CN

ERetinopathy of

Prematurity

Improving Outcomes Through Evidence-Based

Practice

Sandra Bellini, DNP, NNP-BC, APRN

INtRoduCtIoNOne of the major goals of the World Health Organization’s (WHO) “Vision 2020” program is the reduction of childhood blindness worldwide (Gilbert & Foster, 2001). According to the WHO, a wide range of socioeconomic influences have a significant impact on the causes and rates of childhood blind-ness. While much of the focus of the WHO program is targeted at reducing rates of childhood blindness in developing coun-tries where poverty, poor nutrition and poor access to quality medical care are significant issues, retinopathy of prematu-rity (ROP) has also been identified as a significant problem. In countries with middle- and high-income levels, ROP has been identified as a significant cause of childhood blindness. This disparity is likely due to the high rates of infant mortal-ity among preterm infants in developing nations. As long-term survival rates of premature infants in developing countries continue to improve, health care providers should also antici-pate an increase in ROP as a long-term complication associ-ated with prematurity.

According to the National Eye Institute, each year an esti-mated 1,100 to 1,500 infants in the United States develop ROP

severe enough to require medical treatment (National Eye In-stitute [NEI], 2010). Of these infants, 400 to 600 become legally blind from ROP each year (NEI). As ROP is a known cause of childhood blindness, it is critical that nurses working with premature infants understand the pathophysiology and classi-fication of ROP, the research supporting current treatment and prevention and, most importantly, strategies that best ensure improved outcomes for their patients.

HIstoRICal CoNtExt of RoPWith the increased survival of premature infants beginning in the 1940s, researchers began to recognize the association between prematurity and subsequent visual impairment and blindness (Pollan, 2009; Wheatley, Dickinson, Mackey, Craig, & Sale, 2002) although the etiology for that association had not

• Retinopathy of prematu-rity (ROP) is caused by high concentrations of excessive oxygen therapy and can cause childhood blindness.

• Slightly lower oxygen saturation target ranges can safely reduce rates and severity of ROP.

• It is imperative that NICU nurses advocate for careful targeting of oxygen saturation parameters.

Bottom Line

384 © 2010, AWHONN http://nwh.awhonn.org

Sandra Bellini, DNP, NNP-BC, APRN, is the coordinator for the DNP Program at the University of Connecticut School of Nursing in Storrs, CT, and a neonatal nurse practitioner at Connecticut Children’s Medical Center in Hartford, CT. The author and planners of this activity report no conflicts of interest or relevant financial relationships. No off-label drug or device use is mentioned in this article. No commercial support was re-ceived for this learning activity. Address correspondence to: sandra.bel-lini@uconn.edu.

DOI: 10.1111/j.1751-486X.2010.01577.x

objectivesUpon completion of this activity, the learner will be able to:

1. Examine the historical emergence and significance of retinopathy of prematurity (ROP).

2. Describe the pathophysiology and developmental classifications of ROP.

3. Identify potential treatments and preventive practice strategies for ROP.

Continuing Nursing Education (CNE) Credit

A total of 2 contact hours may be earned as CNE credit for reading “Retinopathy of Prematurity: Improving Outcomes Through Evidence-Based Practice” and for completing an online post-test and participant feedback form.

To take the test and complete the participant feedback form, please visit http://journalscne.awhonn.org. Certificates of completion will be issued on receipt of the completed participant feedback form and processing fees.

AWHONN is accredited as a provider of continu-ing nursing education by the American Creden-tialing Center’s Commission on Accreditation.

Accredited status does not imply endorsement by AWHONN or ANCC of any commercial products displayed or discussed in conjunction with an educational activity.

AWHONN also holds a California BRN number California CNE provider #CEP580.

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October November 2010 Nursing for Women’s Health 385

yet been clearly articulated. In 1951, Australian pediatrician Kate Campbell suggested that ROP, known at that time as retro-lental fibroplasia, resulted from the toxic effects of uncontrolled oxygen administration given to premature newborns. At that time she recommended that oxygen be administered to infants with cyanosis, rather than for respiratory distress or atelectasis as had been the practice (Reedy, 2004; Wheatley et al.).

