Treatment for Retinopathy of Prematurity in Denmark in a Ten-Year Period (1996–2005): Is the Incidence Increasing?
a Departments of Ophthalmology
c Neonatology, Copenhagen University Hospital, Rigshospitalet, Copenhagen, Denmark
b Department of Ophthalmology, Copenhagen University Hospital, Glostrup Hospital, Copenhagen, Denmark
d National Board of Health, Copenhagen, Denmark
OBJECTIVE. The objective of this study was to analyze the population incidence of retinopathy of prematurity treatment in Denmark in the 10-year period from 1996 to 2005.
METHODS. Patient charts of infants treated for retinopathy of prematurity and the national birth registry provide information about neonatal parameters. These parameters, along with birth in the latter half of the period (2001–2005), were analyzed as risk factors for retinopathy of prematurity. The national registry for blind and visually impaired children was accessed to obtain information about visual impairment attributable to retinopathy of prematurity in both treated and untreated infants.
RESULTS. The study population consisted of 5467 Danish preterm infants born in 1996 to 2005, with a gestational age of <32 weeks, who survived for 
5 postnatal weeks; 2616 were born in 1996 to 2000, and 2851 were born in 2001 to 2005. The incidence of treated retinopathy of prematurity cases increased significantly from 1.3% in 1996 to 2000 to 3.5% in 2001 to 2005. Significant risk factors for retinopathy of prematurity treatment were low gestational age, small for gestational age, male gender, and multiple birth. Other, yet unknown factors contributed to the increased incidence in the latter half of the period. Of the study population, 0.6% were registered as visually impaired because of retinopathy of prematurity within 2 years after birth (early-detected visual impairment). The incidences were not significantly different between 1996 to 2000 and 2001 to 2005. Of all of the early-detected, visually impaired children, 16% had not been treated for retinopathy of prematurity and were considered screening failures.
The above article can be found here.
14 comments:
I wasn't able to read the entire article (subscription needed), so I am just going to throw this out without much background.
In North America, ROP should actually be declining, if only because we have put the brakes on with respect to the use of steroids to wean kids from vents. Steroids had been implicated in ROP.
Do we have Vermont-Oxford data on what is happening with respect to ROP? Anybody know? I am a bit out of the loop with respect to getting Vermont-Oxford data easily.
There is something in the wording of the abstract about (not) treating ROP, in addition to the incidence. What is THAT about?!
I guess the people with recent experience with their own kids would be the best ones to tell their stories.
Chris and Vic
To Chris and Vic,
If my notes are reliable... a big *if* ... there is a 20.6% rate of stages 3-4 ROP among the Vermont Oxford ELBW infants. This data, presented by Roger Soll in 2006, is from about 3597 babies born in 1998-2003 who were followed to age 2. All were born at less than 1001 g and ranged in gestational age from <22 weeks to >31 weeks.
I'm not sure (haven't read the Danish study in Pediatrics carefully, yet) but I *think* the not treating of ROP may relate to children who weren't identified as having problems when examined (and so weren't treated) but who later developed ROP anyway.
Do you know of any evidence that ROP is declining in the US with the decrease in steroid use? Severe CP may be declining with a decrease in postnatal steroids, Cognitive outcomes and retardation do not seem to have changed.
I can't recall anything on changes in ROP rates in the US related to the steroid decrease, but would love to see any such data.
In other ROP news, Dale Phelps talked at the last Hot Topics about an epidemic of ROP worldwide, especially in 3rd world countries (Denmark does *not* qualify) where oxygen monitoring skills do not match oxygen administration capability.
The gestational ages at risk for ROP are, she said, much higher in the 3rd world than elsewhere, with children born almost at term still being at risk.
In my previous post I said that CP may be on the decline among <1000 g. infants *because of the decrease in use of steroids*.
That was based largely on Maureen Hack's recent data that showed a reduction in CP among a
(relatively small) number of <1000 grammers whose survival
coincided with the time when postnatal steroid use was being discouraged.
However...I've just read the new study on <1000 grammers in Maureen Hack's study who had BPD. BPD was defined as oxygen dependence at 36 weeks post conceptional age.
These BPD infants made up over half of the <1000 grammers. They are the children most likely to be affected by changes in the use of postnatal steroids, yet any improvements in their outcomes in the post-2000 era has been largely due to a decrease in deafness.
(due to changes in antibiotic or diuretic usage?)
There was no significant decrease in CP with the decrease in steroid use among these children and there was no improvement in overall neurodevelopmental outcomes. However, exposure to postnatal steroids (they are still being
used, though more conservatively) did predict both CP and other neurodevelopmental ipairment. PDA ligation also predicted neurodevelopmental impairment, as did duration of ventilator dependence and severe ultrasound abnormalities.
