retinopathy of prematurity.org :    

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Footnotes:

 

70. NOELL WK. Possible mechanisms of photoreceptor damage by light in mammalian eyes. Vis Res 1980: 20: 1163-71 (see page 1165 bottom right).

 

71. MCKECHNIE NM, JOHNSON NF, FOULDS WS. The combined effects of light and acute ischemia on the structure of the rabbit retina: a light and electron microscopic study. Invest Ophthalmol Vis Sci 1982: 22: 449-59 (quote on page 458 bottom right).

 

72. LAGERCRANTZ H, SLOTKIN TA. The stress of being born. Scientific American 1986: 107.

 

73. Encyclopedia Britannica, 15th Edition, 1980, Volume 15, entry "Radiation, Biological Effects of", page 385.

 

74. ROBINSON J, MOSELEY MJ. THOMPSON JR, FIELDER AR. Eyelid opening in preterm neonates. Arch Dis Child 1989: 64: 943-8.

 

75. HASSETT J. A Primer of Psychophysiology. San Francisco: W. H. Freeman & Co., 1978: page 82 (bottom).

 

76. SPRUNGEN LB. KURTZBERG D. VAUGHAN HG. Patterns of looking behavior in full-term and low birth weight infants at 40 weeks post-conceptional age. Dev Behav Ped 1985: 6: 287-94.

 

77. WILKSCH PA, JACKA F. Studies of light propagation through tissue. Prog Clin Biol Res 1984: 170: 149-61 (see pages 155 and 156).

 

78. SLINY DH. Quantifying retinal irradiance levels in light damage experiments. Curr Eye Res 1984: 3: 175-9, see page 178 top left.

 

79. HARPER RG, YOON JJ. Handbook of Neonatology, 2nd edn. Chicago: Year Book Medical Publishers, pp. 590 and 591.

 

80. NILSSON L, LINDBERG J, INGVAR DH, NORDFELDT S, PETTERSSON R. Behold Man: A Photographic Journey of Discovery inside the Body. Boston: Little Brown and Co., 1974: p. 186 (top left).

 

81. TERRY TL. Retrolental fibroplasia in premature infants. Arch Ophthalmol 1945: 33: 203-8 (see p. 208 right).

 

82. TERRY TL. Retrolental fibroplasia. J Pediatr 1946: 29: 770-3, see page 770.

 

83. RAPP LM, WILLIAMS TP. The role of ocular pigmentation in protecting against retinal light damage. Vis Res 1980: 20: 1127-31.

 

84. SAID FS, WEALE RA. The variation with age of the spectral transmissibility of the living human crystalline lens. Gerontologia 1959: 3: 213-31 (see page 219 top).

 

85. KINSEY VE. Spectral transmission of the eye to ultraviolet radiations. Arch Ophthalmol 1948: 39: 508-13 (see page 510 top).

 

86. SLINEY DL, WOLBOPSHT ML. Safety standards and measurement techniques for high intensity light sources. Vision Res 1980: 1133-41, see page 1138.

 

87. ROSENFELD W, SADHEV S, BRUNOT V, JHAVERI R, ZABALETA I, EVANS HE. Phototherapy effect on the incidence of patent ductus arteriosus in premature infants: Prevention with chest shielding. Pediatrics 1986: 78: 10-14.

 

88. JOHNSON K, S D, BOGGS TR. The premature infant, Vitamin E deficiency and retrolental fibroplasia. Am J Clin Nutrition 1974: 27: 1158-73, see pages 1169 ff.

 

89. NOELL WK. Possible mechanisms of photoreceptor damage by light in mammalian eyes. Vis Res 1980: 20: 1163-71, see pages 1168 top left, 1170 bottom left.

 

90. WEITER JJ. Phototoxic Changes in the Retina. In: MILLER D, ed. Clinical Light Damage to the Eye. New York: Springer Verlag, 1987: 79-125. (See pages 99 to 101: "Antioxidant Protection in the Retina").

 

91. LI ZY. TSO MOM. WANG HM, ORGANISCIAK DT. Amelioration of photic injury in rat retina by ascorbic acid: A histopatholoeic study. Invest Ophthalmol Vis Sci 1985: 26: 1589-98 (See page 1589).

 

92. ORGANISCIAK DT, WANG HINI, LO ZY, TSO MOM. The protective effect of ascorbate in retinal light damage of rats. Invest Ophthalmol Vis Sci 1985: 26: 1580-8 (see page 1580).