Subsequent studies in the 1950s demonstrated a causal asso-ciation between premature newborns exposed to high concen-trations of supplemental oxygen therapy and obliterated retinal blood vessels (Ashton, Ward, & Serpell, 1954; Patz, Hoeck, & De La Cruz, 1952). Following publication of these studies, ROP rates declined significantly in the United States between 1950 and 1965 as practitioners began to carefully control the amount of oxygen administered to premature newborns (Pollan, 2009; Wheatley et al., 2002).

While this was good news in terms of preserving vision, there were concurrent increases in rates of both neonatal mor-tality and cerebral palsy during the same time period (Pollan, 2009), leading to concerns about whether restricted oxygen use had played a role in these trends. This had led to an ongo-ing challenge among today’s health care providers to balance the need for providing supplemental oxygen to preserve lung and neurologic function in premature infants while recog-nizing that high concentrations of supplemental oxygen may cause ROP.

PatHogENEsIs of RoPPredisposing factors for the development of ROP include premature birth, low birth weight and severity of underlying illness (Olitsky, Hug, & Smith, 2007). Additionally, the level of oxygen saturation and genetics seem to play a role in the severity of ROP in various infants (Olitsky et al.; Wheatley et al., 2002). Other endogenous factors that likely play a role in the progression of ROP are vascular endothelial growth factor (VEGF) (DiBiasie, 2005; Pollan, 2009) and insulin-like growth factor (IGF-1) (Harrell & Brandon, 2007; Pollan). Both VEGF and IGF-1 are endogenously produced growth factors that are necessary for normal vessel development (Harrell & Brandon).

When a fetus is delivered prematurely, the normal processes for further fetal growth and development are interrupted. In terms of the developing retina, premature birth interrupts the

normal process of the developing vascular bed that will nourish the eye. Normal retinal angiogenesis begins at the optic disc at about 16-week gestation and extends to the periphery by about 36- to 40-week gestation. Disturbances in this process result in arrest of vasculogenesis, known as Phase I ROP (Harrell & Brandon, 2007; Olitsky et al., 2007). In utero, the fetus receives IGF-1 via the placenta. IGF-1 levels are deficient after prema-ture birth, thereby predisposing the infant to Phase I ROP due to an inherent lack of normally developed vessels (Harrell & Brandon; Pollan, 2009). Production of VEGF is also inhibited in Phase I ROP and is caused by the high levels of supplemental

oxygen infants premature receive in the neonatal intensive care unit (NICU), which subsequently causes the death of vascular endothelial cells (Box 1).

As the infant grows and develops, the lack of blood vessels in the retina initiates anaerobic metabolism, further increasing the already existing hypoxia. Without blood flow through the eye, the retina is deprived of oxygen and its metabolic needs increase (Harrell & Brandon, 2007; Pollan, 2009). This hypoxia causes stimulation of VEGF, precipitating rapid neovasculari-zation—excessive, abnormal formation of vessels—known as Phase II ROP (DiBiasie, 2005; Harrell & Brandon; Olitsky et al., 2007; Pollan). Phase II ROP does not proceed with a gradual transition from avascularized to vascularized areas but rather as a demarcated, ridged line that develops along the retina. While vascular development from this stage may resume with-out significant disruption, infants with significant ROP may develop an abnormal proliferation of retinal vessels into the vitreous and over the surface of the retina (Olitsky et al.). As vessels become more tortuous, traction on the retina with sub-sequent blinding detachment can result.

ClassIfICatIoN of RoPThe International Classification of Retinopathy of Prematu-rity (ICROP) system identifies five stages of ROP (Harrell & Brandon, 2007). First developed in 1984 and revised in 1987 and 2005, the system provides a standardized method for oph-thalmologists to grade ROP by three criteria: (1) severity, (2) location and (3) extent (DiBiasie, 2005; Harrell & Brandon).

As long-term survival rates of premature infants in developing countries continue to improve, health care providers

should also anticipate an increase in ROP as a long-term complication

associated with prematurity

BOx 1 PHasEs of RoP

Phase I: Arrest of vasculogenesis

Phase II: Hypoxia causes stimulation of vascular endothelial growth factor, precipitating rapid neovascularization (excessive, abnormal forma-tion of vessels)

386 Nursing for Women’s Health Volume 14 Issue 5

Severity of ROP is graded on a worsening scale of stage 1 through stage 5. Location is described using three zones on the retina, depicted as increasingly larger concentric circles. The zones indicate how far normal vascularization has occurred from the optic nerve out to the periphery and where abnor-mal vascularization begins (DiBiasie; Harrell & Brandon). The

extent of the disease is defined by describing the proportion of the entire retinal circumference that is involved, and is in-dicated by the number of “clock hours” (DiBiasie; Harrell & Brandon).

