Sleeve gastrectomy and the risk of leak: a systematic analysis of 4,888 patients.

INTRODUCTION: Sleeve gastrectomy has become a popular stand-alone bariatric procedure with comparable weight loss and resolution of comorbidities to that of laparoscopic gastric bypass. The simplicity of the procedure and the decreased long-term risk profile make this surgery more appealing. Nonetheless, the ever present risk of a staple-line leak is still of great concern and needs further investigation. METHODS: An electronic literature search of MEDLINE database plus manual reference checks of articles published on laparoscopic sleeve gastrectomy for morbid obesity and its complications was completed. Keywords used in the search were "sleeve gastrectomy" OR "gastric sleeve" AND "leak." We analyzed 29 publications, including 4,888 patients. We analyzed the frequency of leak after sleeve gastrectomy and its associated risks of causation. RESULTS: The risk of leak after sleeve gastrectomy in all comers was 2.4%. This risk was 2.9% in the super-obese [body mass index (BMI) > 50 kg/m(2)] and 2.2% for BMI < 50 kg/m(2). Staple height and use of buttressing material did not affect leak rate. The use of a size 40-Fr or greater bougie was associated with a leak rate of 0.6% compared with those who used smaller sizes whose leak rate was 2.8%. Leaks were found at the proximal third of the stomach in 89% of cases. Most leaks were diagnosed after discharge. Endoscopic management is a viable option for leaks and was documented in 11% of cases as successful. CONCLUSIONS: Sleeve gastrectomy has become an important surgical option for the treatment of the ever growing morbidly obese population. The risk of leak is low at 2.4%. Attention to detail specifically at the esophagogastric junction cannot be stressed enough. Careful patient selection (BMI < 50 kg/m(2)) and adopting the use of a 40-Fr or larger bougie may decrease the risk of leak. Vigilant follow-up during the first 30 days is critical to avoid catastrophe, because most leaks will happen after patient discharge.

General anesthesia delays the inflammatory response and increases survival for mice with endotoxic shock.

Anesthesia is an indispensable component of any operative procedure. In this study, we demonstrate that continuous isoflurane anesthesia for 1 h after a lethal dose (20 mg/kg of body weight) of Escherichia coli lipopolysaccharide (LPS) results in a significant increase in survival of C57BL/6J (B6) mice in comparison with survival of nonanesthetized mice. Protection by anesthesia correlates with a delay in plasma LPS circulation, resulting in a delayed inflammatory response, particularly DNA binding activity of NF-kappaB and serum levels of tumor necrosis factor alpha, interleukin-6 (IL-6), and IL-10. Disparate classes of anesthetic agents produce the same effects on the inflammatory response, which is also independent of the inbred mouse strain used. These results suggest that anesthesia has an important impact on the outcome from endotoxemia. Moreover, the immunomodulatory effects of anesthetics should be considered when interpreting data from experimental animal models.

CO2 abdominal insufflation pretreatment increases survival after a lipopolysaccharide-contaminated laparotomy.

Carbon dioxide (CO(2))-pneumoperitoneum is known to favorably modify the systemic immune response during laparoscopic surgery. The presented studies were designed to determine whether treating animals with CO(2) abdominal insufflation before undergoing a lipopolysaccharide (LPS)-contaminated laparotomy would serve as "shock prophylaxis" and thus improve survival and attenuate cytokine production. Rats were randomized into five groups: CO(2)-pneumoperitoneum, helium-pneumoperitoneum, anesthesia control, laparotomy/LPS control, and LPS only control. Animals in the first four groups all received a laparotomy and a lethal dose of LPS. Immediately preceding their laparotomy, animals in the pneumoperitoneum groups received a 30-minute pretreatment of abdominal insufflation with either CO(2) or helium. The anesthesia control group received a 30-minute pretreatment of isoflurane. Animal mortality was then recorded during the ensuing 72 hours. Subsequently, a similar protocol was repeated for measurements of cytokines. CO(2)-pneumoperitoneum increased survival at 48 hours compared with LPS control (P <.05), and decreased interleukin-6 plasma levels at 2 hours (P <.05). Abdominal insufflation with CO(2) before the performance of a laparotomy contaminated with endotoxin increases survival and attenuates interleukin-6. The beneficial immune-modulating effects of CO(2)-pneumoperitoneum endure after abdominal insufflation. CO(2)-pneumoperitoneum pretreatment may improve outcomes among patients undergoing gastrointestinal surgery who are at high risk for abdominal fecal contamination.

Abdominal insufflation with CO2 causes peritoneal acidosis independent of systemic pH.

