Bariatric Times - June 2008 - (Page 31)

Bariatric Times • June 2008 Surgical Perspective produce toxins that increase their ability to invade a host or survive in host tissue—endotoxin, which stimulates cytokine production, is one such example. Other bacteria inhibit phagocytosis by secretion of a polysaccharide capsule, which also contributes to SSI. Certain strains of clostridia and streptococci produce exotoxins, disrupting cell membranes and altering cellular metabolism. Regardless of the pathogenetic mechanism, for most SSIs, the source of pathogens is the endogenous flora of the patient’s skin, mucousmembranes, or hollow viscera.3 Exogenous sources can contribute to SSI as well. They include surgical personnel, the operating room environment (including air), tools, and instruments brought into the sterile field. Several very good studies have demonstrated the role of certain risk factors in the pathophysiology of SSI. These risk factors have been identified by both univariate and multivariate analyses. In broad terms, these risk factors can be classified as “patient factors” and “operative factors.” Patient factors include age, nutritional status, diabetes, smoking, obesity, and several others. Operative factors include surgical scrub duration, skin antisepsis, preoperative shaving, skin prep, duration of the operation, antimicrobial prophylaxis, foreign material, drains, and surgical technique (Table 3).3 Despite various speculations explaining SSI in obese patients, there are few studies offering rigorous scientific explanations. Clearly, obesity is a surrogate for other known risk factors for SSI, namely diabetes mellitus (DM).1 One recent study demonstrated that gastric bypass patients with elevated fasting blood glucose concentrations have a higher risk of SSI, which highlights the importance of preoperative hyperglycemia as well as that of DM.1,16 Obesity is associated with insulin resistance and hyperglycemia. A number of studies in the cardiac literature have shown a higher rate of SSI in patients with perioperative hyperglycemia. Furthermore, obesity is associated with longer operations, which is one of the independent predictors of SSI that is commonly significant in multiple series as well as in the NNIS data.1 It is generally agreed that obese patients have tissue hypoperfusion, which may predispose to SSI through a greater risk of ischemia, necrosis, and suboptimal neutrophil oxidative killing.1 Possibilities include a high ratio of tissue mass: capillaries in adipose tissue, larger wound surface areas, and decreased oxygen tension in adipose tissues. All of these point toward poor balance between tissue oxygen demand and supply. Kabon, et al., demonstrated that the measured incision oxygen tension during and after operation in obese 31 obese patients had a significantly higher rate of nosocomial infections, including SSI, clostridium difficile diarrhea, pneumonia, and bacteremia.11 Obesity increases the risk of perioerative complications of the skin and underlying tissue, including wound infection, dehiscence, pressure ulcers, and deep tissue injury.18,19 SSI and its risk factors have been studied extensively in cardiac surgery. The cardiac literature has consistently demonstrated that obese patients are at a significantly higher risk of developing SSI. These findings hold true for non-cardiac surgical specialties as well.1 SSI is one of the most common complications of bariatric surgery. Large series of open gastric bypass operations have described SSI rates between 15 and 25 percent.1 Christou, et al., retrospectively reviewed their prospectively collected database, specifically addressing the incidence and risks for SSI in patients undergoing open bariatric surgery. They observed an SSI rate of 20 percent, despite an expected score of four percent based on the NNIS system.12 Laparoscopic procedures, particularly in high-volume centers, have reduced the high risk of SSI in patients undergoing bariatric operations.1,13 Schauer and colleagues, as well as DeMaria and colleagues, have reported much lower rates of SSI compared to the open literature (5% and 1.5%, respectively).14,15 Several other recent studies have demonstrated similar low rates of SSI in patients undergoing laparoscopic bariatric operations compared to open procedures. As stated, an exhaustive discussion of SSI as outlined in the CDC guidelines is beyond the purview of this paper; however, several issues are worth discussing. First, the distribution of pathogens has not changed markedly over the last decade (Table 2).3,5,6 There is no difference in distribution between obese and non-obese patients. Staphylococcus aureus, coagulase-negative staphylococci, enterococcus, and Escherichia coli remain the most frequently isolated pathogens.3 So what causes SSI? Microbial contamination of the surgical site is a necessary precursor. The risk is conceptualized according to the following relationship:3 (Dose of bacterial contamination x virulence)/Resistance of the host patient=Risk of SSI. In fact, if a surgical site is contaminated with greater than 105 microorganisms per gram of tissue, the risk of SSI is markedly increased.3 The dose of contaminating microorganisms needed to produce infection may be much lower when foreign material such as silk suture, for example, is present at the site.3 Microorganisms may contain or http://www.exemplomedical.com http://www.exemplomedical.com http://www.carbessentials.net

Table of Contents Feed for the Digital Edition of Bariatric Times - June 2008

Bariatric Times - June 2008 Endoluminal Treatment Options for Morbid Obesity: Devices and Techniques for Natural Orifice Approaches The Multidisciplinary Approach to Weight Loss: Defining the Roles of the Necessary Providers Acute Bleeding after Gastric Bypass Editorial Message Contents ASMBS: 25 Years Editorial Board Surgical Site Infection In The Morbidly Obese Patient: A Review Consultant's Corner The Link Between Sleep Loss and Obesity: Understanding the Mechanisms Responsible for Weight Gain with Sleep Deprivation Volume Matters Journal Watch Advertiser Index

Bariatric Times - June 2008

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