In addition to the above criteria, ROP is also described as existing at either prethreshold or threshold levels. Threshold levels require immediate treatment by any standard, although recent research has focused on treatment at the prethresh-old level in the hope of improving long-term outcome (Early Treatment for Retinopathy of Prematurity Cooperative Group, 2003). Finally, the progression and grading of ROP includes notation regarding the presence or absence of “plus” disease, whereby retinal vessels are shunting blood and becoming en-gorged. At any stage of ROP, infants may develop plus disease, indicating rapid advancement of pathology and increased risk of retinal detachment. Decisions regarding need for treatment at prethreshold versus threshold levels are sometimes based on whether the infant also exhibits signs of plus disease (DiBiasie, 2005; Harrell & Brandon, 2007).

EvIdENCE BasE foR MaNagEMENt of RoPTreatmentFortunately, only 6 percent of infants who develop some degree of ROP will require treatment (Palmer, 2003). Surgical inter-vention using either cryotherapy or laser photocoagulation is the current standard of care (Harrell & Brandon, 2007). Cryo-surgery first became the standard of care in 1988 (Harrell & Brandon) and involves repeated applications of an extremely cold probe that cauterizes the hypoxic areas of the retina. The cryosurgery procedure essentially ablates the unvascularized peripheral portion of the retina in an attempt to stop secre-tion of VEGF and other factors that promote the progression of ROP (Harrell & Brandon). While the procedure limits some peripheral vision, it preserves central vision.

One group has reported that following adoption of cryo-surgery, unfavorable ROP structural outcomes decreased by more than 40 percent and visual acuity outcomes improved by 30 percent (Cryotherapy for Retinopathy of Prematurity Coop-erative Group, 1990). In another study, the number of infants suffering from retinal detachment following cryotherapy also decreased from 43 percent to 21 percent (Palmer et al., 2005). While these numbers are promising, the search continues for even better outcomes with newer therapies.

Laser photocoagulation for the treatment of ROP has dem-onstrated promising outcomes, although the studies have been less robust than the cryosurgery studies. In laser treatment, ophthalmologists use either an argon or a diode laser, which is applied directly to the retina to destroy the unvascularized tissue (DeJonge, Ferrone, & Trese, 2000). DeJonge et al. have reported better ROP outcomes with laser ablation therapy than with cryosurgery, although larger studies over longer time peri-ods are indicated to provide more conclusive evidence.

PreventionIdeally, ROP is preventable. Much research over the past 15 years has focused on patient care strategies that prevent or minimize the development and progression of ROP. Current research supports the fact that oxygen concentrations have dif-ferent implications in the development of ROP. In Phase I ROP, high saturations can be especially deleterious; in Phase II ROP, slightly higher saturations (although still lower than tradition-ally accepted ranges) may be less harmful. Consequently, the focus of many research studies has been the identification of “optimal” oxygen saturation ranges for premature infants at various postnatal ages. However, the clinical outcomes of in-fants in terms of severity of ROP must be balanced with long-term severity of chronic lung disease and neurologic outcomes.

One of the earliest studies of the last decade to try to pre-vent significant ROP was the STOP-ROP trial. STOP-ROP was a multicenter, randomized controlled trial designed to evaluate the safety and efficacy of maintaining higher than usual oxygen saturations (96-99 percent) for infants with prethreshold ROP to determine whether the higher oxygen saturations would re-duce the number of infants who went on to develop threshold ROP (STOP-ROP Multicenter Study Group, 2000). Outcomes of the study suggested that while the higher oxygen saturation range did not appear to advance the progression of ROP to threshold standards, there were no significant differences be-tween the control and the experimental groups in the number of infants who went on to require peripheral ablative surgery for advanced ROP.

