Is Roux-en-Y Feeding Jejunostomy a Safe and Effective Operation in Children? A Systematic Review Exploring Outcomes.

OBJECTIVES: Roux-en-Y jejunostomy (REYJ) may establish feeding in children with foregut dysmotility or severe gastro-esophageal reflux disease (GERD). Nevertheless, concerns have been raised about safety and efficacy. We, therefore, evaluated outcomes of REYJ by systematic review to determine if this was a satisfactory option for achieving enteral autonomy in children with complex nutritional needs. METHODS: A PRISMA-adherent systematic review was conducted of studies reporting children undergoing feeding REYJ. Two authors performed processes independently; the senior author resolved disagreements. Embase, CINAHL and Medline were searched (inception-01/21). Additional databases, references, and 'grey' literature were searched. Methodological Index for Non-randomized Studies (MINORS) and a bespoke system assessed methodological quality. RESULTS: Of 362 articles, 10 met eligibility criteria (9 retrospective series; 1 conference proceeding). Unpublished data were also attained. Interobserver agreement for MINORS (kappa = 0.47) and bespoke scoring (kappa = 0.58) were moderate. After consensus, median MINORS score was 37.5% (IQR 6.3%) and bespoke 50% (IQR 20.8%), indicating poor methodological quality. One hundred sixty-four patients were reported (age range: 2 months to 19 years). Time to full feeds and length of stay were inadequately reported but most achieved enteral autonomy. No studies reported patient/caregiver-questionnaires. Seventy-six complications were documented (Clavien-Dindo grading was infeasible). Morbidity included peristomal leakage (N = 26), internal hernia/volvulus (N = 8), and SSI (N = 7). Thirty-eight patients died (2 procedure-attributable) during follow-up (range: 1 month to 15 years). CONCLUSIONS: Up to 50% patients experience complications after REYJ (often minor) with 23% patients dying during follow-up, often comorbidity-attributable. REYJ can achieve enteral autonomy although parents/caregivers of children should be counselled accordingly.

Inhibition of Signal Transducer and Activator of Transcription 3 (STAT3) reduces neonatal hypoxic-ischaemic brain damage.

Hypoxic-ischaemic encephalopathy is a leading cause of child death, with high mortality and morbidity, including cerebral palsy, epilepsy and cognitive disabilities. Hypoxia-ischaemia (HI) strongly up-regulates Signal Transducer and Activator of Transcription 3 (STAT3) in the immature brain. Our aim was to establish whether STAT3 up-regulation is associated with neonatal HI-brain damage and evaluate the phosphorylated STAT3-contribution from different cell types in eliciting damage. We subjected postnatal day seven mice to unilateral carotid artery ligation followed by 60 min hypoxia. Neuronal STAT3-deletion reduced cell death, tissue loss, microglial and astroglial activation in all brain regions. Astroglia-specific STAT3-deletion also reduced cell death, tissue loss and microglial activation, although not as strongly as the deletion in neurons. Systemic pre-insult STAT3-blockade at tyrosine 705 (Y705) with JAK2-inhibitor WP1066 reduced microglial and astroglial activation to a more moderate degree, but in a pattern similar to the one produced by the cell-specific deletions. Our results suggest that STAT3 is a crucial factor in neonatal HI-brain damage and its removal in neurons or astrocytes, and, to some extent, inhibition of its phosphorylation via JAK2-blockade reduces inflammation and tissue loss. Overall, the protective effects of STAT3 inactivation make it a possible target for a therapeutic strategy in neonatal HI. Current data show that neuronal and astroglial STAT3 molecules are involved in the pathways underlying cell death, tissue loss and gliosis following neonatal hypoxia-ischaemia, but differ with respect to the target of their effect. Y705-phosphorylation contributes to hypoxic-ischaemic histopathology. Protective effects of STAT3 inactivation make it a possible target for a therapeutic strategy in neonatal hypoxia-ischaemia.