Internal herniation through the falciform ligament of the liver: a case report

<p><b>Background:</b> An internal abdominal hernia is defined as the protrusion of a viscus through a mesenteric or peritoneal aperture within the peritoneal cavity. A less common type of internal herniation is a small bowel herniation through a defect in the falciform ligament of the liver. This defect can be congenital or iatrogenic after penetration of the falciform ligament with a trocar during laparoscopic surgery.</p> <p><b>Methods:</b> We present a case report illustrating an internal herniation through an iatrogenic defect in the falciform ligament of the liver.</p> <p><b>Results:</b> A 78-year-old man comes to the emergency department with severe abdominal pain for several hours. Laparoscopic exploration shows a small bowel herniation through an iatrogenic defect of the falciform ligament after laparoscopic cholecystectomy. Reduction of the internal herniation is performed. Due to subsequently small bowel necrosis, a small bowel resection with primary anastomosis has to be performed too.</p> <p><b>Conclusion:</b> Small bowel herniation through an iatrogenic defect in the falciform ligament is very rare. However, it can lead to severe complications such as small bowel necrosis. To prevent internal herniation, we strongly suggest immediate repair or division of the falciform ligament when an iatrogenic defect is created during laparoscopic procedures.</p

Pro-inflammatory cytokines correlate AST levels.

<p>Using Spearman correlation analysis we detected a significantly, positive correlation between plasma AST levels and cytokines IL8, TNFα and the chemokine CCL3 (Fig 5A-5C).</p

A schematic representation of the study design

<p>A schematic representation of the study design</p

Pro-Inflammatory Cytokines but Not Endotoxin-Related Parameters Associate with Disease Severity in Patients with NAFLD

<div><p>Intestinal dysbiosis and elevated lipopolysaccharides (LPS) levels have been implicated in the development of obesity, insulin resistance and non-alcoholic steatohepatitis (NASH). In order to determine if LPS levels are elevated in patients with NASH compared to patients with non-alcoholic fatty liver (NAFL) and, if elevated LPS levels correlated with histological severity of non-alcoholic fatty liver disease (NAFLD) we compared LPS, markers of LPS bioactivity and pro-inflammatory cytokines/chemokines in patients undergoing bariatric surgery. At the time of surgery a liver biopsy was taken allowing the stratification into well-delineated subgroups including: No NAFL/NAFL; NASH; NASH with fibrosis and NASH cirrhotics, using the NAFLD Activity Score (NAS). Anthropometric data and plasma were collected for assessment of LPS, lipopolysaccharide binding protein (LBP), soluble CD14 (sCD14), intestinal-type fatty acid binding protein (iFABP), Toll-like receptors 2 and 4 (TLR2, 4) and a panel of cytokines/chemokines. Similar analysis was performed on plasma from a cohort of healthy controls. Our data indicate elevated levels of LPS, LBP, sCD14, iFABP and TLR2,4 in obese patients compared to healthy controls, however, these parameters remained unaltered within patients with limited liver disease (NAFL) compared to NASH/NASH with fibrosis subgroups. Hierarchic cluster analysis using endotoxin-related parameters failed to discriminate between lean controls, NAFLD. While similar cluster analysis implementing inflammation-related parameters clearly distinguished lean controls, NALFD subgroups and NASH cirrhotics. In addition, LPS levels was not associated with disease severity while TNFα, IL8, and CCL3 featured a clear correlation with transaminase levels and the histological severity of NALFD. In conclusion our data indicate a stronger correlation for circulating inflammatory- rather than endotoxin-related parameters in progression of NAFLD and highlights the need for additional larger studies in unravelling further mechanistic insights.</p></div

Plasma cytokine and chemokine levels across histological subgroups.

<p>Plasma IL8, TNFα and CCL3 were significantly different between histological subgroups (Fig 4A-4C). Plasma IL6 and CCL2 were significantly higher in patients with cirrhosis compared to other patient groups (Fig 4D and 4E) (see also <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0166048#pone.0166048.g002" target="_blank">Fig 2</a>).</p

Hierarchic clustering was performed of patients using plasma levels of cytokines, chemokines and markers of endotoxemia to investigate global distribution along the 5 histological subgroups.

<p><b>Fig 3A.</b> Hierarchic cluster analysis was performed using iFABP, LBP, LPS and sCD14. Using these markers only a group enriched with cirrhotic patients could be distinguished from the rest. In <b>Fig 3B</b> we used clustering on 5 cytokine/inflammation markers (CCL2, CCL3, TNFα, IL6 and IL8), whereby 3 blocks could be distinguished with some patients misclassified, using the same statistical setting (Euclidian distance, McQuitty’s linkage rule and normalized Z-score, see [<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0166048#pone.0166048.ref022" target="_blank">22</a>]). Abbreviations: CIR: cirrhosis; OB: obese with no NAFL; NFL: NAFL; NFR: NASH with fibrosis and NSH: NASH. </p

Spearman correlation between plasma levels of inflammatory cytokines and liver histology.

<p>Plasma TNFα and CCL3 correlate significantly with features of liver histology (Fig 6A-6F), such as NAS, lobular inflammation and fibrosis scores, while plasma IL8 levels correlated with fibrosis stage (Fig 6G) suggesting that these inflammatory mediators might be important in NAFLD pathogenesis.</p

Plasma levels of markers of endotoxemia and intestinal permeability across the different histological subgroups of patients.

<p>Five out of six markers investigated (with exception of iFABP), the concentrations in the lean controls was significantly lower than in the NAFLD subgroups. For 4 markers (LPS, iFABP, TLR2 and TLR4) plasma levels in cirrhosis patients was significantly different from NAFLD subgroups. Brackets indicate that analysis of multiple subgroups with cirrhosis or lean group (as indicated) was statistically relevant for each subgroup separately. When comparison was made between the groups included in the brackets there was no statistical difference (Kruskal-Wallis One Way Analysis of Variance on Ranks). Only if p < 0.05, this was considered significant and indicated in the figures.</p