The Curious Case of the Blind Baby Epidemic
The story of a sad and tragic epidemic that happened just 70 years ago, but which few people know about today. (But you’re familiar with at least one of its victims.)
On February 14, 1941, Dr. Stewart Clifford, a pediatrician in Boston, made a house call to check on one of his patients, the three-month-old daughter of a young rabbi. The girl had been born several weeks premature, weighing just four pounds at birth, but had been doing well in the months since her birth. Unfortunately, something now seemed wrong. There was a grayness in the pupils of the girl’s eyes—and she appeared to have lost her ability to see. Clifford contacted his friend, Dr. Paul Chandler, one of Boston’s leading ophthalmologists. Chandler examined the girl, and told Clifford he had found something he had never seen before: there were strange gray masses attached to the rear of the lenses in both of the child’s eyes. Even worse, Clifford’s diagnosis was correct. The girl was completely blind.
Just days later, another of Clifford’s patients, this one a seven-month-old baby, was discovered to have the same symptoms. That baby had also gone blind. And just as with the prior case, the child had been born prematurely.
By 1942 several other cases of premature babies going blind, with the same symptoms—the appearance of gray masses inside the babies’ eyes—were reported in the Boston area. That same year, Clifford contacted Dr. Theodore Terry, professor of opthalmology at Harvard Medical School, and asked him to look into the mysterious cases. Terry studied five of the cases, and wrote an article about the condition in American Journal of Ophthalmology. When eye doctors around the country saw the article, similar stories were reported outside the Boston area.
By 1945 Terry had collected information on 117 premature infants who’d been affected by what was being called retrolental fibrofasia (RLF)—medical-ese for “scar tissue behind the lens of the eye.” The victims had varying degrees of vision loss—but they all had the characteristic mass of scar tissue inside their eyeballs. It was now obvious that these were not one-off cases: something was affecting the eyes of premature babies in a way that had not been seen before, and all of those cases—or at the very least the majority of them—were related.
Most ophthalmologists studying RLF were convinced that the condition was related to the fact that all its victims had been born prematurely. That was understandable. Premature birth can cause a wide variety of health problems, minor and serious, simply because the bodies of “preemies” haven’t completed the normal in utero development process that makes them ready for life outside the womb.
But Terry wasn’t convinced: if this was just another premature birth complication, why hadn’t it been seen before?
And most of the babies he’d personally examined had perfectly normal eyes at birth. They’d only been affected with the condition in the weeks—and in many cases months—after they were born. Terry was convinced something else was at play. Sadly, he wasn’t able to confirm this—he died of a heart attack in 1946, at the age of 47.
So what exactly was going on inside the eyes of the victims of RLF? First, by 1942 doctors had discovered that the condition primarily affected the retinas in the victims’ eyes, and not the lenses, as had previously been believed. (The retina is the thin layer of tissue that lines the inside of the rear of the eyeball. It holds the photoreceptors that “read” incoming light and sends that information to the brain via the optic nerves, where it’s translated into the images we see.)
The retinas in our eyes are rich in tiny blood vessels, through which they receive the nutrients they need to function. For unknown reasons, the retinas of RLF victims grew far too many blood vessels, many of which were abnormally shaped or defective. In the worst cases, this abnormal blood vessel growth caused an affected retina to detach from its position on the rear inner wall of the eyeball, and to migrate to a position behind the eyes’ lenses—those were the “strange gray masses” that were the first sign of the disease. Because healthy, attached retinas are vital to even rudimentary eyesight, RLF at its worst led to complete blindness.
WHAT’S GOING ON?
In the years after 1946, with the number of cases of RLF increasing in the United States and in other countries, theories about the cause of the condition were studied in hospitals and research labs around the world. Because most experts were convinced that the condition was new, many of the theories centered around recently developed treatments for premature babies. Those included the use of antibiotics, blood transfusions, large doses of vitamins, and hormone treatments. But none of the studies led to the discovery of what was causing RLF—and the number of victims kept increasing.
