Talk:Retinopathy of prematurity

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Stevie Wonder[edit]

The text at Stevie Wonder#Early life is sufficiently muddled that I can't quite decide if it's attempting to be an explanation of ROP, or a contradiction to one. I'm afraid to touch it without any actual reference about Stevie Wonder's medical status to back it up. But perhaps whoever added the Stevie Wonder bit to this page could take a look? -- JVinocur 00:55, 27 April 2006 (UTC)

I didn't add the Stevie Wonder info here, but I'll have a look at it. -AED 21:41, 2 June 2006 (UTC)
Also can't find the SW info in published text, but is all over the web--perhaps it is mentioned in the unconnected reference: "4. Medicine's Strangest Cases - Michael O'Donnell"? Found additional reference for the history section and removed the O'Donnell reference as it is not currently connected with any of the text that I can see. If it is the source, will replace reference in correct format.Hallbrianh 03:50, 19 February 2007 (UTC)


The text in the pathophysiology section contradicts that in the History section: "Supplemental oxygen exposure, while a risk factor, is not the main risk factor for development of this disease. Restricting supplemental oxygen use does not necessarily reduce the rate of ROP, and may raise the risk of other hypoxia-related systemic complications." vs "Some were given the usual oxygen concentrations in their incubators, while the other group had "curtailed" oxygen levels. The latter group was shown to have a lower incidence of the disease. As a result, oxygen levels in incubators were lowered and consequently the epidemic was halted." Clearly there is a level at which oxygen does become the main risk factor. Obviously, once the level of oxygen in incubators is reduced below this level, the first paragraph may be true. Also you can't be born with a disease caused by incubators. Mkovari (talk) 20:57, 2 September 2009 (UTC)

The pathophysiology section was completely unsourced. I added a cited section which claims the oxygen chambers are specifically to blame for ROP. This page needs more citations anyway. Bloomingdedalus (talk) 23:03, 20 June 2011 (UTC)
Supplemental oxygen (incubators) is not necessary for the development of ROP. I have had ROP patients who were not given supplemental O2. PedEye1 (talk) 21:50, 10 July 2011 (UTC)
I don't think anyone is challenging whether oxygen is necessary for the development of ROF in all cases, only whether it is the main risk factor. If most cases of ROF are associated with oxygen supplementation, then it might still be (correctly) considered the primary risk factor. Rytyho usa (talk) 12:49, 11 December 2012 (UTC)

Is ROP (Retinopathy Of Prematurity) curable?[edit]

I was blessed with twins (Girl & Boy) seven months back (20th Nov 2012). They are premature babies with 6.5 months pregnancy & were of very low weight ( 675 & 725 gms respectively). Both were diagnosed with ROP in regular checkups in NICU & nursery. Laser treatment was done on both the babies to curtail further progress of disease on 29th Dec 12 & 4th Jan 13. The baby Boy responded well to laser treatment & doctors confirmed that they had controlled the disease. But unfortunately baby girl didn’t responded to laser treatment & currently she has been diagnosed with APROP in both the eyes with following details -

Right Eye – Stage 5 Left Eye – Stage 4B

On 14-Mar-13 doctors had conducted LSV surgery on left eye with stage 4B but unfortunately the results weren’t as expected.

I had consulted expert doctors In PGI Chandigarh, R.P. Center AIIMS New Delhi, Sankara Nethralaya Chennai but all had confirmed that nothing can be done.