 

93. WEITER JJ. Phototoxic Chances in the Retina. In: MILLER D. ed. Clinical Light Damage to the Eye. New York: Springer Verlag 1987: 79-125, see pages 86 and 87.

 

94. HAM WT, MUELLER HA, RUFFOLO JJ, et al. Basic mechanisms underlying the production of photochemical lesions in the mammalian retina. Curr Eye Res 1984: 3: 165-74 (see page 170 top).


 


 

  

 

  

  Preemies get more retinal irradiance

 

than safety guidelines allow for adults 

 
 

DavidNursery01.jpg (9641 bytes)

Baby-blinding retinopathy of prematurity and intensive care nursery lighting
by H. Peter Aleff

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A preemie's retinal vulnerability

Preemies, who belong in a dark womb, are going through their period of highest vulnerability to light immediately after birth.

As soon as the fetus becomes a Preemie, fluorescent lamps irradiate her/him in the delivery room, on the examination table, and then around-the-clock in the intensive care nursery. A number of perinatal events further increases the already high damage potential from light:

  • (1) Newborns come from a dark womb. Light damage in test animals is "strikingly potentiated when the animals have been maintained in constant darkness prior to the damaging light exposure" (70).

  • (2) Newborn preemies often suffer from ischemia, or lack of blood in some areas, until their circulation can adapt itself to the world outside the womb. This further enhances the damage potential: experiments on rabbits have shown that the combined insults of light exposure and ischemia produced considerably more damage to the retina than the same light exposure alone (71).

  • (3) Many babies, particularly those delivered vaginally, have at birth widely dilated pupils which close only slowly despite the strong nursery lights (72). This failure to adapt the size of their pupils immediately to the unnatural brightness in the delivery room and nursery increases the retinal irradiance.

  • (4) Radiation damage is generally worse for preemies than for term babies because of their still undifferentiated retinal cells. As an example, the retinae of a still developing fetus are much more vulnerable to irradiation by X-rays than those of a child or of an adult (73).

Even if some preemies manage to avoid having their retinae overexposed upon birth, their odds of escaping damage are slim, as they spend weeks or months in the glare of the nursery lighting.

Three additional factors further increase their risk: preemies cannot prevent light from reaching their retinae; their retinae are highly sensitized to light damage; and they cannot self-repair as well as adults.

1.) A preemie cannot prevent light from reaching the retinae: To begin with, she cannot look away, being too feeble to lift or even turn her head. Her still soft head lies immobile on one side, and the upper part of her visual field is filled with rows of ceiling lights.

Her next line of defense would be to shut her eyes, but she does not yet know that. According to a British study of eyelid opening, in preemies (74), those with a gestational size of 26 wk typically kept their eyes open 45% of the time. The preemies in that study had their eyes shut most often at 28 wk -- during 93% of the observations. Unfortunately, even then the eye-open time adds up to 100 min a day - more than enough time to absorb the adult danger dose of light many times over.

Preemies also cannot blink to give their retinae brief periods of rest; infants do not acquire this reflex until they are about 6 months old (75).

Preemies stare a lot. When their eyes are open, they fix their graze for long times at whatever attracts their attention, more so even than term newborns who also have a tendency to stare (76). Bright light is likely to fascinate them.

Even among adults educated about the dangers of intense light, the fascination with a bright light source at times overcomes all injunctions against staring into it. The medical literature on accidental retinal burns reports many cases where patients just kept staring at the sun or at a welding arc in light-induced absentmindedness. Preemies have not yet acquired mental barriers against such behavior.

A preemie's thin eyelids do not offer much protection. Measurements of light propagation through slices of pig and cow tissue 0.55 mm and 0.94 mm thin (and therefore about comparable to the thickness of preemie eyelids) showed that only about 7.5 to 10% of the light was absorbed in the tissue; the rest was scattered, mostly forward (77).

Such scattering through the eyelids will simply diffuse the light over the retina but will not exclude it. David Sliney, a U.S. Government researcher on light damage to the eye, states:

"In the albino rat, the iris is not very effective, and some scattered light reaches the retina. Nevertheless, imaging of a light source still occurs, and" [the above formula for calculating the retinal irradiance] "is still valid if the contribution of scattered light (which falls over the entire retina) is added" (78).

Furthermore, baby skin is not yet as pigmented as adult skin or as the above pig and cow tissue, and is quite translucent. Neonatologists rely on this translucency in procedures such as thoracic trans- illumination where a light shining inside the baby's chest is observed outside after it has passed through layers of tissue much thicker than the paper-thin eyelids of a preemie (79).

