Perioperative Fluid Accumulation Impairs Intestinal Contractility to a Similar Extent as Peritonitis and Endotoxemia.

BACKGROUND: Perioperative resuscitation with large amounts of fluid may cause tissue edema, especially in the gut, and thereby impairing its functions. This is especially relevant in sepsis where capillaries become leaky and fluid rapidly escapes to the pericapillary tissue. We assessed the effects of endotoxemia and peritonitis, and the use of high and moderate volume fluid resuscitation on jejunal contractility. We hypothesized that both endotoxemia and peritonitis impair jejunum contractility and relaxation, and that this effect is aggravated in peritonitis and with high fluid administration. METHODS: Pigs were randomized to endotoxin (n = 16), peritonitis (n = 16), or sham operation (n = 16), and either high (20 mL/kg/h) or moderate volume (10 mL/kg/h) fluid resuscitation for 24 h or until death. At the end of the experiment, jejunal contractility and relaxation were measured in vitro using acetylcholine and sodium nitroprusside reactivity, and the effect of nitric oxide synthase inhibition (NOS-I) was assessed. RESULTS: Mortality in the respective groups was 88% (peritonitis high), 75% (endotoxemia high), 50% (peritonitis moderate), 13% (endotoxemia moderate and sham operation high), and 0% (sham operation moderate volume resuscitation). Although gut perfusion was preserved in all groups, jejunal contractility was impaired in the two peritonitis and two endotoxemia groups, and similarly also in the sham operation group treated with high but not with moderate volume fluid resuscitation (model-fluid-contraction-interaction, P = 0.036; maximal contractility 136 ±â€Š28% [average of both peritonitis, both endotoxemia and sham operation high-volume groups) vs. 170 ±â€Š74% of baseline [sham operation moderate-volume group]). NOS-I reduced contractility (contraction-inhibition-interaction, P = 0.011) without significant differences between groups and relaxation was affected neither by peritonitis and endotoxemia nor by the fluid regimen. CONCLUSIONS: Intestinal contractility is similarly impaired during peritonitis and during endotoxemia. Moreover, perioperative high-volume fluid resuscitation in sham-operated animals also decreases intestinal contractility. This may have consequences for postoperative recovery.

Different contribution of splanchnic organs to hyperlactatemia in fecal peritonitis and cardiac tamponade.

BACKGROUND: Changes in hepatosplanchnic lactate exchange are likely to contribute to hyperlactatemia in sepsis. We hypothesized that septic and cardiogenic shock have different effects on hepatosplanchnic lactate exchange and its contribution to hyperlactatemia. MATERIALS AND METHODS: 24 anesthetized pigs were randomized to fecal peritonitis (P), cardiac tamponade (CT), and to controls (n = 8 per group). Oxygen transport and lactate exchange were calculated during 24 hours. RESULTS: While hepatic lactate influx increased in P and in CT, hepatic lactate uptake remained unchanged in P and decreased in CT. Hepatic lactate efflux contributed 20% (P) and 33% (CT), respectively, to whole body venous efflux. Despite maintained hepatic arterial blood flow, hepatic oxygen extraction did not increase in CT. CONCLUSIONS: Whole body venous lactate efflux is of similar magnitude in hyperdynamic sepsis and in cardiogenic shock. Although jejunal mucosal pCO2 gradients are increased, enhanced lactate production from other tissues is more relevant to the increased arterial lactate. Nevertheless, the liver fails to increase hepatic lactate extraction in response to rising hepatic lactate influx, despite maintained hepatic oxygen consumption. In cardiac tamponade, regional, extrasplanchnic lactate production is accompanied by hepatic failure to increase oxygen extraction and net hepatic lactate output, despite maintained hepatic arterial perfusion.

Mesh shrinkage and pain in laparoscopic ventral hernia repair: a randomized clinical trial comparing suture versus tack mesh fixation.

BACKGROUND: Mesh fixation during laparoscopic ventral hernia repair can be performed using transfascial sutures or metal tacks. The aim of the present study is to compare mesh shrinkage and pain between two different techniques of mesh fixation in a prospective randomized trial. METHODS: A randomized trial was performed. Patients with ventral hernia of maximal diameter 8 cm were assigned to mesh fixation using either transfascial nonabsorbable sutures or metal tacks for fixation of a parietene composite mesh. The borders of the mesh were marked using clips, and radiological images in prone position were used for assessment of mesh size and location. The primary endpoint was mesh shrinkage; secondary endpoints included postoperative pain, mesh dislocation, and surgical morbidity. RESULTS: Demographic parameters were similar in both groups. A total of 40 patients were randomized, and 36 patients were available for follow-up. There was one hernia recurrence in each group. Pain was significantly higher following suture fixation after 6 weeks, but no difference was found after 6 months. Mesh shrinkage after 6 months was significantly higher using tacks for mesh fixation. CONCLUSIONS: Transfascial sutures are associated with more pain within the first 6 postoperative weeks and less mesh shrinkage after 6 months compared with mesh fixation using metal tacks.

