Surgical Considerations of Endogenous Infections — Sources, Types, and Methods of Control

Altemeier, William A.; Culbertson, W. R.; Hummel, Robert P.

doi:10.1016/s0039-6109(16)38448-1

Cited by 156 publications

(72 citation statements)

References 10 publications

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“…Both regimens differ from that used for total gut decontamination (1,14). Rats generally do not acquire yeast infections, an observation we also made during our preliminary trials.…”

Section: Materuils and Methodsmentioning

confidence: 78%

Bacteria: a major pathogenic factor for anastomotic insufficiency

Schardey

Kamps

Rau

et al. 1994

Antimicrob Agents Chemother

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The aim of this study was to determine the influence of bacteria on the development of anastomotic insufficiency following gastrectomy in the rat. Fifty-seven male Wistar rats were randomly assigned to three groups and subjected to gastrectomy. Group I (n = 20) was orally inoculated with 109 Pseudomonas aeroginosa organisms on postoperative day 1. Group II (n = 20) served as the control group. Group III (n = 17) was decontaminated with 320 mg of tobramycin, 400 mg of polymyxin B, and 500 mg of vancomycin per liter of fluid administered from preoperative day 7 to postoperative day 10. Swabs from the oropharynx and rectum were cultured and analyzed daily for gram-positive and gram-negative bacteria. Surviving animals were sacrificed on postoperative day 10. All animals were autopsied immediately following death. Anastomotic insufficiency was defined as a histologically proven transmural defect at the suture line. Along with an effective reduction of pathogenic bacteria colonizing the oropharynx, the rate of anastomotic insufficiency could be reduced significantly, to 6% in decontaminated animals compared with 80% in controls (P < 0.001 by Fisher's exact test). Inoculation of group I animals with P. aeruginosa led to an increase of anastomotic insufficiency up to 95% and a significant increase in mortality (P < 0.05). We conclude that bacteria play a major role in the pathogenesis of anastomotic insufficiency following gastrectomy in the rat.Anastomotic insufficiency is one of the major causes of morbidity and mortality following total gastrectomy. The pathogenesis of esophago-intestinal anastomotic insufficiency, however, is not completely understood. Impaired blood supply or local microcirculatory disturbances leading to necrosis (13), as well as foreign bodies (6, 7), have been thought to be the cause of anastomotic insufficiency for more than 100 years. Anastomotic insufficiency, however, is a septic disease. Exogenous or endogenous potentially pathogenic microorganisms colonizing the digestive tract may play a causative role in the pathogenesis in addition to microcirculatory disturbances. This idea led us to examine the influence of bacterial colonization on the incidence of anastomotic insufficiency.By topical application of nonresorbable bactericidal antibiotics (16, 18), the colonizing microflora of the oropharynx and upper gastrointestinal tract can be easily manipulated. We therefore used deliberate colonization and topical decontamination with tobramycin, polymyxin and vancomycin to test the following hypotheses in an experimental study: (i) anastomotic insufficiency occurs as a result of bacterial infection, and (ii) anastomotic insufficiency can be prevented by preventing bacterial colonization. MATERUILS AND METHODSFifty-seven male Wistar rats were randomly assigned to three groups. In group I (bacterial inoculation), all animals received one oral dose of 109 Pseudomonas aeruginosa organisms on the first postoperative day. P. aeruginosa was chosen because it is commonly causes nosocomial infections i...

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“…Both regimens differ from that used for total gut decontamination (1,14). Rats generally do not acquire yeast infections, an observation we also made during our preliminary trials.…”

Section: Materuils and Methodsmentioning

confidence: 78%

Bacteria: a major pathogenic factor for anastomotic insufficiency

Schardey

Kamps

Rau

et al. 1994

Antimicrob Agents Chemother

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“…A prolonged preoperative stay with exposure to hospital environment, its ubiquitous diagnostic procedures, therapies, and microflora, including multidrug resistant organisms, have been shown to increase the rate of SSI [32]. Kowli in their study demonstrated an infection rate of 1.76% when preoperative stay was up to one day, which increased to 5% when preoperative stay was more than one week [6].…”

Section: Discussionmentioning

confidence: 99%

Risk Factor Analysis and Microbial Etiology of Surgical Site Infections following Lower Segment Caesarean Section

Saxena

Mehta

et al. 2013

International Journal of Antibiotics

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Background. Lower segment caesarean section (LSCS) is a common mode of delivery now and surgical site infection is the second most common infectious complication in these patients. This study was planned with this background to have a comprehensive approach to SSI following LSCS. Methods. 500 consecutive patients undergoing LSCS, irrespective of indication, were studied. A questionnaire was developed to assess the risk factors associated with development of SSI. All patients were followed up from day one of surgery till discharge and then up till the postoperative day 30 after discharge. Results. SSI was identified in 121 (24.2%) out of 500 patients. In all age groups, Gram-negative bacilli were the commonest finding. The commonest isolate was Acinetobacter species (32.03%) followed by Staphylococcus aureus and coagulase negative Staphylococcus (21.09%). 23.8% of Staphylococcus aureus strains were MRSA. By multivariate logistic regression premature rupture of membrane (PROM), antibiotics given earlier than 2 hours and increased duration of stay in the hospital were found to be significant. Conclusions. A proper assessment of risk factors that predispose to SSI and their modification may help in reduction of SSI rates. Also, frequent antimicrobial audit and qualitative research could give an insight into the current antibiotic prescription practices and the factors affecting these practices.

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“…For most SSIs, the source of pathogens is the endogenous flora of the patient's skin, mucous membranes or hollow viscera (15). When mucous membranes or skin is incised, the exposed tissues are at risk for contamination with endogenous flora.…”

Section: Discussionmentioning

confidence: 99%