ObjectiveThe authors review current definition, classification, scoring, microbiology, inflammatory response, and goals of management of secondary peritonitis.
Summary Background DataDespite improved diagnostic modalities, potent antibiotics, modern intensive care, and aggressive surgical treatment, up to one third of patients still die of severe secondary peritonitis. Against the background of current understanding of the local and systemic inflammatory response associated with peritonitis, there is growing controversy concerning the optimal antibiotic and operative therapy, intensified by lack of properly conducted randomized studies. In this overview the authors attempt to outline controversies, suggest a practical clinical approach, and highlight issues necessitating further research.
MethodThe authors review the literature and report their experience.
ResultsThe emerging concepts concerning antibiotic treatment suggest that less-in terms of the number of drugs and the duration of treatment-is better. The classical single operation for peritonitis, which obliterates the source of infection and purges the peritoneal cavity, may be inadequate for severe forms of peritonitis; for the latter, more aggressive surgical techniques are necessary to decompress increased intra-abdominal pressure and prevent or treat persistent and recurrent infection. The widespread acceptance of the more aggressive and demanding surgical methods has been hampered by the lack of randomized trials and reportedly high associated morbidity rates.
ConclusionsSepsis represents the host's systemic inflammatory response to bacterial peritonitis. To improve results, both the initiator and the biologic consequences of the peritoneal infective-inflammatory process should be addressed. The initiator may be better controlled in severe forms of peritonitis by aggressive surgical methods, whereas the search for methods to abort its systemic consequences is continuing.Intra-abdominal infections after spontaneous gastro-overview is to present the "state of the art" in the manintestinal perforation and those resulting from injuries agement of secondary peritonitis, to emphasize persistor complicating abdominal operations, still represent the ing controversies, and to identify the gaps in our knowl-"bread and butter" for surgeons. The purpose of this edge that require further study.
The effectiveness of short-term, low-dose, preoperative oral administration of neomycin and erythromycin base combined with vigorous purgation in reducing the incidence of wound infections and other septic complications of elective colon and rectal operations has been studied in a prospective, randomized, double-blind, clinical trial. One hundred and sixteen patients completed the study; all received mechanical preparation; 56 received neomycin-erythromycin base while 60 received an identical appearing placebo. The two patient groups were comparable in age distribution, clinical diagnoses, associated systemic diseases, types of operation performed and similar clinical features. The overall rate of directly related septic complications was 43 per cent in the placebo group and 9% in the group receiving neomycin and erythromycin base. The wound infection rates were 35% in placebo and 9% in antibiotic treated patients. Oral administration of neomycin and erythromycin base together with vigorous mechanical cleansing reduces the risk of septic complications after elective colo-rectal operations.
We report here the characteristics of a cyclic motor activity in the colon of conscious dogs and its relationship to small intestinal migrating motor complexes (MMCs). The colonic motor activity was recorded by four equispaced strain gauges and small intestinal myoelectric activity by four equispaced bipolar electrodes. The colonic motor activity was characterized by rhythmic bursts of contractions. The mean durations of bursts of contractions varied from 7.0 to 11.5 min at the four colonic recording sites. Those bursts of contractions which migrated over at least three recording sites were called colonic migrating motor complexes (CMMCs). All other patterns of bursts of contractions were called colonic nonmigrating motor complexes (CNMCs). A total of 160 CMMCs were recorded during a total recording period of 132 h; 151 CMMCs migrated caudad and 9 orad. The mean period of caudad migrating CMMCs was 53.3 +/- 5.4 (SE) min, and their mean migration time was 11.3 +/- 1.2 (SE) min. The onset of CMMCs was not temporally related to the onset of small intestinal migrating myoelectric complexes in the duodenum or their arrival in the terminal ileum. CMMCs did not have phases I to IV like those of small intestinal MMCs, but two consecutive CMMCs were separated by a quiescent state or by one or more randomly occurring bursts of contractions (CNMCs).
The role of tachykinins in stimulating phasic and giant migrating contractions (GMCs) in the normal and inflamed colon in conscious dogs was investigated by close-intra-arterial infusions of test substances. At low doses (0.1 nmol), substance P and neurokinin (NK1) receptor agonist ([Sar9,Met(O2)11]substance P] stimulated phasic contractions only. At higher doses (2.0 nmol), they stimulated phasic contractions and GMCs. The phasic contractions were blocked partially but significantly by prior close-intra-arterial infusions of tetrodotoxin and atropine but not by hexamethonium. NK1 receptor antagonist partially but significantly inhibited the phasic contractile response to substance P, whereas NK2 and NK3 receptor antagonists had no significant effect. The contractile response to NK2 receptor agonist was less than one-half of the response to substance P; NK3 receptor agonist did not stimulate any contractile activity. The stimulation of GMCs by higher doses of substance P was not blocked by prior infusions of atropine, tetrodotoxin, or NK1, NK2, and NK3 receptor antagonists, nor was the contractile response to substance P blocked by H1 and H2 receptor antagonists. Inflammation depressed the phasic contractile response but enhanced the stimulation of GMCs by substance P. The ability of substance P to stimulate GMCs is novel and suggests its potential role in increasing the frequency of these contractions during colonic inflammation.
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