We have shown that the inflammation-attenuating effects of CO(2) pneumoperitoneum during laparoscopy are not due to changes in systemic pH. However, acidification of peritoneal macrophages in an in vitro CO(2) environment has been shown to reduce LPS-mediated cytokine release. We tested the hypothesis that the peritoneum is locally acidotic during abdominal insufflation with CO(2)--even when systemic pH is corrected. Rats (n = 20) were anesthetized and randomized into two groups: continued spontaneous ventilation (SV) or intubation and mechanical ventilation (MV). All animals were then subjected to abdominal insufflation with CO(2). Mean arterial pH among SV rats decreased significantly from baseline after 15 and 30 minutes of CO(2) pneumoperitoneum (7.329 --> 7.210 --> 7.191, P < 0.05), while arterial pH among MV rats remained relatively constant (7.388 --> 7.245 --> 7.316, P = NS). In contrast, peritoneal pH dropped significantly from baseline and remained low for both groups during CO(2) abdominal insufflation (SV 6.74 --> 6.41 --> 6.40, P < 0.05; MV 6.94 --> 6.45 --> 6.45, P < 0.05). In a second experiment, rats (n = 10) were randomized to receive abdominal insufflation with either CO(2) or helium. Abdominal insufflation with helium did not significantly affect peritoneal pH (7.10 --> 7.02 --> 6.95, P = NS), and the decrease in pH among CO(2)-insufflated animals was significant compared with helium-insufflated animals (P < 0.05). Peritoneal pH returned to baseline levels in all groups within 15 minutes of desufflation in both experiments. A significant local peritoneal acidosis occurs during laparoscopy which is specifically attributable to the use of CO(2) and which is independent of systemic pH. These data provide additional evidence that localized peritoneal acidosis is central to the mechanism of CO(2)-mediated attenuation of the inflammatory response following laparoscopic surgery.

Anesthesia-specific protection from endotoxic shock is not mediated through the vagus nerve.

BACKGROUND: We have shown recently that volatile anesthetics significantly decrease inflammatory cytokine production and dramatically increase survival among rodents challenged with lipopolysaccharide (LPS). Because acetylcholine's interaction with nicotine receptors on tissue macrophages during vagus nerve stimulation has been implicated in the modulation of LPS-stimulated tumor necrosis factor alpha (TNF-alpha) production, we hypothesized that the mechanism of anesthetic immunoprotection is mediated through the vagus nerve. METHODS: Male Sprague-Dawley rats underwent bilateral cervical vagotomy (n = 20) or sham operation (n = 6). Twenty-four hours postoperatively, vagotomized rats were randomized into 3 groups: LPS injection (V+LPS, n = 6), LPS injection followed by 60 minutes of isoflurane anesthesia (V+LPS+ISO, n = 7), or saline injection (V+S, n = 7). Sham animals were also given LPS (Sham+LPS). A sublethal dose of LPS (8 mg/kg) was used. Blood samples were collected via cardiac puncture 90 minutes after LPS or saline injection, and plasma was isolated for the measurement of cytokines by enzyme-linked immunosorbent assay. Statistical differences between groups were detected by 1-way analysis of variance. RESULTS: Serum TNF-alpha was reduced significantly and interleukin (IL)-6 was abrogated completely among V+LPS+ISO rats, compared with both V+LPS and Sham+LPS animals (P < or = .05 for all). In contrast, levels of the anti-inflammatory cytokine IL-10 were similar among all LPS groups. CONCLUSIONS: Isoflurane anesthesia administered simultaneously with the injection of LPS decreases serum production of TNF-alpha and IL-6 despite bilateral transection of the vagus nerve. Isoflurane-mediated attenuation of proinflammatory cytokine production occurs via a mechanism other than modulation of vagal output.

Videoendoscopic endotracheal intubation in the rat: a comprehensive rodent model of laparoscopic surgery.

BACKGROUND: Peritoneal absorption of CO(2) during abdominal insufflation in laparoscopy may disrupt the acid-base equilibrium and alter the physiological response to stress. Current nonventilated rodent models of laparoscopy do not manage the CO(2) load of pneumoperitoneum, but ventilated surgical rodent models are invasive (tracheotomy) and may independently induce the inflammatory response. MATERIALS AND METHODS: A comprehensive rodent model of laparoscopy was developed. Rats were randomized to receive anesthesia alone, anesthesia plus CO(2) pneumoperitoneum, or anesthesia plus CO(2) pneumoperitoneum with videoendoscopic intubation and mechanical ventilation. Arterial blood-gas analysis was performed at baseline and after 30 min of intervention. RESULTS: Baseline pH, pCO(2), and HCO(3)(-) arterial blood gas parameters were normal for all rats. After 30 min, pCO(2) and pH changed slightly but remained normal among rats receiving anesthesia alone (pCO(2) = 46.5 +/- 1.9; pH = 7.365 +/- 0.009) whereas animals receiving anesthesia plus CO(2) pneumoperitoneum that were dependent on spontaneous respiration for ventilation developed significant hypercarbic acidosis (pCO(2) = 53.2 +/- 1.9, P < 0.05; pH = 7.299 +/- 0.011, P < 0.001). This acidosis was completely corrected with increased minute ventilation in intubated rats receiving mechanical ventilation (pCO(2) = 36.8 +/- 1.5, P < 0.001; pH = 7.398 +/- 0.011, P < 0.001). CONCLUSIONS: CO(2) pneumoperitoneum induces significant hypercarbic acidosis in nonventilated rats. Noninvasive endotracheal intubation is feasible in the rat with videoendoscopic assistance. Our noninvasive rodent model of laparoscopic surgery controls for anesthesia- and capnoperitoneum-related acid-base changes and provides an environment in which the biological response to pneumoperitoneum can be studied precisely.