Several other significant studies during the last decade ex-plored whether oxygen saturations that were slightly lower than standard-of-care protocols would have a positive outcome on rates of advanced ROP requiring treatment. The first of these studies (Tin, Milligan, Pennefather, & Hey, 2001) compared

Surgical intervention using either cryotherapy or laser photocoagulation

is the current standard of care

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outcomes of infants who had received supplemental oxygen to targeted saturation ranges of 88 percent to 98 percent with those who had received targeted saturation levels of 70 percent to 90 percent. Among other notable results, the higher satura-tion group had four times the incidence of ROP than the lower saturation group. The need for supplemental oxygen at 36-week gestational age was also greater in the higher saturation group although the incidence of subsequent cerebral palsy was the same in both groups.

The BOOST Trial was a multicenter, double-blind, rand-omized controlled clinical trial that included 358 infants born at less than 30 weeks of gestation who remained dependent on supplemental oxygen at 32 weeks of postmenstrual age (Askie, Henderson-Smart, Irwig, & Simpson, 2003). Infants were randomly assigned to a cohort group with a standard tar-get oxygen saturation range of 91 percent to 94 percent or to a cohort group with a slightly higher target saturation range of 95 percent to 98 percent. In comparison to findings by Tin et al. (2001), similar pulmonary and neurodevelopmental out-comes were noted in the BOOST Trial (Askie et al.), although the BOOST Trial did not demonstrate differences in severity of ROP between groups.

The hypothesis that slightly lower oxygen saturation target ranges were both safe and potentially beneficial in terms of re-ducing rates and severity of ROP sparked a number of stud-ies with similar design, criteria and findings (Chow, Wright, Sola, & the CSMC Oxygen Administration Study Group, 2003; Coe et al., 2006; Sears, Pietz, Sonnie, Dolcini, & Hoppe, 2009; VanderVeen, Mansfield, & Eichenwald, 2006). Thus, a signifi-cant evidence base now supports the fact that (1) oxygen satu-ration target ranges in the mid 80s to lower-mid 90s are safe and can reduce the severity of ROP in infants <32 weeks gesta-tion and (2) slightly higher target ranges at >32 to 34 weeks can be attempted in an effort to reduce the hypoxia/increased neovascularization progression seen in Phase II ROP.

EvIdENCE-BasEd PRaCtICE guIdElINEsBy integrating the most recent research findings with clini-cal practice management and reducing variation in practice, adherence to evidence-based practice guidelines can improve patient outcomes as much as 28 percent (Heater, Becker, & Olson, 1988). In light of the growing body of evidence regard-ing ROP prevention, many NICUs have adopted new practice guidelines pertaining to the management of supplemental oxygen and that specifically target lower oxygen saturations ranges for premature infants. The goal for targeting oxygen saturation is to avoid hyperoxia in infants at risk of ROP and chronic lung disease. While there are still many questions pertaining to the ideal methods of managing supplemental oxygen delivery to preterm infants, there is substantial Level 2 evidence supporting the need for targeted oxygen saturations in preterm infants.

The Oxygen With Love (OWL) ProtocolIn a 2007 commentary, Goldsmith and Greenspan (2007) echo other investigators (Chow et al., 2003) who endorse multidis-ciplinary “buy in” and appropriate staff education to achieve successful changes in clinical practice. The OWL protocol (Goldsmith & Greenspan), resulted from an effort to improve visual outcomes in premature infants by using quality improve-ment strategies based on evidence-based practices, rather than on a protocol related to a single research study. The OWL proto-col is a clinical practice guideline designed to ensure that NICU staff adhere to targeted oxygen saturation ranges (Goldsmith & Greenspan). It includes settings for oxygen saturation limits for infants based on adjusted gestational age, birth weight and sup-plemental oxygen needs that are slightly lower than tradition-ally accepted ranges, as well as documentation requirements for deviations from saturation targets that are standard with unit policy. Compliance with policies is optimized by requiring all staff to sign a document of agreement following educational activities that are focused on the need for targeted saturation ranges.

Bedside cards with an OWL icon are placed at the patient’s bedside to remind the staff that the infant is an “OWL” baby,

identified as at risk for ROP and therefore requiring special atten-tion to supplemental oxygen management (Goldsmith & Green-span, 2007). The OWL icon is a cartoon-owl named Seymour (as in, “see more”), invoking wordplay reflecting the concept that OWLs have keen eyesight. The bedside cards are intended to raise staff consciousness that the team goal is preservation of sight. Staff adherence to the protocol is critical to achieving the OWL goal of minimizing infants’ exposure to higher oxygen saturation levels, which can increase the risk of ROP over time. Unpublished data suggest that monitoring targeted ranges in this unit resulted in 80 percent compliance with a similar reduction in ROP for inborn infants (Goldsmith & Greenspan).

