Surgical approach to neonatal intestinal perforation. An analysis on 85 cases (1991-2001).

AIM: Primary gastrointestinal perforations have an incidence of between 1% and 3% in NICU patients. The 3 Centers participating in this study cover nearly 40% of the NICU population of the Lazio Region--Italy. The aim of this study is to discuss factors affecting survival in patients affected by a primary intestinal perforation. METHODS: From 1991 to 2001, 67 cases of 85 with a neonatal gastrointestinal perforation, were related to primary bowel lesions. Necrotizing enterocolitis (NEC) was not always the cause of perforation and in many patients an isolated bowel lesion without signs of NEC was found. The aim of this study was to examine clinical and intraoperative findings of NEC and non NEC perforations and their impact on survival. A relevant number of these patients were extremely low-birth weight (ELBW). Controversies about treatment of this category of neonates are discussed. RESULTS: Patients were 37 males and 30 females (mean birth weight 1 274.8 g, mean gestational age 28.9 weeks, mean age at perforation 10 days). Overall survival was 56.8%. Patients were divided by intraoperative findings in 2 groups: NEC (n=48), or isolated intestinal perforation (IIP) without signs of NEC (n=19). Differences between these 2 groups with regard to birth weight, maturity, associated cardiac anomalies (patent ductus arteriosus, PDA) were significant. NEC and IIP behaved as 2 distinct entities, each with peculiar clinical (age at perforation, oral feeding, need of ventilatory support) and radiological aspects. At surgery, multiple lesion on necrotic bowel were typical of NEC versus single, isolated perforations on healthy bowel typical of IIP. Overall survival was almost identical in the 2 groups (59% vs 58%). ELBW patients (55% of the total neonatal intestinal perforations) were also studied. There were 21 patients with NEC and 16 with IIP. The 2 groups were different in age at perforation, previous oral feeding and associated cardiac anomalies (PDA). Overall survival was 62% for NEC and 50% for IIP. A laparotomy was always performed. Temporary peritoneal drainage was done in 4 cases only. Results were better when intestinal diversion was performed rather than resection and primary anastomosis. Almost all NEC patients had multiple perforations and extended bowel necrosis. CONCLUSION: NEC is the most frequent cause of neonatal intestinal perforation. This is a quite distinct entity from IIP, which must always be differentiated preoperatively and which is most frequently found among low birth weight newborns. As far as surgical treatment of perforation among ELBW neonates is concerned, peritoneal drainage might be reasonably performed when a single lesion on healthy bowel as in IIP is clearly diagnosed but it could be inadequate for NEC patients.

Umbilical cord interleukin-6 levels are elevated in term neonates with perinatal asphyxia.

BACKGROUND: A correlation between elevation of pro-inflammatory cytokines and white matter injury or abnormal neurologic outcome has been established in the preterm infant. In the full-term neonate, few studies exist linking elevation of cytokines with encephalopathy and poor neurodevelopmental outcome. Our aims were to investigate if serum interleukin-6 concentrations in delivering mothers and their offspring at birth are associated with perinatal asphyxia, and to examine the relation of interleukin-6 levels to the severity of hypoxic-ischemic encephalopathy and to the neurological outcome. DESIGN AND METHODS: Serum interleukin-6 levels were measured at birth, 24 and 48 h of life in 50 consecutive term uninfected newborns with perinatal asphyxia and 113 randomly selected healthy term newborns, and at delivery in their mothers. RESULTS: The median cord interleukin-6 concentrations in the infants who developed hypoxic-ischemic encephalopathy was 376-fold as high as the values in the normal infants (P < 0.0001) and 5.5-fold as high as those in the infants with asphyxia who did not develop hypoxic-ischemic encephalopathy (P < 0.05). There was also a significant relationship between interleukin-6 and the degree of hypoxic-ischemic encephalopathy, and between interleukin-6 and neurodevelopmental outcome at 2 years of age. Regardless of outcome, in the asphyxiated infants the interleukin-6 values were significantly lower at both 24 and 48 h of life than at birth, with a significant decline from 24 to 48 h of life. Among mothers of the asphyxiated neonates, there were no significant differences in interleukin-6 concentrations between those delivering neonates with and without hypoxic-ischemic encephalopathy. CONCLUSIONS: Measurement of IL-6 concentrations in the umbilical cord of neonates with perinatal asphyxia may be useful to identify early, and in a relatively simple way, those who are most likely to have subsequent brain injury and adverse outcome.