Once past the eyelids, the light penetrates not just through the pupil, which is likely to be fully dilated (59, 60), but also through the surrounding iris. The iris of a preemie looks bluish-transparent and still lacks the pigment that will later form the variously colored streaks and spots of the iris pattern (80). This lack of iris color seems particularly pronounced in victims of ROP.

Already Terry, the early observer of this disease, repeatedly drew attention to "the fetal blue color of the iris [which] persists longer, its speed of disappearance being in direct proportion to the rapidity of growth of the involved eye" (81). He also described the irises of the babies with ROP as "abnormally light colored" (82).

The effective aperture of the preemie's eyes is therefore not just the pupil opening but includes much of the iris area. A greater aperture of the lens increases the speed with which the retina incurs light damage. This proportionality of dose and effect is confirmed by experimental evidence.

Normal rats with pigmented eyes show considerable resistance to light damage compared with albinos whose iris is as unpigmented as that of the preemie. When the eyes of pigmented rats were maximally dilated, they incurred damage much faster than before, at up to half the rate of albino rats. The authors concluded:

"... the inherent susceptibility of the retina to light damage is about the same in albino and pigmented rats, and ocular pigmentation protects against damage primarily by lowering the retinal irradiance" (83).

Add to these risk factors the transparency of the preemie's lens to the lower and more energetic wavelengths which the older eye screens out. The blue-light hazard function on which the light exposure safety standards are based shows less danger to the retina for wavelengths below 415 nm, because those short wavelengths mostly do not reach the adult retina.

But a preemie's eyes are more transparent to more wavelengths and let through about 90% of the visible light above 400 nm plus 80 to 85% of the ultraviolet light down to about 320 nm. For comparison, the age-yellowed lens of a 25-yr-old lets through only 46 to 50% of the visible light, and next to nothing in the ultraviolet range (55, 84, 85).

That is good for adults because ultraviolet would harm their retinae. The visible wavelengths next to ultraviolet are almost as energetic and could destroy the light receptors over the years if our species had not evolved an adaptive protection. The violet and blue light that enters the lens causes chemical reactions that gradually turn the mass of the lens yellow just as varnish exposed to sunlight gradually turns yellow. The yellowed lens filters out a large part of the blue and violet light which would be most harmful to the retina.

Children, and particularly preemies, have not yet built up this protective barrier. The hazard value of the violet and blue spectrum region is therefore much higher for preemies than the blue-light hazard function for adults in Table 1. The left side of the retinal protection barrier in Fig. 2 may be much lower for preemies than shown, or it may not exist at all.

So: the preemie cannot prevent light from reaching her retina; her eyes are often open and she stares at light: even her closed eyelids let through most of the light that shines on them, and this light passes unhindered through her pupil and most of her iris.

2.) Sensitizers: Upon arrival, each photon of light does more damage to the preemie than it would to the adult. The occupational exposure limits are designed "for an awake, task-oriented individual who is neither photosensitive nor on medications which would drastically alter retinal exposure conditions" (86). This description does not fit preemies, who are at much higher risk than the adults whom the occupational safety laws protect because:

  • Preemies are extremely photosensitive. Their blood chemistry reacts to bilirubin lights shining through their almost transparent skin and bloodvessels. Even the contraction of blood channels deep inside their chest can be delayed or prevented by bright light. This reaction prolongs heart murmurs for which many preemies undergo surgery (87).

  • Preemies are often on powerful medications which can have known and unknown side-effects, among which may be the addition of damage-causing free radicals to those caused by the irradiation.

  • Many preemies are deficient in a variety of minerals and vitamins, including free radical scavengers such as Vitamins' C and E (88) that have been shown to offer some protection against free radical reactions such as those caused by excess light (89-92).

  • Many preemies are receiving supplemental oxygen. Without oxygen, none of the free-radical reactions caused by the light could occur, and no one could live. All living tissues always contain enough oxygen to sustain the light damage, even when breathing normal room air. Among these tissues, the retina has the highest concentration of oxygen and consumes it the fastest (93). Consequently, there is no "safe" retinal concentration of oxygen compatible with life below which the light damage reactions could not proceed. Increasing the amount of oxygen accelerates these reactions: if a given intensity of light causes a certain amount of retinal damage in room air with 20% oxygen and 80% nitrogen, then the same light takes only half that time to cause the same damage in a 60/40 blend of oxygen and nitrogen, and only one third that time if the oxygen level is raised further to 80% of the breathing mix (94).

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