IMPlICatIoNs foR NuRsINg PRaCtICEWhile it may seem intuitive that staff members generally fol-low recommended plans of care for infants with ROP, evidence suggests otherwise. Several recent studies testing the effects of various target ranges for oxygen saturations have noted vari-able staff compliance to the study protocol (Chow et al., 2003; Clucas, Doyle, Dawson, Donath, & Davis, 2007; Hagadorn et

Oxygen saturation target ranges in the mid 80s to lower-mid 90s are safe

and can reduce the severity of ROP in infants <32 weeks gestation

388 Nursing for Women’s Health Volume 14 Issue 5

al., 2006). These studies all found higher than prescribed oxy-gen saturation limits a significant portion of the time. There-fore, it is imperative that the multidisciplinary NICU staff be educated that oxygen can be potentially damaging as well as lifesaving, depending on the circumstance. In particular, nurses play a major role in ensuring target ranges are maintained in the hour-to-hour provision of care (Coe, 2007).

Specifically, neonatal nurses should be vigilant about en-suring that the settings of the saturation monitor alarms are consistent with those recommended for the gestational and weight of the infant. Changes in traditional nursing practice—such as more cautious increases in supplemental oxygen and avoidance of fluctuations in saturations—should be encour-aged and promoted by other nursing staff or nurses in clini-cal leadership positions (Goldsmith & Greenspan, 2007; Sola, Seldeno, & Favareto, 2008). Staff nurses should also take an ac-tive role in assuring multidisciplinary compliance with target-ed saturation settings through optimum communication with neonatologists, nurse practitioners, other staff nurses, respira-tory therapists and most importantly, parents. Clear evidence exists that oxygen saturation levels once considered insuffi-cient are in fact safe, and have fewer harmful effects. There-fore, nurses—integral members of the NICU team—can play a significant role in advancing optimal care for their patients by being knowledgeable advocates with regard to management of supplemental oxygen and by sharing their knowledge with others.

CoNClusIoNAdvancing survival rates of premature infants over the past sev-eral decades have led to an increase in the prevalence of ROP as a complication of prematurity. Through careful study and evaluation of the development of ROP, better treatment and prevention strategies have emerged—including the careful tar-

geting of oxygen saturation parameters once thought too low for optimal lung and neurologic outcome. To help them under-stand oxygen may be harmful to premature infants, particularly in light of its role in the development of ROP, multidisciplinary NICU staff must receive ongoing education. It is imperative that nurses practicing at the bedside understand the evidence base upon which newer preventive strategies are predicated, so

that they can manage patients, mentor other staff and educate parents in the interest of improving visual outcomes for prema-ture infants. NWH

REfERENCEsAshton, N., Ward, B., & Serpell, G. (1954). Effect of oxygen on de-

veloping retinal vessels with particular reference to the problem of retrolental fibroplasia. British Journal of Ophthalmology, 38(7), 397–430.

Askie, L. M., Henderson-Smart, D., Irwig, L., & Simpson, J. M. (2003). Oxygen-saturation targets and outcomes in extremely preterm infants. New England Journal of Medicine, 349(10), 959–967.

Chow, L. C., Wright, K. W., Sola, A., & the CSMC Oxygen Admin-istration Study Group. (2003). Can changes in clinical practice decrease the incidence of severe retinopathy of prematurity in very low birth weight infants? Pediatrics, 111(2), 339–345.

Clucas, L., Doyle, L. W., Dawson, J., Donath, S., & Davis, P. G. (2007). Compliance with alarm limits for pulse oximetry in very preterm infants. Pediatrics, 119(6), 1056–1060.

Coe, K. (2007). Nursing update on retinopathy of prematurity. Journal of Obstetric, Gynecologic, & Neonatal Nursing, 36(3), 288–292.

Coe, K., Butler, M., Reavis, N., Klinepeter, M. E., Purkey, C., Oliver, T., et al. (2006). Special premie oxygen targeting: A program to decrease the incidence of blindness in infants with retinopathy of prematurity. Journal of Nursing Care Quality, 21(3), 230–235.

Cryotherapy for Retinopathy of Prematurity Cooperative Group. (1990). Multicenter trial of cryotherapy for retinopathy of pre-maturity: One year outcome—Structure and function. Archives of Ophthalmology, 108(10), 1408–1416.