Cytogenetic and molecular characterization of a de novo 4q24qter duplication and correlation to the associated phenotype.

We report on a newborn with severe psychomotor retardation, minor anomalies, congenital heart defects, thumb and urogenital abnormalities. Cytogenetic analysis showed a 4q24qter duplication, never described before, as the result of a de novo t(4;14). The extension of the duplicated 4q region was defined by FISH using YAC probes. The breakpoint was localized between 106.3cM (YAC 800f2, D4S1572) and 111 cM (YAC 744e4, D4S1564). Comparing our patient with those previously reported in literature, we observed some features mature frequently reported in these patients: psychomotor retardation, retromicrognathia, low set and/or malformed ears and some more specific traits: congenital cardiac defects, hypoplastic thumb and urogenital abnormalities.

Serial measurements of C-reactive protein and interleukin-6 in the immediate postnatal period: reference intervals and analysis of maternal and perinatal confounders.

BACKGROUND: There is a wide range of reported sensitivities and specificities for C-reactive protein (CRP) and interleukin-6 (IL-6) in the detection of early-onset neonatal infection. This prompted us to assess reference intervals for CRP and IL-6 during the 48-h period immediately after birth and to identify maternal and perinatal factors that may affect them. METHODS: CRP and IL-6 values were prospectively obtained for 148 healthy babies (113 term, 35 near-term) at birth and at 24 and 48 h of life, and from their mothers at delivery. RESULTS: Upper reference limits for CRP at each neonatal age were established. At birth, CRP was significantly lower than at 24 and 48 h of life. Rupture of membranes > or =18 h, perinatal distress, and gestational hypertension significantly affected the neonatal CRP dynamics, but at specific ages. There was no correlation between CRP concentrations in mothers and their offspring at birth. The IL-6 values observed in the delivering mothers and in their babies at all three neonatal ages were negatively associated with gestational age. In the immediate postnatal period, IL-6 dynamics for term babies were significantly different from those for near-term babies. Maternal IL-6 concentrations correlated with babies' IL-6 concentrations only for term deliveries. Apgar score had a significant effect on babies' IL-6 values at birth. CONCLUSIONS: The patterns of CRP and IL-6 responses in the healthy neonate should be taken into account to optimize their use in the diagnosis of early-onset neonatal sepsis.

Serum procalcitonin concentrations in term delivering mothers and their healthy offspring: a longitudinal study.

BACKGROUND: The reported sensitivities and specificities of procalcitonin (PCT) concentrations for the diagnosis of neonatal infection vary widely. A postnatal increase of PCT has been observed in healthy term newborns with a peak at approximately 24 h of age, and many questions remain regarding maternal and perinatal factors that may influence the normal PCT kinetics during the immediate postnatal period. METHODS: We prospectively investigated the association between the serum PCT values obtained from 121 mothers at delivery and serum PCT in their healthy, term offspring at birth as well as at 24 and 48 h of age. We also analyzed whether obstetric and perinatal factors would alter maternal and neonatal PCT response. RESULTS: PCT concentrations in the babies at birth were significantly higher than in the mothers (P <0.0001), with even larger differences at 24 and 48 h of age. None of the variables identified from maternal and perinatal histories had a significant effect on maternal PCT response. In the healthy neonate, the variables that significantly affected the concentration of PCT at birth were the mothers' PCT (P <0.01), maternal group B streptococcus colonization (P <0.05), and rupture of membranes >/=18 h (P <0.01). The coefficient of linear correlation between the mother's PCT concentration and that of the baby at birth was 0. 32 (P <0.01). The only variable that significantly altered the PCT concentration at both 24 (P <0.01) and 48 (P <0.01) h of age was rupture of membranes >/=18 h. Nonetheless, the PCT response observed during the 48-h period after birth among healthy babies born to mothers with risk factors for infection was well below that reported previously among age-matched neonates with sepsis. CONCLUSIONS: The postnatal increase of PCT observed in the healthy neonate with peak values at 24 h of age most likely represents endogenous synthesis. In estimating the sensitivities and specificities of PCT for diagnosis of sepsis throughout the initial 48 h of life, it is important to consider the normal PCT kinetics and the pattern(s) of PCT response in the healthy neonate.