And poor outcomes persisted among the BPD children even in the absence of identified neurologic abnormalities (such as IVH, PVL, etc). The authors speculate that BPD, in and of itself, or time on the ventilator, or poor growth may be the chief cause of the continued poor outcomes (half of the BPD children had a neurodevelopmental impairment at age 20 months).
Kobaly et al. Outcomes of extremely low birth weight (<1 kg) and extremely low gestational age (<28 weeks) infants with bronchopulmonary dysplasia: effects of practice
changes in 2000 to 2003. Pediatrics 2008;121:73-81
Obviously nowhere near close to scientific since the n in this study is 1 :-), but my 28 weeker got only to Stage 1 Zone 3 in each eye and then it "resolved". At his 1 year opthamology appointment his vision was normal for his age. We have his 2 year check up in 2 weeks, so we shall see then.
I am not sure if the oxygen sat limits in his NICU had anything to do with it or not. I know when he was at a younger gestation that the upper limit was lower and it was raised as his gestation age increased. Sorry I can't remember the exact numbers, but I do know that satting 100 was not considered good for babies of his gestation in his NICU.
Helen,
Can you please go deeper into the correlation between PDA ligation and neurodevelopmental impairment.
I'm very interested in how they are connected and would appreciate the education.
To anon:
A number of studies are showing this (PDA ligation is related to poor outcome), and I can only speculate as to the reasons. I would appreciate it some of the neos reading the blog would weigh in with their more informed speculations.
I suspect that the need for PDA ligation (usually after a failure of medical treatment) may indicate severe circulatory problems that adversely affect the brain. The other possiblity is that the major circulatory changes brought about by the surgery itself may be harmful to the brain, at least initially.
This is only a guess on my part and I would very much like to hear from the experts.
It is frightening to realize, but almost everything done in the NICU to treat almost every neonatal problem directly or indirectly involves the brain from lung treatment (ventilator, o2 treatment, suctioning) to nutritional strategies, and everything in between. Anything that causes changes in circulation or blood pressure can affect the brain and PDA and PDA surgery do these things.
Helen:
"And poor outcomes persisted among the BPD children even in the absence of identified neurologic abnormalities (such as IVH, PVL, etc). The authors speculate that BPD, in and of itself, or time on the ventilator, or poor growth may be the chief cause of the continued poor outcomes (half of the BPD children had a neurodevelopmental impairment at age 20 months)"
I'm curious if this could even be a fair judgment of BPD babies... only because at 20 months the children with severe BPD haven't even come close to 'catch up' age.
We were told that besides early gestational age, the length of hospitalization contributes to delay.. so someone like my son, with obvious severe BPD and an extremely long NICU stay, would still be significantly delayed at 20 months (though right now he is developmentally consistent with his corrected age - slightly advanced cognitively), but at 20 months he wouldn't even be close to an age that he could be compared to his term peers.
I wonder if considering severe BPD babies as delayed would have to be something done later in age, say at 2 years or even 3 years, because severe BPD babies tend to have longer hospital stays anyway but also because their growth, and therefore development, is slower than non-BPD babies.
To Sarah, who asked:
"I wonder if considering severe BPD babies as delayed would have to be something done later in age, say at 2 years or even 3 years, because severe BPD babies tend to have longer hospital stays anyway but also because their growth, and therefore development, is slower than non-BPD babies."
***
Long hospitalization and impairment of early development is an important issue, but what is being talked about here isn't simply delay for medical reasons, but early detection of the sorts of serious disabilities that tend not to change with age, such as ROP, deafness, cerebral palsy and severe retardation.
Changes in the brain from BPD are also seen on MRI, and unfortunately they cause problems that persist.
I have about a dozen references I can give here (and there are many more out there).
I will list all the ones in my files, if you would like. I can also send you via email the paper by Kobaly et al. I have mentioned here that has about 1/2 dozen of these references.
email me at
Helen1144@aol.com
if you are interested
Helen
"I have about a dozen references I can give here (and there are many more out there)."
No, I think I misunderstood (which you explained). I was thinking only of delay as opposed to long-term and permanent disabilities.
FAO Sarah
I have just read your comment about the advice provided to you about catch-up,a wide and undefined term.
I have to say that it perhaps more helpful to consider your child "moving on" in terms of how your son develops in all areas. Catch-up as a term implies that your son is on the same developmental path as healthy children born at full term. Again, it is perhaps more helpful to regard your son as simply starting his journey from a different place and that his development will follow his own trajectory as opposed to mimicking the developmental path of a healthy baby born at 40 weeeks ga.
Kind regards
Sarah Manns
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