Cardiorespiratory performance capacity and airway microbiome in patients following primary repair of esophageal atresia.

BACKGROUND: Patients following repair of an esophageal atresia (EA) or tracheoesophageal fistula (TEF) carry an increased risk of long-term cardiopulmonary malaise. The role of the airway microbiome in EA/TEF patients remains unclear. METHODS: All EA/TEF patients treated between 1980 and 2010 were invited to a prospective clinical examination, spirometry, and spiroergometry. The airway microbiome was determined from deep induced sputum by 16 S rRNA gene sequencing. The results were compared to a healthy age- and sex-matched control group. RESULTS: Nineteen EA/TEF patients with a mean age of 24.7 ± 7 years and 19 age- and sex-matched controls were included. EA/TEF patients showed a significantly lower muscle mass, lower maximum vital capacity (VCmax), and higher rates of restrictive ventilation disorders. Spiroergometry revealed a significantly lower relative performance capacity and lower peak VO2 in EA/TEF patients. Alpha- and beta-diversity of the airway microbiome did not differ significantly between the two groups. Linear discriminant effect size analysis revealed significantly enriched species of Prevotella_uncultured, Streptococcus_anginosus, Prevotella_7_Prevotella_enoeca, and Mogibacterium_timidum. CONCLUSION: EA/TEF patients frequently suffer from restrictive ventilation disorders and impaired cardiopulmonary function associated with minor alterations of the airway microbiome. Long-term examinations of EA/TEF patients seem to be necessary in order to detect impaired cardiopulmonary function. IMPACT: The key messages of the present study are a significantly decreased VCmax and exercise performance, as well as airway microbiome differences in EA/TEF patients. This study is the first to present parameters of lung function and exercise performance in combination with airway microbiome analysis with a mean follow-up of 24 years in EA/TEF patients. Prospective, long-term studies are needed to unravel possible interactions between alterations of the airway microbiome and impaired pulmonary function in EA/TEF patients.

Oesophageal atresia: The growth gap.

Poor growth is an under-recognised yet significant long-term sequelae of oesophageal atresia (OA) repair. Few studies have specifically explored the reasons for growth impairment in this complex cohort. The association between poor growth with younger age and fundoplication appears to have the strongest supportive evidence, highlighting the need for early involvement of a dietitian and speech pathologist, and consideration of optimal medical reflux management prior to referring for anti-reflux surgery. However, it remains difficult to reach conclusions regarding other factors which may negatively influence growth, due to conflicting findings, inconsistent definitions and lack of validated tool utilisation. While swallowing and feeding difficulties are particularly frequent in younger children, their relationship with growth remains unclear. It is possible that these morbidities impact on the diet of children with OA, but detailed analysis of dietary composition and quality, and its relationship with these complications and growth, has not yet been conducted. Another potential area of research in OA is the role of the microbiota in growth and nutrition. While the microbiota has been linked to growth impairment in other paediatric conditions, it is yet to be investigated in OA. Further research is needed to identify the most important contributory factors to poor growth, the role of the intestinal microbiota, and effective interventions to maximise growth and nutritional outcomes in this cohort.

Bacterial colonisation of the upper pouch in neonates with oesophageal atresia.

The bacterial flora in the upper oesophageal pouch of forty neonates with oesophageal atresia was studied at daily intervals preoperatively. Of the twenty-nine infants whose oesophagus was anastomosed within 24 hours of admission, no organisms were isolated in sixteen, despite the fact that only nine of these patients had antibiotics. The remaining thirteen grew oropharyngeal organisms. Of eleven infants having delayed anastomosis eight received antibiotics. All eleven grew organisms in the upper pouch. Pseudomonas and serratia grew only in those receiving antibiotics. These results suggest that prophylactic antibiotics are rarely indicated. Efficient continuous aspiration of the pouch is probably more important.

Faecal flora in neonates with oesophageal atresia.

The bacteriological findings of a study of intestinal colonisation in 24 neonates with oesophageal atresia are reported. Only five of the patients received antibiotics. When compared with published findings in healthy neonates, the rate of intestinal colonisation in our series was prolonged, with Staphylococcus albus predominating in the first week. Anaerobic colonisation was delayed and bacteroides spp were present in only five patients by the third week. Bifidobacteria were almost completely absent. The onset of intestinal colonisation seemed to be related temporally to enteral feeding. The use of antibiotics in five patients resulted in colonisation by candida in four and clinical thrush in three.

[The infectious risk in neonatal surgery : an evaluation of frequency and consequences from a study of 300 cases (author's transl)]. / Evaluation et interprétation du risque infectieux en chirurgie néo-natale. A propos de 300 observations.

This study is an evaluation of the infectious risk related to neonatal surgery in 300 patients between 1968 and 1978, and its consequences to mortality and morbidity. Bacteriological species, circumstances, chronology of infection, related to each type of surgical pathology prove the endogenous way of contamination to be usual and predominant. When intestinal obstruction occurs, the risk of hematogenous diffusion is directly dependent from local stasis and bacterial pullulation which can be evaulated with duodenal, jejunal or fecal samples. Both mechanical factors and antibiotictherapy can induce qualitative and quantitative changes in bacterial flora of the bowel, and then increase the incidence of endogenous septicemia.