Necrotizing enterocolitis

2021 ◽  
pp. 317-324
Author(s):  
Michael Obladen

Necrotizing enterocolitis is not a new disease but one that has been reported since special care units began to house preterm infants. It was observed in the foundling hospitals of Paris (Billard 1828) and Vienna (Bednar 1850) and, as it occurred in clusters, was regarded as a nosocomial infection in the infant hospitals of Zurich (Willi 1944) and Berlin (Ylppö 1931). Clinical and pathoanatomical characterization was achieved by Schmidt and Quaiser in 1952. The unproven hypothesis of mesenteric hypoperfusion as a major aetiological factor arose from animal models and analogous perforating disorders in term infants. Despite similarities between necrotizing enterocolitis and clostridial infections, few studies employed anaerobic culture techniques. The pathogenesis remains unclear and its distinction from related disorders uncertain. It is unlikely that strategies to prevent necrotizing enterocolitis will be successful unless the disease is better understood.

2018 ◽  
Vol 2018 ◽  
pp. 1-6 ◽  
Author(s):  
Jayasree Nair ◽  
Rachel Longendyke ◽  
Satyan Lakshminrusimha

Necrotizing enterocolitis (NEC) is a devastating morbidity usually seen in preterm infants, with extremely preterm neonates (EPT ≤28 weeks) considered at highest risk. Moderately preterm infants (MPT 28–34 weeks) constitute a large percentage of NICU admissions. In our retrospective data analysis of NEC in a single regional perinatal center, NEC was observed in 10% of extremely EPT and 7% of MPT, but only 0.7% of late-preterm/term admissions. There was an inverse relationship between postnatal age at onset of NEC and gestational age at birth. Among MPT infants with NEC, maternal hypertensive disorders (29%) and small for gestational age (SGA-15%) were more common than in EPT infants (11.6 and 4.6%, resp.). Congenital gastrointestinal anomalies were common among late preterm/term infants with NEC. SGA MPT infants born to mothers with hypertensive disorders are particularly at risk and should be closely monitored for signs of NEC. Identifying risk factors specific to each gestational age may help clinicians to tailor interventions to prevent NEC.


PEDIATRICS ◽  
1995 ◽  
Vol 96 (5) ◽  
pp. 923-932 ◽  
Author(s):  
Deborah M. Buehler ◽  
Heidelise Als ◽  
Frank H. Duffy ◽  
Gloria B. McAnulty ◽  
Jacqueline Liederman

Objective. We assessed the effectiveness of individualized developmental support in the special care nursery for low-risk preterm infants. Setting. A university-affiliated teaching hospital. Participants. Twelve healthy full-term infants, and 24 low-risk preterm infants randomly assigned to a control or an experimental group. Design. The preterm control group received standard care and the preterm experimental group received individualized developmental care at the same special care nursery. Outcome Measures. Medical, behavioral (Assessment of Preterm Infants' Behavior and Prechtl's Neurological Examination of the Full-Term Newborn Infant), and electrophysiologic outcome (using quantitative electroencephalography with topographic mapping) of all three groups was assessed 2 weeks after the expected due date. Results. No between-or among-group medical differences were seen for this low-risk, healthy sample. The preterm experimental group showed behavioral and electrophysiologic performances comparable to those of the full-term group, whereas the preterm control group performed significantly less well. Behavioral measures suggested significantly poorer attentional functioning for the preterm control group. Electrophysiologic results implicated the frontal lobe. Conclusions. Individualized developmental intervention supports neurobehavioral functioning as measured at 2 weeks post-term. It appears to prevent frontal lobe and attentional difficulties in the newborn period, the possible causes of behavioral and scholastic disabilities often seen in low-risk preterm infants at later ages.


Nutrients ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 1005
Author(s):  
Walter Mihatsch ◽  
Izaskun Dorronsoro Martín ◽  
Vicente Barrios-Sabador ◽  
María L. Couce ◽  
Gabriel Á. Martos-Moreno ◽  
...  

The present study longitudinally evaluated growth, bone mineral density, body composition, and metabolic health outcome in very low birth weight (VLBW) infants whose in-hospital target nutrient intake was within recent recommendations. From six months to three years, bone mineral density (dual-energy X-ray absorptiometry, DXA), body composition, and metabolic health outcome were compared with a reference group of term infants. The aim was to test whether in-hospital achieved weight gain until 36 weeks of gestation (light or appropriate for term equivalent age; LTEA or ATEA) predicts later growth, bone mineral density (BMD), abdominal obesity, or metabolic health outcomes such as insulin resistance, relative to term infants, during the first three years of life. Target in-hospital energy and protein intake was not achieved. Growth in weight, length and head circumference, mid arm circumference, adiposity, fat free mass (FFM), and bone mineralization in VLBW infants was less than those in term infants and influenced by nutritional status at discharge. Preterm infants had poorer motor and cognitive outcomes. Post-discharge body composition patterns indicate FFM proportional to height but lower fat mass index in LTEA preterm infants than term infants, with no evidence of increased truncal fat in preterm infants. The hypothesis of early BMD catch-up in VLBW infants after discharge was not supported by the present data. The clinical significance of these findings is unclear. The data may suggest a reduced obesity risk but an increased osteoporosis risk. Since postnatal growth restriction may have permanent negative health effects, LTEA VLBW infants would especially appear to benefit from targeted preventive interventions. Further follow-up of the infants is required.