I am looking for treatments available in Allopathic, Ayurvedic, Homeopathic etc, which can benefit my daughter.

````Ajay Malik — Preceding unsigned comment added by Ajaymalik3007 (talkcontribs) 08:02, 20 June 2013 (UTC)

Confusing sentence, what does it mean?[edit]

"...prematurely-born babies generally having received intensive neonatal care, in which oxygen therapy is often used and advantageous."

What is intended by the phrase "is advantageous" here? (talk) 10:49, 9 February 2014 (UTC)

"ROP prevalence varies, from 5–8% in developed countries with adequate neonatological facilities, to up to 30% in middle-income developing countries."

Percent of what group? (talk) 10:54, 9 February 2014 (UTC)

No mention of CCFL (fluorescent, mercury based) and White-LED energy saving light exposure dangers[edit]

"Medical scientists have discovered that blue light is strongly absorbed in the retina tissues. This absorption, if at high energy levels like that found in welding, has the capability to ultimately cause ocular problems such as macular degeneration and retina damage." "There is growing evidence implicating welding as a possible risk factor for uveal melanoma. The major culprit is high-energy blue light exposure" High energy blue light filtration: An evidence-based assessment

CCFL (most common lighting technology because of energy saving and efficiency - ignoring health risks) light has such spikes:

White-LEDs that are becoming common in computer and phone displays recently are actually UV (black body) sources where the UV light is modified through either coating or some other method into visible light. From the datasheets of these lights (such as Cree's white-leds) it can be seen that these can also have spikes in blue energy.

My personal experience (and confirmed by numerous reports on product reviews from people who have developed damage to eyes from use of computer displays and have become sensitive to the light - causing quick eye strain) is that CCFL and White-LED, when not filtered to completely smooth the spikes from the output spectum to resemble natural or incandescent type light is the cause of the eye strain. My own anecdotal evidence to this is that I have two phones, one causes eye strain within *minutes* and another does not. Visibly the image quality is similar. The only explanation is that there are high energy spikes either in blue,UV or both - I've ruled out PWM dimming flicker as the source for the eye-strain by trying these displays at various backlight intensities and verifying that the PWM is not in effect.

Current hypothesis: Eye adapts to the broad spectra - it can not adapt to the spikes in spectra, thus these are comparatively high energy and are absorbed more intensely since eyes are adapted to lower overall light input (broad spectra).

If eye adapted to the maxima of these spikes in the spectra, it would cause everything else to look dim. This is just common sense to me but I don't have a reference unfortunately if this has been demonstrated already.

Following site provides further support to the hypothesis above and I've quoted key sections and added references:

"Each year, thousands of premature babies in intensive care nurseries lose their sight to ROP. This blinding began with the introduction of fluorescent lamps. Industrial safety researchers have determined the wavelengths where the retina is most vulnerable to blue-light damage. The most intense energy spike in the spectrum of the fluorescent lamp shines precisely into that vulnerability window. Typical nursery lighting exposes the preemie in 15 minutes or less to the US industrial safety regulations' danger-limit dose of retinal irradiation for adults. Preemies have none of the adults' protections against damaging light. Light hitting a preemie's still migrating retinal cells can garble the cells' migrating instructions and make them stick to other cells. Under the electron microscope, retinae damaged by light and by ROP show the same abnormal adhesions between cells."

"The first babies to develop ROP were born in 1940. ROP had never been observed before and could not be traced in retrospective studies of older blind people. Its sudden appearance coincided with the appearance of fluorescent lamps which had been introduced commercially at the New York World Fair in 1938/39." "Like the lamps, ROP long remained unknown anywhere else until 1948/49, when fluorescent lamps became available in post-war Europe and other industrial countries; then, ROP suddenly affected preemies in these countries, too."

"Because the disease had appeared so suddenly, some physicians wondered if it had been there all along but had simply not been recognized before. They organized several large-scale retrospective studies on ROP among older blind people. Some of these studies found a few isolated and uncertain cases beginning, in 1937 (34, 35), but they all concluded that if ROP had existed before 1940 in the U.S.A., or before 1946 in the U.K., it must have been exceedingly rare (36)."

