Too Little & Too Much

More and better incubators were just what the doctors ordered, and by the late 1930s a steadily increasing number of premature babies was surviving the dangerous weeks after birth. But by 1942, medical statisticians were already calculating the cost. Of premature babies who weighed 4 Ibs. or less at birth, one out of every eight reared in hospital incubators was going blind. Suddenly, and for no apparent reason, the blood vessels of the retina would fan out in wild profusion. Fibrous tissue growing behind the lens would cloud the eyes and ruin the retina. Doctors were baffled. They could do little more than tag the disease with a name, retrolental fibroplasia (R.L.F.).

The sharpest eye specialists plugged away at the problem. Some blamed too early exposure to light; some suspected insufficient vitamins, and a few insisted that an unidentified virus was to blame. Then, in 1951, Dr. Thaddeus S. Szewczyk of East St. Louis, Ill. suggested that careful control of incubator oxygen might control the disease.

The inquiry quickly focused on oxygen. At Harvard, experiments with mice proved that too little oxygen at critical stages of fetal development caused a host of abnormalities, including a condition similar to R.L.F. In Melbourne, Australia, Dr. Kate Campbell recalled that R.L.F. had first appeared in Women's Hospital when new incubators were installed and all premature babies began to get liberal doses of oxygen. In Birmingham, England, doctors pointed out that the incidence of R.L.F. rose when premature infants began to get larger and longer doses of oxygen. When oxygen was reduced, the frequency of the disease decreased.

In the current British Journal of Ophthalmology, doctors from the University of London report on research that goes a long way toward proving Dr. Szewczyk's early guess. Working with kittens (whose eyes, at birth, are similar to the eyes of premature babies), the English scientists kept a record of the aftereffects of exposure to varying amounts of oxygen. Litters of kittens were kept for clays in an atmosphere rich (70% to 80%) in oxygen. At first, their retinal blood vessels shriveled and all but disappeared. Returned to ordinary air, the blood vessels quickly began to grow. They ruptured and spread in uncontrollable disorder--exactly as they do in human R.L.F. And strangely, litters kept in low oxygen concentrations (10% to 15%) developed a similar condition.

As every lab worker knows, humans seldom react in exactly the same manner as lab animals. But the English ophthalmologists are hopeful that their preliminary experiments contain some preliminary answers. It now seems more probable than ever that too much oxygen in the incubator, combined with sudden removal to normal air, may cause retrolental fibroplasia in premature children. And too little oxygen in the fetal blood stream may help to bring about the same condition.

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