And one of the most puzzling aspects about RLF: it was occurring almost exclusively in modern, developed nations—including the United States, Canada, the UK and several other western European nations, Australia, and Cuba—where the care of premature babies had improved and the infant mortality rate for preemies had fallen dramatically over the previous decades.
In 1949 doctors started examining a treatment for premature babies that prior studies had overlooked: incubators. Incubation devices had been used to keep delicate babies warm since the late 1800s, but in the 1930s, a new kind was developed—airtight incubators that could maintain abnormally high air-oxygen levels. Throughout the 1940s, it had become increasingly common in the developed world to treat preemies with high concentrations of oxygen, often for several weeks at a time. The treatment had been credited with lowering the mortality rate…but had there been an unknown price for that lower rate? By the early 1950s, a lot of doctors thought that might be the case.
Over the next few years, several studies involving premature babies that were kept in oxygen-supplying incubators were conducted in countries around the world. The most notable was one led by two doctors, Arnall Patz, an ophthalmologist, and Leroy Hoeck, a pediatrician, at Gallinger Municipal Hospital in Washington, D.C.—and the results were shocking.
TRIAL AND ERROR
Over the course of two years (1951 to 1953), Patz and Hoeck studied 65 premature babies, all weighing less than 3.5 pounds at birth, divided into two groups. One group was kept in incubators with 65 percent oxygen levels and higher for four to seven weeks at a time (the standard treatment for premature babies at the time). The other group was given lower levels—40 percent oxygen or less—but only when it was deemed medically necessary, and only for from one to 14 days at a time. (Note: The parents were not asked for permission to have their children participate in the study, and were only told about it after it had begun—which was pretty normal for the era.)
Results: only 16 percent of the babies in the low-oxygen group developed RLF, compared to about 61 percent of those in the high-oxygen group. (Twelve of the babies in the high-oxygen group went blind, compared to just one in the low-oxygen group.)
The results of Patz and Hoeck’s study led to the National Institutes of Health (NIH) to begin a much larger study, involving 18 U.S. hospitals and thousands of children. The results of that study—confirming that high levels of oxygen over long periods of time indeed played a major role in the development of RLF—were published in 1955.
In the years following the Patz-Hoeck and the NIH studies, the use of prolonged exposure to high levels of oxygen in the care of premature babies was drastically curtailed in hospitals worldwide, and by the late 1950s the epidemic of blindness in premature babies was over. Here’s some information about the epidemic, and the state of the disease since that time:
- The process through which high levels of oxygen causes RLF is quite complex, but here’s a basic explanation: retinal blood vessels normally develop in utero, in just the last few weeks of pregnancy, and require relatively low levels of oxygen in the developing retinas. Because this vessel growth process is incomplete in premature babies, high levels of oxygen adversely affect that normal vessel growth process, causing the vessels to grow too fast, too large, and in abnormal shapes, which can lead to RLF.
- An estimated 12,000 preemies developed RLF during the epidemic. More than 10,000 of them lost their sight.
- The name of retrolental fibroplasia was changed in the years after it was discovered it involved the retinas, and not the lenses, of the affected eyes. It is now known as retinopathy of prematurity (ROP).
- Some well-known victims of RLF include jazz singer/pianist Diane Schuur (born in 1953) and actor/singer Tom Sullivan (born in 1947). The most famous victim of RLF: Stevie Wonder, who was born in 1950.
This article is reprinted with permission from Uncle John’s OLD FAITHFUL 30th Anniversary Bathroom Reader. Uncle John and the Bathroom Readers’ Institute! Every year for the past three decades, Uncle John and his team of tireless researchers have delivered an epic tome packed with thousands of fascinating factoids. And now this extra-special 30th anniversary edition has everything you’ve come to expect from the BRI, and more! It’s stuffed with 512 pages of all-new articles sure to please everyone, from our longtime readers to newbies alike. You’ll get the scoop on the latest “scientific” studies, weird world news, surprising history, and obscure facts.
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