34. HEPNER WR, KRAUSE AC, NARDIN HE. Retrolental fibroplasia (11. Encephala-ophthalmic dysplasia). Study of 66 cases. Pediatrics 1950: 5: 771-82. (These authors mentioned one isolated case each in 1937, 1938, and 1939 in Chicago). 35. ZACHARIAS L. Retrolental fibroplasia: A survey. Am J Ophthalmol 1952: 35: 1426-54. See page 1434. This survey listed four cases in 1938 and one in 1939 in Boston. 36. SILVERMAN WA. Retrolental Fibroplasia: a modem parable. Monographs in Neonatology. New York: Grune & Stratton, 1980: page 17.

"Wombs have no fluorescent lamps, and preemies meant to have stayed in their protected darkness are much more vulnerable to harsh light than adult workers."

"It appears that a common exciting factor is related to premature birth and incubator life. It seems logical that, of the etiologies limited to the eyes alone, precocious exposure to light is still the leading factor in the cause of ocular developmental abnormalities"

"The lowest threshold value for light damage to animal retinae is reported for non-coherent blue light (42) like that from the most intense of the energy spikes in the fluorescent lamp spectrum. When the photons emerge from the phosphor atoms in the fluorescent lamp, they shoot out in specific wavelengths and form intense spikes of concentrated energy radiation. These spikes occur in all fluorescent lamps at the same wavelengths 365.0 nm; 404.7 nm; 435.8 nm; 546.1 nm; and 578 nm -- and approximately with the same relative intensities (43). The differences between the different types of fluorescent lamps are mostly in the broadband spectrum reradiated by the different phosphor formulations. "

42. SPERLING G. Functional Changes and Cellular Damage Associated with Two Regimens of Moderately Intense Blue Light Exposure in Rhesus Monkey Retinae. Association for Research in Vision and Ophthalmoloy, Spring 1978 meeting, ARVO Abstracts page 267. 43. Sylvania Engineering Bulletin 0-283: "Spectral Energy Distribution Curves of Sylvania F40T12 Fluorescent Lamps", Code 753. undated, received in 1985.

"Figure 1 does not show the full height of these spikes, since it averages the energies over bandwidths of 10 nm. The spike at 435.8 nm, for instance, is only 0.1 nm wide (45) and would appear almost 100 times higher on the graph if it was not averaged with the neighboring wavelengths. This spike packs 8.5% of a typical nursery lamp's total energy output (see Table 1).

Due to the higher photochemical energy of shorter wavelengths, this spike in the short-wave end of the visible spectrum accounts for an even higher percentage of the total photochemical activity produced by the lamp: in vitro experiments of bilirubin conversion by fluorescent lamps have shown that the single energy spike at 435.8 nm is responsible for more than 50% of the conversion reaction (46)."

46. AGATI G, FUSI F, PRATESI R. Configurational photoisomerization of bilirubin in vitro - II. A comparative study of phototherapy fluorescent lamps and lasers. Photochem Photobiol 1985: 41: 381-92 (Ref. 45, page 382 top left).

"The 1974 Symposium on Illumination, sponsored by the U.S. National Institute of Occupational Safety and Health, NIOSH, warned that high lighting levels in that region of the spectrum could cause much damage to the eye, particularly retinal and macular degeneration (the macula is the most light-sensitive part of the retina).

Included in the Public Health Service's "Guide to the Recognition of Occupational Diseases" is this statement in the section on laser light:

'even a diffuse reflection from a high power laser can present an ocular hazard. An action spectrum has been recently developed to account for the variation in retinal sensitivity with wavelength for exposure times greater than ten seconds. The minimum threshold dose for retinal lesions occurs at 440 nm and is thought to be due to a photochemical process rather than to a thermal mechanism as in wavelengths greater than 500 nm' (47). "

47. KEY MM, HENSCHEL AF, BUTLER J, LIGO RN, TABERSHAW IR, EDE L. Occupational Diseases - A Guide to their Recognition. National Institute for Occupational Safety and Health, U.S. Government Printing Office, June 1977, page 496 top. (from )

"The NIOSH data for this table and graph derive mostly from experiments which destroyed the retinae of monkeys, pigs, rats, and a variety of other mammals. The retinal structure of all mammals is virtually the same (49). Clinical experience with victims of welding accidents and accidental exposures to excess laser light confirms that humans are just as vulnerable in the same wavelength region as test animals. There is, thus, no basis for assuming that the developing preemie retina during its period of greatest vulnerability is immune to irradiation in a wavelength which quickly burns the retinae of other mammals. Much of the nursery lamps' energy is concentrated in precisely the wavelength that is known to cause the most damage to the retina."

49. Y CAJAL SR. (first published in 1892 in "La Cellule", Paris), translated by THORPE SA, GLICKSTERN M. The Structure of the Retina. Springfield: Charles C. Thomas Publishers. 1972: pp. 93 and 153.

