Intra-Abdominal Hypertension Causes Bacterial Growth in Lungs: An Animal Study.

To study the effect of intra-abdominal hypertension (IAH) on the frequency of pneumonia with an experimental study, thirteen Sprague-Dawley rats were included. Eight out of thirteen animals were randomly assigned to receive 10 ml of benzalkonium chloride 0.2% (megacolon group) and five animals received 10 ml NaCl 0.9% (controls). Animals were anaesthetized by intramuscular delivery of ketamine. The incidence of positivity for bacteria lung tissue cultures and mesenteric lymph node cultures was assessed at the 21st day after animals' sacrification, or before in case of death. All megacolon group animals presented progressive increase of the abdomen and increased IAP (≥10 mmHg) whereas the frequency of their evacuations was almost eliminated. Controls presented normal evacuations, no sign of abdominal distention, and normal IAP. In megacolon group animals, there was evidence of significant amount of bacteria in lung cultures. In contrast, no bacteria were found in control animals.

The Effect of Elevated Intra-Abdominal Pressure on TLR4 Signaling in Intestinal Mucosa and on Intestinal Bacterial Translocation in a Rat.

BACKGROUND: Recent evidence suggests that elevated intra-abdominal pressure (IAP) may adversely affect the intestinal barrier function. Toll-like receptor 4 (TLR-4) is responsible for the recognition of bacterial endotoxin or lipopolysaccharide and for initiation of the Gram-negative septic shock syndrome. The objective of the current study was to determine the effects of elevated IAP on intestinal bacterial translocation (BT) and TLR-4 signaling in intestinal mucosa in a rat model. METHODS: Male Sprague-Dawley rats were randomly assigned to one of two experimental groups: sham animals (Sham) and IAP animals who were subjected to a 15 mmHg pressure pneumoperitoneum for 30 minutes. Rats were sacrificed 24 hours later. BT to mesenteric lymph nodes, liver, portal vein blood, and peripheral blood was determined at sacrifice. TLR4-related gene and protein expression (TLR-4; myeloid differentiation factor 88 [Myd88] and TNF-α receptor-associated factor 6 [TRAF6]) expression were determined using real-time PCR, western blotting, and immunohistochemistry. RESULTS: Thirty percent of sham rats developed BT in the mesenteric lymph nodes (level I) and 20% of control rats developed BT in the liver and portal vein (level II). abdominal compartment syndrome (ACS) rats demonstrated an 80% BT in the lymph nodes (Level I) and 40% BT in the liver and portal vein (Level II). Elevated BT was accompanied by a significant increase in TLR-4 immunostaining in jejunum (51%) and ileum (35.9%), and in a number of TRAF6-positive cells in jejunum (2.1%) and ileum (24.01%) compared to control animals. ACS rats demonstrated a significant increase in TLR4 and MYD88 protein levels compared to control animals. CONCLUSIONS: Twenty-four hours after the induction of elevated IAP in a rat model, increased BT rates were associated with increased TLR4 signaling in intestinal mucosa.

[Non-perforation tensionpneumoperitoneum resulting from primary non-aerobic bacterial peritonitisin a previously healthy middle-aged man: A case report].

Background: Tension pneumoperitoneumis a rare surgical emergency in which free intra-peritoneal gas accumulates under pressure. The known sources of free gas are perforated hollow viscera. We believe this is the first published case of atension non-perforation pneumoperitoneum secondary to anaerobic gas production. This occurred in a background of primary non-aerobic bacterial peritonitis, which developed in an immunocompetent adult male. Case presentation: A previously healthy 45-year-old Bulgarian male presented with a 3-week history of abdominal pain. He displayed signs of shock, peritonitis, and abdominal compartment syndrome. A plain abdominal X-ray showed thepathognomonic "saddlebag sign" with the liver displaced downwards and medially. An emergency laparotomy released pressurized gas, accompanied by 3100 mL of foamy pus. A sudden haemodynamic deterioration occurred soon after decompression. The sources of infection and tension pneumoperitoneum were not found. The peritoneal exudate sample did not recover aerobes. A laparostomy was created and three planned re-laparotomies were performed. During the second re-operation we placed an intraperitoneal silo and the abdomen was closed with skin sutures. Definitive fascial closure was achieved through separation of the two rectus muscles from their posterior sheaths. The patient was discharged in good healthon the 25th postoperative day. Conclusion: Our case provides evidence supporting the theory that anaerobic infection may underlie the etiology of tension pmeumoperitoneum. Prior to decompressive laparotomy the patient should receive an intravenous volume bolus to compensate for possible hypotension. If laparostomy leads to lateralization of the rectus muscles with a gap of 6 cm or less, the posterior part of the components separation technique is effective in achieving fascial closure. We present an original classification of tension pneumoperitoneum defining it as primary or secondary.