DeJonge, M. H., Ferrone, P. J., & Trese, M. T. (2000). Diode laser ablation for threshold retinopathy of prematurity: Short-term structural outcome. Archives of Ophthalmology, 118(3), 365–367.

DiBiasie, A. (2005). Evidence-based review of retinopathy of pre-maturity prevention in VLBW and ELBW infants. Neonatal Net-work, 25(6), 393–403.

Early Treatment for Retinopathy of Prematurity Cooperative Group. (2003). Revised indications for the treatment of retinopa-thy of prematurity: Results of the early treatment for retinopathy of prematurity randomized trial. Archives of Ophthalmology, 121, 1684–1696.

Gilbert, C., & Foster, A. (2001). Childhood blindness in the context of VISION 2020—The right to sight. Bulletin of the World Health Organization, 79(3), 227–232.

Goldsmith, J. P., & Greenspan, J. S. (2007). Neonatal intensive care unit oxygen management: A team effort. Pediatrics, 119(6), 1195–1196.

Hagadorn, J. I., Furey, A. M., Nghiem T. H., Schmid, C.H., Phelps, D. L., Pillers, D. A., et al. (2006). Achieved versus intended pulse oximeter saturation in infants born less than 28 weeks’ gestation: The AVIOx Study. Pediatrics, 118(4), 1574–1582.

Clear evidence exists that oxygen saturation levels once considered

insufficient are in fact safe, and have fewer harmful effects

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Reedy, E. (2004). The discovery of retrolental fibroplasia and the role of oxygen: A historical review, 1942-1956. Neonatal Net-work, 23(2), 31–38.

Sears, J. E., Pietz, J., Sonnie, C., Dolcini, D., & Hoppe, G. (2009). A change in oxygen supplementation can decrease the incidence of retinopathy of prematurity. Ophthalmology, 116(3), 513–518.

Sola, A., Seldeno, Y. P., & Favareto, V. (2008). Clinical practices in neonatal oxygenation: Where have we failed? What can we do? Journal of Perinatology, 28(Suppl. 1): S28–S34.

STOP-ROP Multicenter Study Group. (2000). Supplemental therapeutic oxygen for prethreshold retinopathy of prematurity (STOP-ROP), a randomized, controlled trial. I: Primary out-comes. Pediatrics, 105(2), 295–310.

Tin, W., Milligan, D. W., Pennefather, P., & Hey, E. (2001). Pulse oximetry, severe retinopathy, and outcome at one year in babies of less than 28 weeks gestation. Archives of Diseases in Childhood, Neonatal Edition, 84(2), F106–F110.

VanderVeen, D. K., Mansfield, T. A., & Eichenwald, E. C. (2006). Lower oxygen saturation alarm limits decrease the severity of retinopathy of prematurity. Journal of the American Association for Pediatric Ophthalmology and Strabismus, 10(5), 445–448.

Wheatley, C. M., Dickinson, J. L., Mackey, D. A., Craig, J. E., & Sale, M. M. (2002). Retinopathy of prematurity: Recent advances in our understanding. British Journal of Ophthalmology, 86(6), 696–700.

Harrell, S. N., & Brandon, D. H. (2007). Retinopathy of prema-turity: The disease process, classifications, screening, treatment, and outcomes. Neonatal Network, 26(6), 371–378.

Heater, B. S., Becker, A. M., & Olson, R. K. (1988). Nursing in-terventions and patients outcomes: A meta-analysis of studies. Nursing Research, 37(5), 303–307.

National Eye Institute. 2010. National Institutes of Health. Re-trieved from http://www.nei.nih.gov/health/rop/rop.asp#2

Olitsky, S. E., Hug, D., & Smith, L. P. (2007). Disorders of the retina and vitreous. In R. Kliegman, R. Behrman, R., H. Jenson, & B. Stanton. (Eds.), Nelson Textbook of Pediatrics (pp. 2598–2600). Philadelphia, PA: Saunders.

Palmer, E. A. (2003). Implications of the natural course of retin-opathy of prematurity. Pediatrics, 111(4, Pt. 1), 885–886.

