Outcomes of laparotomy in preterm infants with extremely low operative weight (< 1000 g).

PURPOSE: Most studies on outcomes of surgery in extremely premature neonates include cases based on birth weight irrespective of weight at the time of surgery. Reported figures may not accurately reflect what is truly experienced in babies with smaller weight at the time of surgery. This study sought to document the outcomes of laparotomy in preterms at extremely low operative (ELOW) of < 1000 g. METHODS: Preterm infants weighing < 1000 g at the time of laparotomy were identified from a prospectively collected database. Data were collected over 12 years (Sept 2007-Mar 2020). Primary outcome investigated was in-hospital mortality. Other outcomes including long-term morbidities are reported. RESULTS: 79 ELOW infants were included. Median gestational age was 25 weeks (23-29 weeks) and median birth weight 680 g (382-986 g). The median weight at laparotomy was 755 g (380-993 g) at a median age of 11 days of life (1-38 days). The commonest diagnoses at laparotomy included: necrotising enterocolitis 44 (56%), spontaneous intestinal perforation 20 (25%) and meconium obstruction of prematurity 5 (6%). The median predicted mortality using CRIB II scoring system was 35%. 21 (27%) in-hospital mortality was recorded. Babies who died had significantly lower operative weight (610 vs 767 g p = 0.0303) compared to those who survived despite no significant difference in birth weight. 30% had one or more surgical complications. 50% had no recorded morbidity at 2-year assessment while 19% had severe impairment. CONCLUSION: 73% of preterm infants that underwent laparotomy at < 1000 g survived to discharge and 50% of survivors had no long-term morbidity. Association between mortality and lower operative weight at laparotomy is shown. This study provides a focused data on the ELOW category of patients which could more accurately guide counselling and management decisions.

Alleviated mucosal and neuronal damage in a rat model of Crohn's disease.

AIM: To establish a rat model suitable to investigate the repetitive relapsing inflammations (RRI) characteristic to Crohn's disease. METHODS: Colitis was induced by 2,4,6-trinitrobenzenesulfonic acid (TNBS). RRI were mimicked by repeating administrations of TNBS. Tissue samples were taken from control, once, twice and three times treated rats from the inflamed and adjacent non-inflamed colonic segments at different timepoints during the acute intestinal inflammation. The means of the ulcerated area were measured to evaluate the macroscopic mucosal damage. The density of myenteric neurons was determined on whole mounts by HuC/HuD immunohistochemistry. Heme oxygenase-1 (HO-1) expression was evaluated by molecular biological techniques. RESULTS: TNBS-treated rats displayed severe colitis, but the mortality was negligible, and an increase of body weight was characteristic throughout the experimental period. The widespread loss of myenteric neurons, and marked but transient HO-1 up-regulation were demonstrated after the first TNBS administration. After repeated doses the length of the recovery time and extent of the ulcerous colonic segments were markedly decreased, and the neuronal loss was on a smaller scale and was limited to the inflamed area. HO-1 mRNA level was notably greater than after a single dose and overexpression was sustained throughout the timepoints examined. Nevertheless, the HO-1 protein up-regulation after the second TNBS treatment proved to be transient. Following the third treatment HO-1 protein expression could not be detected. CONCLUSION: Experimentally provoked RRI may exert a protective preconditioning effect against the mucosal and neuronal damage. The persistent up-regulation of HO-1 mRNA expression may correlate with this.

Gut region-specific rearrangement of the cellular and subcellular compartments of nitric oxide synthase isoforms after chronic ethanol consumption in rats.

We recently provided evidence of cell-type-specific differences in the subcellular distributions of the three nitric oxide synthase (NOS) isoforms in the myenteric neurons, enteric smooth muscle cells and the capillary endothelium of the rat duodenum. We hypothesized that the presence of three NOS isoforms in the same type of cells with differences in subcellular compartmentalization might reflect a functional plasticity. Therefore, investigation of the possible rearrangement of cellular and subcellular NOS compartments in different gut segments following chronic ethanol treatment was the aim of this study. Rats were randomly divided into two groups and received water or 20% ethanol solution, preceded by short periods of adaptation with 10% and 15% ethanol. After 8 weeks, segments of duodenum, ileum and colon of the control and the alcohol-treated rats were processed for post-embedding immunohistochemistry and RT-PCR. The quantitative differences in the numbers of gold particles indicative of the different NOSs and their relative mRNA levels between the two experimental groups varied greatly, depending on the gut segment, and also on the cellular and subcellular compartments investigated. The chronic ethanol administration had the opposite effect on the quantitative distribution of the neuronal and endothelial NOS labelling gold particles in the different cellular compartments and resulted in subcellular rearrangement of NOS labels along the gastrointestinal tract. The intestinal region-specific rearrangement of the cellular and subcellular NOS compartments may possibly result in functional plasticity and help to maintain the optimum NO level under pathological conditions.