"60 ftc intensive care nursery lightning will expose a preemie's retinae in 15 min or less to the dose of retinal irradiance which NIOSH has established as the occupational danger limit for healthy adult industrial workers."

"Direct sunshine can be hazardous to unprotected eyes also. In more primitive times, societies punished some of their worst criminals by making them stare into the sun until their eyes were destroyed. Nowadays some nursery staffs appear unaware of the dangers from sunlight.

A report from a nursery in Washington, D.C., describes how a group of babies near the nursery windows had "on occasion" been left lying with the sun in their faces, exposed to light intensities in excess of 400 ftc. Most of them went blind. The authors of the report computed the chances as 199 in 200 that it was this exposure to sunlight which had blinded the babies (69).

69. GLASS P, AVERY GB, SLUBRAMIANIAN KNS, KEYS MP, SOSTEK AM, FRIENDLY DS. Effects of bright light in the hospital nursery on the incidence of retinopathy of prematurity. New Engl J Med 1985: 313: 401-4 (see page 402 bottom right and 403 middle left).

Such carelessness about sunlight is not an isolated case. The above-mentioned nursery in Seattle, for instance, that had the high light levels and a tripling of babies with ROP in the early 1980s, reported measurements of nursery luminance with direct sunlight entering the room. The mean of these measurements taken right next to the isolettes works out to 226 ftc, and the maximum measured was given as 1124 ftc (66)."

66. HAMIER RD, DOMN V, MAYER MJ. Absolute thresholds in human infants exposed to continuous illumination. Invest Ophthalmol Vis Sci 1984: 25: 381-8 (see page 383 top right).

"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. "

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.

"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."

"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). "

"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. "

"Electron microscope pictures of light-damaged retina segments from albino rats (100) show that after exposure to light the cell membranes of the photoreceptors and of the pigment epithelium cells form massive microvilli, little hairlike tendrils, which grip each other like the hooks and loops on a patch of Velcro. This causes the cell membranes to stick together permanently. "

100. KURABARA T, GORN RA. Retinal damage by visible light. Arch Ophthalmol 1968: 79: 69-70.

"Neonatologists who say that the nursery lights do preemies no harm base this assertion on a small scale trial published in 1952 which claimed to have ruled out a connection between exposure to light and ROP. The authors reported that just as many preemies had developed the disease when their eyes were patched with gauze as when they were not. However, in that study the babies' eyes were patched, not immediately, but within up to 24 h after birth (103). That is more than enough time for the fluorescent light to overdose their fragile retinae with damaging blue radiation.

103. LOCKE JC, REESE AB. Retrolental fibroplasia - the negative role of light, mydriatics, and the ophthalmoscopic examination in its etiology. Arch Ophthalmol 1952: 48: 44 47 (see page 46 top).

A year after this misleading study, another flawed but very influential study asserted that oxygen was the major cause of ROP. In that study, 18 nurseries withheld oxygen from some of the preemies and found fewer cases of ROP among the survivors of that group (104). This result was acclaimed as a victory over ROP and led to severe oxygen rationing for most preemies that has endured to this day. However, the unacknowledged reason for the apparent reduction in the incidence of ROP was that fewer preemies, with immature lungs and eyes, survived long enough to display the symptoms of ROP. In fact, the lack of sufficient oxygen killed most of the babies whom ROP would have blinded, plus many more whom ROP would have spared (105).

105. SILVERMAN WA. Retrolental fibroplasia: a modem parable. Monographs in Neonatology. New York: Grune & Stratton, 1980. Chapter 9: "The Determinative Era of Oxygen Treatment", see particularly pp. 62 ff.

A British researcher estimated two decades later that each case of ROP avoided by withholding oxygen "may have cost some 16 deaths" (106)."

106. SILVERMAN WA. Retrolental fibroplasia: a modem parable. Monographs in Neonatology. New York: Grune & Stratton. 1980. Chapter 8: "The Consequences of Oxygen Restriction", see particularly pages 54-57 and 63, 65.

"By the mid and late 1960s, researchers studying the safety of laser light for industrial applications discovered that light could damage eyes not just by burning, the retina with heat as in welding accidents or Sun-staring -- but also through a slower, non-thermal process which they found to be photochemical (108-110). "

