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Low-tidal-volume ventilation with positive end-expiratory pressure is the standard of care in acute respiratory distress syndrome. In this trial, the use of protective ventilation during surgery, as compared with nonprotective ventilation, reduced postoperative complications. Worldwide, more than 230 million patients undergoing major surgery each year require general anesthesia and mechanical ventilation. 1 Postoperative pulmonary complications adversely affect clinical outcomes and health care utilization, 2 so prevention of these complications has become a measure of the quality of hospital care. 3 Previous, large cohort studies have shown that 20 to 30% of patients undergoing surgery with general anesthesia are at intermediate to high risk for postoperative pulmonary complications. 4 , 5 Mechanical ventilation with the use of high tidal volumes (10 to 15 ml per kilogram of predicted body weight) has traditionally been recommended to prevent hypoxemia and atelectasis in . . .

PurposePostoperative ileus (POI) occurrence within enhanced recovery programs (ERPs) has decreased. Also, intra-abdominal complications (IAC) such as anastomotic leakage (AL) generally present late. The aim was to characterize the link between POI and the other complications occurring after surgery.MethodsThis retrospective analysis of a prospective database was conducted by the Francophone Group for Enhanced Recovery after Surgery. POI was considered to be present if gastrointestinal functions had not been recovered within 3 days following surgery or if a nasogastric tube replacement was required.ResultsOf the 2773 patients who took part in the study, 2335 underwent colorectal resections (83.8%) for cancer, benign tumors, inflammatory bowel disease, and diverticulosis. Among the 2335 patients, 309 (13.2%) experienced POI, including 185 (59.9%) cases of secondary POI. Adjusted for well-known risk factors (male gender, need for stoma, right hemicolectomy, surgery duration, laparotomy, and conversion to open surgery), POI was associated with abdominal complications (OR = 4.55; 95% confidence interval (CI): 3.30–6.28), urinary retention (OR = 1.75; 95% CI: 1.05–2.92), pulmonary complications (OR = 4.55; 95% CI: 2.04–9.97), and cardiological complications (OR = 3.01; 95% CI: 1.15–8.02). Among the abdominal complications, AL and IAC were most strongly associated with POI (respectively, OR = 5.97; 95% CI: 3.74–8.88 and OR = 5.76; 95% CI: 3.56–10.62).ConclusionWithin ERPs, POI should not be considered as usual. There is a significant link between POI and IAC. Since POI is an early-onset clinical sign, its occurrence should alert the physician and prompt them to consider performing CT scans in order to investigate other potential morbidities.

When the original article was first published the given name and family names of Francophone Group for Enhanced Recovery After Surgery (GRACE) individually cited within the author list were inadvertently interchanged. The author list are correctly cited in this Correction.

An autosomal recessive neuromuscular disorder characterized by skeletal muscle weakness, fatigability and variable electromyographic or muscular histopathological features has been described in the two related Sphynx and Devon Rex cat breeds (Felis catus). Collection of data from two affected Sphynx cats and their relatives pointed out a single disease candidate region on feline chromosome C2, identified following a genome-wide SNP-based homozygosity mapping strategy. In that region, we further identified COLQ (collagen-like tail subunit of asymmetric acetylcholinesterase) as a good candidate gene, since COLQ mutations were identified in affected humans and dogs with endplate acetylcholinesterase deficiency leading to a synaptic form of congenital myasthenic syndrome (CMS). A homozygous c.1190G>A missense variant located in exon 15 of COLQ, leading to a C397Y substitution, was identified in the two affected cats. C397 is a highly-conserved residue from the C-terminal domain of the protein; its mutation was previously shown to produce CMS in humans, and here we confirmed in an affected Sphynx cat that it induces a loss of acetylcholinesterase clustering at the neuromuscular junction. Segregation of the c.1190G>A variant was 100% consistent with the autosomal recessive mode of inheritance of the disorder in our cat pedigree; in addition, an affected, unrelated Devon Rex cat recruited thereafter was also homozygous for the variant. Genotyping of a panel of 333 cats from 14 breeds failed to identify a single carrier in non-Sphynx and non-Devon Rex cats. Finally, the percentage of healthy carriers in a European subpanel of 81 genotyped Sphynx cats was estimated to be low (3.7%) and 14 control Devon Rex cats were genotyped as wild-type individuals. Altogether, these results strongly support that the neuromuscular disorder reported in Sphynx and Devon Rex breeds is a CMS caused by a unique c.1190G>A missense mutation, presumably transmitted through a founder effect, which strictly and slightly disseminated in these two breeds. The presently available DNA test will help owners avoid matings at risk.

An autosomal recessive neuromuscular disorder characterized by skeletal muscle weakness, fatigability and variable electromyographic or muscular histopathological features has been described in the two related Sphynx and Devon Rex cat breeds (Felis catus). Collection of data from two affected Sphynx cats and their relatives pointed out a single disease candidate region on feline chromosome C2, identified following a genome-wide SNP-based homozygosity mapping strategy. In that region, we further identified COLQ (collagen-like tail subunit of asymmetric acetylcholinesterase) as a good candidate gene, since COLQ mutations were identified in affected humans and dogs with endplate acetylcholinesterase deficiency leading to a synaptic form of congenital myasthenic syndrome (CMS). A homozygous c.1190G>A missense variant located in exon 15 of COLQ, leading to a C397Y substitution, was identified in the two affected cats. C397 is a highly-conserved residue from the C-terminal domain of the protein; its mutation was previously shown to produce CMS in humans, and here we confirmed in an affected Sphynx cat that it induces a loss of acetylcholinesterase clustering at the neuromuscular junction. Segregation of the c.1190G>A variant was 100% consistent with the autosomal recessive mode of inheritance of the disorder in our cat pedigree; in addition, an affected, unrelated Devon Rex cat recruited thereafter was also homozygous for the variant. Genotyping of a panel of 333 cats from 14 breeds failed to identify a single carrier in non-Sphynx and non-Devon Rex cats. Finally, the percentage of healthy carriers in a European subpanel of 81 genotyped Sphynx cats was estimated to be low (3.7%) and 14 control Devon Rex cats were genotyped as wild-type individuals. Altogether, these results strongly support that the neuromuscular disorder reported in Sphynx and Devon Rex breeds is a CMS caused by a unique c.1190G>A missense mutation, presumably transmitted through a founder effect, which strictly and slightly disseminated in these two breeds. The presently available DNA test will help owners avoid matings at risk.