Spontaneously closed gastrocutaneous fistula becomes symptomatic after 30 years with pregnancy.

Percutaneous endoscopic gastrostomy (PEG) is the standard procedure of choice for the provision of enteral nutrition in children who require long-term nutritional support. Removal of gastric tubes has a risk of causing gastrocutaneous fistula and this complication is dealt within childhood. The authors report a 34-year old woman who had a PEG procedure at the age of four years due to caustic esophageal injury and recovered without incident. Thirty years later she becomes pregnant and as her pregnancy progresses, her former fistula opening becomes more obvious and at the 34'h week of the pregnancy she' presents to the hospital with fistula. After a successful delivery, the fistula was evaluated and repaired surgically.

The effect of exogenous melatonin on experimental colonic anastomosis.

UNLABELLED: In this study we investigated the role of exogenous melatonin administration on the healing of colonic anastomoses. MATERIALS AND METHODS: Rats were divided into four groups: control, vehicle, 1 mg/kg and 10 mg/kg melatonin, which was administered postoperatively on days 0, 1, and 2. Following colon resection and anastomosis, the rats were sacrificed on the 3rd and 7th days to measure bursting pressure and hydroxyproline content of the anastomoses. RESULTS: Bursting pressure significantly increased on the 7th day compared with the 3rd day in all groups. Hydroxyproline levels did not show any significant change on the 3rd day compared with the 7th day in any of the groups. Hydroxyproline levels were significantly higher in control groups than in melatonin groups. CONCLUSION: Results suggest that exogenous melatonin has no beneficial effect on the healing of colonic anastomosis.

Adrenalin tolerance does not prevent bacterial translocation in a murine burn model.

Burn injury causes mesenteric vasoconstriction and bacterial translocation. Since catecholamines are powerful vasoconstrictors and elevated immediately after burn injury, we hypothesised that adrenaline tolerance might decrease burn-induced mesenteric vasoconstriction and bacterial translocation. Adrenaline tolerance was developed in Swiss albino mice. Adrenaline tolerant and control animals were subdivided into sham-burn and burn subgroups. 24 h after sham-burn or burn injury, specimens were obtained for microbiological evaluation. Also, in a separate group of adrenaline tolerant and control animals, superior mesenteric blood flow was measured. Burn injury increased bacterial translocation rate in both control (P = 0.001) and adrenaline tolerant groups (P = 0.0351). The caecal bacterial level increase was significant after burn injury in control groups (P = 0.0004) but was not significant in adrenaline tolerant animals (P = 0.743). Mesenteric blood flow was decreased significantly by burn injury in both control and adrenaline tolerant animals (P < 0.00001). The results showed that catecholamines do not mediate postburn mesenteric vasoconstriction or bacterial translocation.

A case of renal artery stenosis secondary to chronic pancreatitis.

We report a case of renal artery stenosis most probably secondary to chronic pancreatitis. The patient had a traumatic pancreatic fistula. This was followed by numerous attacks of pancreatitis in the following years. At a relatively young age, he developed hypertension. Examinations revealed a right renal artery stenosis which was successfully treated by a percutaneous angioplasty. This rare complication should be kept in mind as a possible complication of pancreatitis.

Epinephrine and endotoxin tolerance differentially modulate serum cytokine levels to high-dose lipopolysaccharide challenge in a murine model.

BACKGROUND: The epinephrine tolerance state has been demonstrated to increase survival in endotoxic shock and was claimed to have cross-tolerance with endotoxin tolerance. With use of these data, we aimed to determine the effect of epinephrine and endotoxin tolerance on major cytokine levels in a lipopolysaccharide challenge in mice. METHODS: Epinephrine tolerance was induced by beginning with a low dose and gradually increasing to a lethal dose. Endotoxin tolerance was induced by injecting saline solution for 4 days and lipopolysaccharide 1 mg/kg on the fifth day. After these procedures, saline solution or 20 mg/kg lipopolysaccharide was injected into animals. Peak serum levels of tumor necrosis factor-alpha (TNF-alpha), interleukin 1 beta, interleukin 6 (IL-6), interleukin 10 (IL-10), and interleukin 12 (IL-12) were assayed. RESULTS: The lipopolysaccharide injection increased the levels of all the cytokines in the control and epinephrine-tolerant animals. TNF-alpha, IL-6, and IL-10 levels were lower in endotoxin-tolerant animals compared with controls. Epinephrine-tolerant animals had higher levels of TNF-alpha, IL-6, and IL-12 than the controls did. CONCLUSION: Epinephrine tolerance primes for an exaggerated release of TNF-alpha, IL-6, and IL-12 in response to lipopolysaccharide challenge, suggesting anti-inflammatory and immunosuppressive effects by epinephrine. The anti-inflammatory effect was not mediated through increased IL-10 release. Endotoxin tolerance selectively modulated cytokine release.

Effects of adrenaline or endotoxin tolerance states on mesenteric blood flow in endotoxaemia.

BACKGROUND: Endotoxic shock is associated with release of catecholamines as well as decreased mesenteric vascular perfusion, which is thought to cause remote organ injury. Adrenaline tolerance was reported to decrease mortality in endotoxic shock and have cross-tolerance with endotoxin tolerance. Our aim was to investigate the effect of these two tolerance conditions on the lipopolysaccharide (LPS)-induced decrease in mesenteric blood flow (MBF). METHODS: Adrenaline tolerance was developed by injecting 0.03 mg/kg adrenaline to Swiss-albino mice, gradually increasing the dose to 2 mg/kg over 5 days. Endotoxin tolerance was developed by injecting saline for 4 days and LPS 1 mg/kg at the fifth day. Control animals were injected with saline for 5 days. At 72 h after completion of injections, half of the animals in each group were challenged with saline and the other half with 20 mg/kg LPS, at 0 h. Mesenteric blood flow was measured at 4 and 24 h. RESULTS: Neither endotoxin nor adrenaline tolerance prevented an LPS-induced decrease in MBF. CONCLUSION: A low dose of LPS prior to a higher dose does not prevent an LPS-induced decrease in MBF and may actually prime for a decrease. Also, catecholamines are not primary mediators of LPS-induced decreases in MBF.

Experimental study of the effect of adrenaline tolerance on intestinal ischaemia-reperfusion.

BACKGROUND: Adrenaline tolerance improves survival in animal models of shock. The purpose of this study was to determine the effects of adrenaline tolerance on intestinal ischaemia-reperfusion in a mouse model. METHODS: Adrenaline tolerance was developed by injecting intravenous adrenaline, gradually increasing the dose to 2 mg/kg over 5 days. In experimental animals the superior mesenteric artery was clamped for 120 min and then released. Evans blue dye was given intravenously to all animals to quantify pulmonary microvascular injury. Some 60 min after clamp release, the animals were killed and the effects of reperfusion assessed on tissue samples. RESULTS: Evans blue dye concentrations were significantly higher in animals with intestinal ischaemia-reperfusion than in those having sham intestinal ischaemia-reperfusion or in adrenaline-tolerant mice having intestinal ischaemia-reperfusion or sham ischaemia-reperfusion (P< 0.01). Malonyldialdehyde levels increased significantly in the lung in the intestinal ischaemia-reperfusion group compared with those in the sham ischaemia-reperfusion group (P< 0.001 for liver, lung and small intestine), whereas there was no difference in adrenaline-tolerant animals. There was no significant change induced by adrenaline tolerance in myeloperoxidase levels in any organ. CONCLUSION: Adrenaline tolerance reduced the lung permeability caused by intestinal ischaemia-reperfusion. Catecholamines may play a role in free radical generation induced by ischaemia-reperfusion.