Delayed gastropleural fistula: a rare cause of a persistent pleural effusion after blunt force trauma.

A gastropleural fistula (GPF) is a rare pathological connection between the stomach and pleural cavity. Diagnosis and treatment are frequently delayed due to the lack of specific clinical, laboratory and radiological findings. We describe a case of a 53-year-old gentleman who presented to our institution with respiratory sepsis and a massive haemopneumothorax on imaging. Uniquely, he was discharged a week prior after a splenectomy for a traumatic fall. Gut flora in the pleural fluid and a subsequent positive dye test suggested an aero-digestive connection. Repeat imaging revealed a fistula between stomach and the left pleural cavity through a ruptured diaphragm. He underwent an open sleeve gastrectomy and primary repair of the diaphragm. This is the first GPF in literature presenting in such a fashion. Although rare, a persistent effusion with a history of blunt thoracoabdominal trauma may herald a GPF, which, if not diagnosed promptly, may result in significant morbidity.

The ecology of antibiotic use in the ICU: homogeneous prescribing of cefepime but not tazocin selects for antibiotic resistant infection.

BACKGROUND: Antibiotic homogeneity is thought to drive resistance but in vivo data are lacking. In this study, we determined the impact of antibiotic homogeneity per se, and of cefepime versus antipseudomonal penicillin/ß-lactamase inhibitor combinations (APP-ß), on the likelihood of infection or colonisation with antibiotic resistant bacteria and/or two commonly resistant nosocomial pathogens (methicillin-resistant Staphylococcus aureus and Pseudomonas aeruginosa). A secondary question was whether antibiotic cycling was associated with adverse outcomes including mortality, length of stay, and antibiotic resistance. METHODS: We evaluated clinical and microbiological outcomes in two similar metropolitan ICUs, which both alternated cefepime with APP-ß in four-month cycles. All microbiological isolates and commensal samples were analysed for the presence of antibiotic-resistant bacteria including MRSA and P. aeruginosa. RESULTS: Length of stay, mortality and overall antibiotic resistance were unchanged after sixteen months. However, increased colonisation and infection by antibiotic-resistant bacteria were observed in cefepime cycles, returning to baseline in APP-ß cycles. Cefepime was the strongest risk factor for acquisition of antibiotic-resistant infection. CONCLUSIONS: Ecological effects of different ß-lactam antibiotics may be more important than specific activity against the causative agents or the effect of antibiotic homogeneity in selection for antibiotic resistance. This has important implications for antibiotic policy.

The effect of midazolam on neutrophil mitogen-activated protein kinase.

BACKGROUND: Neutrophil p38 mitogen-activated protein kinase (MAPK) is a key enzyme in the intracellular signalling pathway that is responsible for many neutrophil functions, which are important in neutrophil-endothelial interaction. The imidazole compounds are inhibitors of this enzyme system. The objectives of this in-vitro investigation were to examine the effect of midazolam on neutrophil p38 MAPK activation (phosphorylation) following in-vitro ischaemia-reperfusion injury, and the expression of adhesion molecule CD11b/CD18. METHODS: In-vitro injury was produced by incubating the neutrophils with N-formyl-methionyl-leucyl-phenylalanine. Neutrophils were treated with either 10 or 50 times the therapeutic plasma concentrations of midazolam and SB203580 (known inhibitor of p38 MAPK). The concentrations of phosphorylated p38 MAPK and expression of neutrophil adhesion molecules CD11b/CD18 were measured. Flow cytometry was used to estimate adhesion molecule expression. RESULTS: The concentration of phosphorylated p38 MAPK was less in neutrophils subjected to ischaemia-reperfusion and treated with midazolam either 10 microg ml [13.6 (3.2) ng ml] or 50 microg ml [12.4 (3.6) ng ml], or SB203580 [13 (2.6) ng ml] than those subjected to ischaemia-reperfusion alone [18 (3.18) ng ml] at a P value of less than 0.05.Following ischaemia-reperfusion injury, CD11b/CD18 expression (expression mean channel fluorescence) on neutrophils was greater when compared with controls. The magnitudes of CD11b and CD18 expression on ischaemia-reperfusion-injured neutrophils were decreased by midazolam (10 microg ml) as compared with control of 10.3 (2.6) vs. 14 (3.1) microg ml and 28.3 (12.9) vs. 44 (12.1) microg ml, respectively, at a P value of less than 0.05. Similarly, the expression of CD11b and CD18 was less in ischaemia-reperfusion-injured neutrophils treated with inhibitor of 10.3 (2.8) vs. 14 (3.18) microg ml and 29.5 (12.5) vs. 44.3 (12.3) microg ml when compared with controls at a P value of less than 0.05. CONCLUSION: Midazolam diminishes in-vitro ischaemia-reperfusion-induced phosphorylation of p38 MAPK in neutrophils. This decrease in p38 MAPK activation results in decreased neutrophil CD11b/CD18 molecule expression.