Author(s):  
Robert Thänert ◽  
Eric C Keen ◽  
Gautam Dantas ◽  
Barbara B Warner ◽  
Phillip I Tarr

Abstract Decades of research have failed to define the pathophysiology of necrotizing enterocolitis (NEC), a devastating pediatric gastrointestinal disorder of preterm infants. However, recent evidence suggests that host-microbiota interactions, in which microbial dysbiosis is followed by loss of barrier integrity, inflammation, and necrosis, are central to NEC development. Thus, greater knowledge of the preterm infant microbiome could accelerate attempts to diagnose, treat, and prevent NEC. Here, we summarize clinical characteristics of and risk factors for NEC, the structure of the pre-event NEC microbiome, how this community interfaces with host immunology, and microbiome-based approaches that might prevent or lessen the severity of NEC in this very vulnerable population.


Children ◽  
2021 ◽  
Vol 8 (2) ◽  
pp. 131
Author(s):  
Satyan Lakshminrusimha

During transition at birth with ventilation of the lungs, pulmonary vascular resistance (PVR) decreases from high fetal values, leading to an 8 to 10-fold increase in pulmonary blood flow (Qp). In some infants, this transition does not occur, resulting in pulmonary hypertension (PH). In infants, PH can present as: (a) primary PH in term neonates (idiopathic), (b) PH secondary to lung disease or hypoplasia in term infants, (c) acute PH in preterm infants with respiratory distress syndrome (RDS), (d) chronic PH with bronchopulmonary dysplasia (BPD) in preterm infants and (e) post-neonatal PH. A hemodynamically significant patent ductus arteriosus (PDA) can exacerbate PH in preterm infants due to increased Qp. Pulmonary vein stenosis (PVS) can complicate BPD with PH. Diagnosis of PH is based on clinical features, echocardiography and, in some intractable cases, cardiac catheterization. Therapy of PH includes oxygen, invasive or non-invasive ventilation, correction of acidosis, surfactant and selective and non-selective pulmonary vasodilators such as inhaled nitric oxide and sildenafil, respectively. Early closure of a hemodynamically significant PDA has the potential to limit pulmonary vascular remodeling associated with BPD and PH. The role of thiamine in pathogenesis of PH is also discussed with the recent increase in thiamine-responsive acute pulmonary hypertension in early infancy. Recognition and prompt therapy of PH can prevent right ventricular dysfunction, uncoupling and failure.


Neonatology ◽  
2021 ◽  
pp. 1-7
Author(s):  
Faiza Latheef ◽  
Hanna Wahlgren ◽  
Helene Engstrand Lilja ◽  
Barbro Diderholm ◽  
Mattias Paulsson

<b><i>Introduction:</i></b> Necrotizing enterocolitis (NEC) is a disease predominantly affecting preterm infants. The administration of hyperosmolar solutions could lead to the development of NEC. The objective of this study was to measure the osmolality of enteral medications used in clinical practice and to assess the risk of NEC following exposure to hyperosmolar medications. <b><i>Methods:</i></b> A retrospective cohort study in extremely preterm infants (gestational age &#x3c;28 weeks) born between 2010 and 2016 at a tertiary neonatal intensive care unit in Sweden. 465 infants were identified via the Swedish Neonatal Quality register. Data relating to enteral administrations received during a two-week period were collected from the medical records. The osmolalities of medications were measured using an osmometer. Logistic regression was used to calculate the odds ratio of developing NEC. <b><i>Results:</i></b> A total of 253 patients met the inclusion criteria. The osmolalities of 5 commonly used medications significantly exceeded the recommended limit of 450 mOsm/kg set by the American Academy of Paediatrics (AAP). Most patients (94%) received at least one hyperosmolar medication. No significant risk of developing NEC could be found. <b><i>Conclusion:</i></b> The medications used in clinical practice can significantly exceed the limit set by the AAP. This study does not indicate an increased risk of developing NEC in extremely preterm infants following exposure to hyperosmolar medications. Further studies in larger cohorts are needed to determine the specific cut-off level of osmolality in relation to the pathogenesis of NEC.


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