Fecal calprotectin correlates more closely with the Simple Endoscopic Score for Crohn's disease (SES-CD) than CRP, blood leukocytes, and the CDAI.

OBJECTIVES: Studies evaluating the correlation between the widely used Simple Endoscopic Score for Crohn's disease (SES-CD) and noninvasive markers are scarce. The aim of this study was to evaluate the correlation between the SES-CD and fecal calprotectin, C-reactive protein (CRP), blood leukocytes, and the Crohn's disease activity index (CDAI). METHODS: Crohn's disease patients undergoing complete ileocolonoscopy were prospectively enrolled and scored independently according to the SES-CD and the CDAI. SES-CD was defined as follows: inactive 0-3; mild 4-10; moderate 11-19; and high > or =20. RESULTS: Values in CD patients (n=140 ileocolonoscopies) compared with controls (n=43) are as follows: calprotectin, 334+/-322 vs. 18+/-5 microg/g; CRP, 26+/-29 vs. 3+/-2 mg/l; and blood leukocytes, 9.1+/-3.4 vs. 5.4+/-1.9 g/l (all P<0.001). The SES-CD correlated closest with calprotectin (Spearman's rank correlation coefficient r=0.75), followed by CRP (r=0.53), blood leukocytes (r=0.42), and the CDAI (r=0.38). Calprotectin was the only marker that could discriminate inactive endoscopic disease from mild activity (104+/-138 vs. 231+/-244 microg/g, P<0.001), mild from moderate activity (231+/-244 vs. 395+/-256 microg/g, P=0.008), and moderate from high activity (395+/-256 vs. 718+/-320 microg/g, P<0.001). The overall accuracy for the detection of endoscopically active disease was 87% for calprotectin (cutoff 70 microg/g), 66% for elevated CRP, 54% for blood leukocytosis, and 40% for the CDAI > or =150. CONCLUSIONS: Fecal calprotectin correlated closest with SES-CD, followed by CRP, blood leukocytes, and the CDAI. Furthermore, fecal calprotectin was the only marker that reliably discriminated inactive from mild, moderate, and highly active disease, which underlines its usefulness for activity monitoring.

Effect of fluid resuscitation on mortality and organ function in experimental sepsis models.

INTRODUCTION: Several recent studies have shown that a positive fluid balance in critical illness is associated with worse outcome. We tested the effects of moderate vs. high-volume resuscitation strategies on mortality, systemic and regional blood flows, mitochondrial respiration, and organ function in two experimental sepsis models. METHODS: 48 pigs were randomized to continuous endotoxin infusion, fecal peritonitis, and a control group (n = 16 each), and each group further to two different basal rates of volume supply for 24 hours [moderate-volume (10 ml/kg/h, Ringer's lactate, n = 8); high-volume (15 + 5 ml/kg/h, Ringer's lactate and hydroxyethyl starch (HES), n = 8)], both supplemented by additional volume boli, as guided by urinary output, filling pressures, and responses in stroke volume. Systemic and regional hemodynamics were measured and tissue specimens taken for mitochondrial function assessment and histological analysis. RESULTS: Mortality in high-volume groups was 87% (peritonitis), 75% (endotoxemia), and 13% (controls). In moderate-volume groups mortality was 50% (peritonitis), 13% (endotoxemia) and 0% (controls). Both septic groups became hyperdynamic. While neither sepsis nor volume resuscitation strategy was associated with altered hepatic or muscle mitochondrial complex I- and II-dependent respiration, non-survivors had lower hepatic complex II-dependent respiratory control ratios (2.6 +/- 0.7, vs. 3.3 +/- 0.9 in survivors; P = 0.01). Histology revealed moderate damage in all organs, colloid plaques in lung tissue of high-volume groups, and severe kidney damage in endotoxin high-volume animals. CONCLUSIONS: High-volume resuscitation including HES in experimental peritonitis and endotoxemia increased mortality despite better initial hemodynamic stability. This suggests that the strategy of early fluid management influences outcome in sepsis. The high mortality was not associated with reduced mitochondrial complex I- or II-dependent muscle and hepatic respiration.