Palmer, E. A., Hardy, R. J., Dobson, V., Phelps, D. L., Quinn, G. E., Summers, C. G., et al. (2005). 15-year outcomes following threshold retinopathy of prematurity: Final results from the multicenter trial of cryotherapy for retinopathy of prematurity. Archives of Ophthalmology, 123(3), 311–318.

Patz, A., Hoeck, L. E., & De La Cruz, E. (1952). Studies on the effect of high oxygen administration in retrolental fibroplasia. I. Nurs-ery observations. American Journal of Ophthalmology, 35(9), 1248–1253.

Pollan, C. (2009). Retinopathy of prematurity: An eye toward bet-ter outcomes. Neonatal Network, 28(2), 93–101.

Get the Facts

National Eye Institute

http://www.nei.nih.gov/health/rop/rop.asp

World Health Organization

http://www.who.int/blindness/causes/priority/en/index4.html

American Academy of Pediatrics

http://www.aap.org/healthtopics/visionhearing.cfm

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Post-test QuestionsInstructions: To receive contact hours for this learning activity, please complete the online post-test and participant feedback form at http://JournalsCNE.awhonn.org. CNE for this activity is available online only; written tests submit-ted to AWHONN will not be accepted.

1. According to Gilbert and Foster (2001), a major goal for the World Health Organization’s “Vision 2020” program is:

a. decreasing rates of preterm birth worldwideb. improving access to care by opthamologists worldwidec. reducing rates of childhood blindness worldwide

2. On a global scale, it is important to reduce rates of ROP because as mortality rates for preterm infants decrease in developing countries, the concomitant rate of ROP would be expected to:

a. decreaseb. increase c. Remain the same

3. In the early 1950s, pediatrician Dr. Kate Campbell sug-gested that ROP:

a. was a complication of atelectasis often seen in the neonatal period following preterm birth

b. was a result of light exposure among preterm infants in hospital nurseries

c. was a result of the toxic effects of uncontrolled oxy-gen administration given to premature newborns

4. During the 1950s, research studies were able to determine the etiology of ROP by demonstrating a causal association between premature newborns exposed to:

a. excessive hours of light in the hospital nursery and subsequent damage to vessels in the eye

b. high concentrations of supplemental oxygen therapy and obliterated retinal blood vessels

c. Inadequate oxygenation levels in the bloodstream and overproduction of endogenous cytokines leading to damaged vascular endothelium

5. Health providers today are challenged to balance admin-istration of oxygen that is necessary versus that which is detrimental to preserve:

a. cerebral function, growth and nutrition, and visionb. lung function, neurologic function, and visionc. motor function, cardiac function, and vision

6. Phase I ROP is characterized by:a. arrest of vasculogenesis b. increase VEGF productionc. rapid neovascularization

7. Phase II ROP is characterized by:a. arrest of vasculogenesis b. decreased VEGF productionc. rapid neovascularization

8. The most signifi cant potential complication to the retina of severe ROP is:

a. blinding detachment b. Plus diseasec. Stage IV ROP

9. The International Classifi cation of Retinopathy of Prema-turity (ICROP) system provides a standardized method for ophthalmologists to grade ROP by which of the following three criteria?

a. degrees, number of clock hours, and oxygen saturationb. gestational age, gender, and risk factorsc. severity, location, and extent

10. The presence of plus disease indicates rapidly advancing ROP, which can occur at which stage of ROP?

a. any stage a. threshold stagec. prethreshold stage

11. What is the current standard of care in the treatment of ROP?a. cryotherapy or laser photocoagulation b. Phototherapy or increased oxygen exposurec. Therapeutic light reduction or anti-infl ammatory

intraocular medications

12. What is the ideal goal regarding ROP?a. early diagnosisb. preventionc. surgery

13. Clinical management strategies for prevention of ROP fo-cus on targeting appropriate _________ ranges for infants at risk.

a. arterial Phb. oxygen saturationc. VEGF concentration

14. When attempting to ensure multi-disciplinary adherence to clinical practice protocols, such as the OWL protocol, what is essential?

a. frequent fi ling of incident reports for non-adherenceb. salary incentives and pay for performancec. staff education and buy-in

15. It is imperative for nurses at the bedside to understand the evidence base supporting the practice of targeting oxygen saturation ranges lower than previously thought safe be-cause these preventive strategies can lead to which of the following?

a. improved outcomes for patients b. improved parent satisfaction surveysc. increased autonomy for nurses