Deaths in preterm infants: changing pathology over 2 decades

Janet Elizabeth Berrington1, Richard Iain Hearn, Mary Bythell

  • 1Newcastle Neonatal Service, Newcastle upon Tyne Hospitals NHS Foundation Trust, Newcastle upon Tyne, UK. janet.berrington@nuth.nhs.uk

Insights

Infection and necrotizing enterocolitis (NEC) are growing causes of death in preterm infants, while respiratory issues have declined. This trend emerged over two decades in a UK population study.

Area of Science:

  • Neonatal Medicine
  • Pediatric Mortality Studies
  • Public Health Surveillance

Background:

  • Preterm infants (24-31 weeks gestation) face significant mortality risks.
  • Understanding evolving causes of death is crucial for improving neonatal care.
  • Longitudinal data analysis can reveal trends in infant mortality.

Purpose of the Study:

  • To analyze changes in causes of death for live-born preterm infants over a 20-year period.
  • To identify shifts in mortality etiologies within specific gestational age groups.
  • To inform strategies for reducing preterm infant mortality.

Main Methods:

  • Population-based survey of over 680,000 live births in the UK (1988-2008).
  • Analysis of deaths within the first postnatal year, categorized by major etiologies: respiratory, infection, malformation, necrotizing enterocolitis (NEC), and other.
  • Data stratified into three 7-year epochs and two gestational age groups (<27 and 28-31 weeks) for trend analysis.

Main Results:

  • Total deaths decreased over the study period (671 to 360).
  • Proportion of deaths from respiratory causes significantly decreased (64% to 49%).
  • Proportion of deaths from infection and necrotizing enterocolitis (NEC) increased (11% to 21%), with a longer median time to death.

Conclusions:

  • Infection and necrotizing enterocolitis (NEC) have become increasingly prevalent causes of mortality in preterm infants.
  • The declining proportion of respiratory deaths suggests improvements in respiratory support for preterm neonates.
  • Shifting mortality patterns necessitate updated clinical focus and interventions for preterm infant survival.
Abstract

Related Concept Videos

Atelectasis II: Pathophysiology01:10

Atelectasis II: Pathophysiology

Atelectasis develops when alveoli lose their air and collapse inward. Because lung tissue is naturally elastic, these air sacs shrink rather than remaining open. Collapsed alveoli are no longer ventilated, reducing their role in gas exchange. Blood flow may continue in these regions, creating a ventilation–perfusion mismatch. Clinical findings include decreased breath sounds, dullness to percussion, reduced chest expansion, and decreased tactile fremitus as sound transmission through collapsed...
Teratogenicity01:07

Teratogenicity

The ability of a drug to produce structural deformations and functional abnormalities in the developing embryo or the fetus is called teratogenicity, and the drug producing this effect is known as a teratogen. Teratogenic effects include stillbirth, miscarriage, intrauterine growth restriction, and neurocognitive delay. A teratogen may affect the embryo at different stages of development, which is important in determining the type and extent of the damage. During blastocyst formation, the early...
Acute Pancreatitis II: Pathophysiology01:21

Acute Pancreatitis II: Pathophysiology

The pathophysiology of acute pancreatitis centers on injury to pancreatic acinar cells, which initiates a cascade of harmful intracellular events.This injury leads to premature activation of trypsinogen to trypsin in the pancreas. Trypsin then activates other digestive enzymes, such as chymotrypsin, elastase, and phospholipase A2, which begin breaking down pancreatic tissue. The resulting autodigestion causes local inflammation, tissue swelling, hemorrhage, and fat necrosis.Injured acinar cells...
Pneumonia II: Pathophysiology01:29

Pneumonia II: Pathophysiology

The pathophysiology of pneumonia involves the following steps:
Pharmacokinetics in Pediatric Patients: Drug Metabolism01:24

Pharmacokinetics in Pediatric Patients: Drug Metabolism

In pediatric care, understanding the nuances of hepatic drug metabolism is crucial, as it significantly differs from that of adults. This divergence is primarily due to the developmental stage of drug-metabolizing enzymes, which affects how medications are processed in the body. In neonates, for instance, the activity of Phase I enzymes—critical for the initial breakdown of drugs—is markedly reduced, functioning at just 20–40% of the levels seen in adults. This reduction poses a challenge in...