New research shows brain injuries stem from infection
January 1, 2005 2 minutes read
New research continues to dispel the once widely accepted belief that premature infants suffer brain injury from a lack of oxygen usually attributed to obstetrician error. In fact, infection plays a larger role, according to high-risk obstetrician Ernest Graham, MD, an assistant professor at The Johns Hopkins University School of Medicine in Baltimore. Graham is lead author of a study presented at the 24th annual meeting of the Society for Maternal-Fetal Medicine last February in New Orleans.
"Infection plays a much larger role than lack of oxygen in brain injury among premature infants," Graham says. "To reduce the risk of brain injury in the premature neonate, physicians may have to pay more attention to infections that occur around the time of birth."
The injury to the premature brain white matter, known as periventricular leukomalacia (PVL), is a condition in which small, cystlike regions of brain tissue die. PVL is the most common form of brain injury in premature infants and results in cerebral palsy in 60% to 100% of those who live to adulthood. Ultrasound, MRI scan, or CT scan of the infant's brain can only identify it.
As part of their analysis, the researchers reviewed the records of 150 cases of white matter injury in premature infants born at Hopkins from 1994 to 2001. Ultrasound recordings taken at three different times after birth assessed rates of PVL. Using control cases without brain injury and matched by length of pregnancy, the researchers studied several factors believed to play a role in causing brain injury, including multiple births, lack of oxygen, and the presence of infections.
Overall, the researchers confirmed previous research that showed in women who had had twins or triplets, subsequent infants were at higher risk for the subsequent development of brain injury.
However, to their surprise, the researchers found a very small portion of cases with brain injury also had metabolic acidosis, a sign that oxygen was lacking. Indeed, the rates of severe metabolic acidosis were statistically the same among the cases with PVL and the in the control cases without brain injury, ranging from 3% to 6%, respectively.
The most striking results came from bacterial cultures of samples from the premature infants’ cerebrospinal fluid, blood and trachea. Researchers found a two- to fourfold increase in the rates of PVL among those premature infants with an infection, tested positive by culture samples. The rates of injury were independent of the type of infection, and more than a dozen different kinds of bacteria were found.
New research continues to dispel the once widely accepted belief that premature infants suffer brain injury from a lack of oxygen usually attributed to obstetrician error. In fact, infection plays a larger role, according to a high-risk obstetrician and assistant professor at The Johns Hopkins University School of Medicine in Baltimore.
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