PubMed · 7258516
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P Arrington, C S Judd. 1981. Cecal diverticulitis.. https://doi.org/10.1016/s0002-9610(81)80012-8
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BACKGROUND: Adhesions after abdominal and pelvic surgery are important complications, although their basic epidemiology is unclear. We investigated the frequency of such complications in the general population to provide a basis for the targeting and assessment of new adhesion-prevention measures. METHODS: We used validated data from the Scottish National Health Service medical record linkage database to identify patients undergoing open abdominal or pelvic surgery in 1986, who had no record of such surgery in the preceding 5 years. Patients were followed up for 10 years and subsequent readmissions were reviewed and outcomes classified by the degree of adhesion. We also assessed the rate of adhesion-related admissions in 1994 for the population of 5 million people. FINDINGS: 1209 (5.7%) of all readmissions (21,347) were classified as being directly related to adhesions, with 1169 (3.8%) managed operatively. Overall, 34.6% of the 29,790 patients who underwent open abdominal or pelvic surgery in 1986 were readmitted a mean of 2.1 times over 10 years for a disorder directly or possibly related to adhesions, or for abdominal or pelvic surgery that could be potentially complicated by adhesions. 22.1% of all outcome readmissions occurred in the first year after initial surgery, but readmissions continued steadily throughout the 10-year period. In 1994, 4199 admissions were directly related to adhesions. INTERPRETATION: Postoperative adhesions have important consequences to patients, surgeons, and the health system. Surgical procedures with a high risk of adhesion-related complications need to be identified and adhesion prevention carefully assessed.
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Intraperitoneal administration of the cytokine interleukin-1beta (IL-1beta) induces brain-mediated sickness symptoms that can be blocked by subdiaphragmatic vagotomy. Intraperitoneal IL-1beta also induces expression of the activation marker c-fos in vagal primary afferent neurons, suggesting that IL-1beta is a key component of vagally mediated immune-to-brain communication. The cellular sources of IL-1beta activating the vagus are unknown, but may reside in either blood or in the vagus nerve itself. We assayed IL-1beta protein after intraperitoneal endotoxin [lipopolysaccharide (LPS)] injection in abdominal vagus nerve, using both an ELISA and immunohistochemistry, and in blood plasma using ELISA. IL-1beta levels in abdominal vagus nerve increased by 45 min after LPS administration and were robust by 60 min. Plasma IL-1beta levels increased by 60 min, whereas little IL-1beta was detected in cervical vagus or sciatic nerve. IL-1beta-immunoreactivity (IR) was expressed in dendritic cells and macrophages within connective tissues associated with the abdominal vagus by 45 min after intraperitoneal LPS injection. By 60 min, some immune cells located within the nerve and vagal paraganglia also expressed IL-1beta-IR. Thus, intraperitoneal LPS induced IL-1beta protein within the vagus in a time-frame consistent with signaling of immune activation. These results suggest a novel mechanism by which IL-1beta may serve as a molecular link between the immune system and vagus nerve, and thus the CNS.