108. NOELL WK, WALKER VS, KANG BS, BEPMAN S. Retinal damage by light in rats. Invest Ophthalmol Vis Sci 1966: 5: 450-73. 109. GORN RA, KUWABARA T. Retinal damage by visible light: a physiologic study. Arch Ophthalmol 1967: 77: 115 ff. 110. KUWABARA T, GORN RA. Retinal damage by visible light: an electron microscope study. Arch Ophthalmol 1968: 79: 69 ff.

"In August 1970, a team of physicians from Boston and Philadelphia described in their paper "Retinal Changes produced by Phototherapy" (67) how they had placed newborn piglets under phototherapy lamps with a total irradiance of 300 ftc "to determine if retinal damage does in fact occur during phototherapy of the newborn infant".

67. SISSON TRC, GLAUSER SC, GLAUSER EM, TASMAN W, KUWABARA T. Retinal changes produced by phototherapy. J Pediatr 1970: 77: 221-7 (see page 225 middle left).

They had picked piglets because "the newborn piglet eye is developmentally of close approximation to the human of comparable age, and since the piglet is a diurnal animal whose eyes are similarly pigmented".

One of the piglets lost the patch over its control eye which had not been dilated, and which remained relatively protected by its heavy eyelids, covered with hair, and thick eyelashes. Although that eye was exposed to the lights for less than 12 h, the next day that piglet had become totally blind. When its retinae were examined 3 weeks later under an electron microscope, both showed virtually the same "marked damage" as the other exposed piglets' retinae.

These researchers concluded that preemie eyes exposed to phototherapy lights should be shielded with the utmost care"

Recommendations ( To prevent retinopathy of prematurity, the following recommendations are made:

1. All fluorescent lamps in intensive care nurseries in hospitals should be immediately removed and replaced with lamps using only incandescent light bulbs at intensities as low as possible and only when needed.

2. Bilirubin phototherapy lamps should be equipped with side shields to prevent their light from reaching neighboring babies

3. Most of the clinical literature on the role of oxygen in ROP treats supplementary oxygen as the cause of ROP, but this literature is incorrect and misleading. There was total absence of ROP before the advent of fluorescent light while many preemies had been receiving oxygen therapy for up to 6 weeks, and in concentrations of 40 to 55% (131). "

What a productive day this has been. I've suffered from computer display eye strain after switching from heavy CRT screen to light and flat CCFL based LCD screen. My eye strain reduced immensely immediately when switching from LCD back to CRT and I can watch the CRT for 2-3 times long (almost full 16 hours in one sitting, where as LCD's make eye strain and burn feeling that results in red eyes from anywhere from minutes to 8 hours depending on the LCD - presumably due to variation in how much filtering is used).

I've been learning and developing ideas of what might possible be the cause of the eye strain in LCD use and only after I learned about these spikes in black body lamps (UV based White-LED, Cold-cathode Fluorescent Lighting /CCFL) I started discovering information where severe exposures (as opposed to mild exposure from spectra spikes at typical home & office settings) have caused more immediate and permanent damage. It's plain obvious that if these light sources can cause blindness, then smaller exposure can cause eye strain and possibly lead to increasing sensitivity the more.

In addition, I don't have a reference to quote from but I read long ago that watching this type of CCFL light directly can lead to alteration in the eye fluid so that eyes will not get properly lubricated. The solution to this is "artificial eye drops". So in order for computer display makes to save a few dollars, everyone will eventually need eye lubricant. Win-win for the tech and pharma biz. I developed this issue after about 2 years of CCFL LCD and the sensitivity and quick eye strain from these type of lights came soon after.

As long as display and computer panel manufacturers are not obligated by law to publicize the emitted spectra and then keep the components the same (today they sell you model X and change backlight and panel suppliers without changing the model name) there is no really good solution for consumers. The best you could do to avoid this is have your display tested by extremely sensitive person but it's possible that a person has sensitivity only at specific frequencies and a display which is emits equally dangerous different frequencies would feel "OK" since the test persons eye has not been sensitized to the frequencies emitted by this other display.

Only a class action suit against LG, AUOptronics, Samsung and the like is likely to bring any resolution to this issue. Overhead CCFL lights are mostly a problem in hospitals where patients are lying down eyes facing the lights - in office and home settings the computer displays are the only direct UV based light source people stare at. — Preceding unsigned comment added by (talk) 17:24, 23 March 2012 (UTC)