemorrhage that was documented but not controlled by endoscopy. Fifty patients were identified over a 7-year period ending in March 1998. ⋯ No differences were found that could be attributed to gastric vs. duodenal sources, number of comorbid diseases, organ failure, APACHE score, age, or whether active bleeding was found at angiography. A total of 20 patients (40%) died including 9 of 17 patients operated on in an attempt to salvage angiographic failure. In summary, angiographic embolization should be performed early in the course of bleeding in otherwise critically ill patients.
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J. Gastrointest. Surg. · Jan 1999
Laparoscopic cholecystectomy as a "true" outpatient procedure: initial experience in 130 consecutive patients.
Laparoscopic cholecystectomy has received nearly universal acceptance and is currently considered the "gold standard" for the treatment of cholelithiasis. Many centers have employed "short-stay" units or "23-hour admissions" for postoperative observation following laparoscopic cholecystectomy. The practice of early discharge as "true" outpatients following this procedure has not been well defined. ⋯ In retrospect, 20.4% of the patients stated that they would have preferred an inpatient to an outpatient procedure. Laparoscopic cholecystectomy can be performed as a true outpatient procedure with patients discharged to home within hours of completion of the procedure. Less than 10% of patients will fail this protocol and another 5% of the patients may require hospitalization after returning to their homes.
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J. Gastrointest. Surg. · Nov 1998
Gastroesophageal reflux disease and mucosal injury with emphasis on short-segment Barrett's esophagus and duodenogastroesophageal reflux.
Gastroeosphageal reflux disease has been associated with long segments of Barrett's esophagus
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J. Gastrointest. Surg. · Nov 1998
Intestinal microcirculation and gut permeability in acute pancreatitis: early changes and therapeutic implications.
Translocation of bacteria from the intestine causes local and systemic infection in severe acute pancreatitis. Increased intestinal permeability is considered a promoter of bacterial translocation. The mechanism leading to increased gut permeability may involve impaired intestinal capillary blood flow. ⋯ Impairment of colonic capillary perfusion correlates with the severity of pancreatitis. A decrease in capillary blood flow in the colon, even in mild pancreatitis not associated with significant protease activation and acinar cell necrosis or impairment of pancreatic capillary perfusion, suggests that colonic microcirculation is especially susceptible to inflammatory injury. There was no significant change in intestinal permeability in the early stage of pancreatitis, suggesting a window of opportunity for therapeutic interventions to prevent the later-observed increase in gut permeability, which could result in improved intestinal microcirculation.
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J. Gastrointest. Surg. · Sep 1998
Reasons for intracranial hypertension and hemodynamic instability during acute elevations of intra-abdominal pressure: observations in a large animal model.
In previous studies we reported that an acute elevation in intra-abdominal pressure (IAP) is responsible for the elevation in intracranial pressure (ICP) and mean blood pressure (MBP). Thus far, the reasons for the increased ICP during an acute elevation in IAP and the combined effects of increased IAP and ICP on hemodynamics have not been reported. Five large animals (swine) were studied. ⋯ Cavograms performed on animals in the supine position with increased IAP showed a narrowing of the IVC at the level of the diaphragm. Increases in IAP will increase ICP and MBP without altering the cerebral perfusion pressure. A mechanical effect mediated by compression of the inferior vena cava at the level of the diaphragm with increased central venous pressure and decreased drainage from the lumbar plexus and central nervous system is responsible for this effect.