Abnormal Development in the Retinal Vessels: Treatment

Prematum, retinopathy (PR) is one of the most important reasons for the development of the gum, treatment, and treatment of children, and the most important causes of childhood [1, 2]

Abnormal development in the retinal vessels seen in premature infants with prematurity, retinopathy, duodenal arthritis is a proliferative vitreoretinopathy. For the first time in 1942, the child doctor Theodore Terry described premature infants as anomalous retrolental fibroplasia. Patients were examined by the ophthalmologist Stewart Clifford and this clinical situation was defined as fibroplastic proliferation of the tunica vasculosa lentis.

The first PR epidemic was in the United States of America in 1950; Which is approximately 7000 babies in the humidity, the color is developed. The etiology is that it can be responsible for the development of diseases such as anemia, anoxia, hypercapnia, infection, exposure to electrolytes, insensitivity, hormone deficiency, iron deficiency, etc., which may be responsible for the development of illness ; tuuml r.

Initiated in 1986, prospective, randomized, center-based, cryotherapy for retinopathy of prematurity (CRYO-ROP) has been reported by the receiving group to include 40,999 newborn infants prematurely re- Useful information on retinopathy, gingivitis, retinopathy, and clinical prognosis has been obtained. One or two goumls have been reported as PRS of 65.8% in any case. [3]

Between 2000 and 2002, newborns with a birth weight of less than 1251 g have been included in this study, which is named as Early Treatment for Retinopathy of Prematurity (ETROP), in 92.7% of newborns receiving less than 750 grams , In 75.8% of newborns with doum arl 750-999 g, and in 43.7% of newborns with 1000-1250 g of doum arl. [4]

Prematurity is a retinopathic disorder characterized by early onset and treatment prognosis due to the fact that it is one of the most prevalent diseases in childhood and has a high incidence of respiratory disease. Appropriate treatment can be avoided if the patient is properly treated and properly treated with appropriate treatment. For this reason, the pathogenesis of the disease is known to be associated with risk factors and can be treated according to the clinical situation.

Pathogenesis

The retina of retinal vessels is retinas; Parts feed. Fotoreseptoumlins are in the form of eren d strata and choroid vessels are feeding. Fetal development is embryonic retina avasculature until the 16th week. This fluid is in the moisture and the blood of the segment and the lens is emitted by the hyaloid artery. The retinan vasculature was developed early in the morning, vasculature in the humidity, Douml is complete with angiogenesis in humid. Vaskuuml, logenezis is hypoxia-dependent, and VEGF, IL, and TNF are released, and at week 15 the balloons are completed at week 21. In vascular endothelium, hyaloid artery colony in the loganezis stage, the innermost primitive mesenchymal spindle huuml, creel endothelium, crelerine douml, nuuml, uuml, muuml; gerccedil; add. Vasculature progresses to angiogenesis during the gestational 18th week to the 40th week, while loganezis continues. This is followed by moisture in the retina of the plant, olive and deep capillary plexus formation. Peripheral capillaries have been in the formation stage. This is caused by the release of physiological hypoxic astrocytes and the release of VEGF from the mesenchymal humorous creams, along with tissue development in humans. However, physiologic stimulation of angiogenesis mediated factors such as serum albumin, angiopoietin, IGF-1, and vasculitic ligation of rats. IGF-I, VEGF Bam1 Endothelial Growth VEGF Induced; Clemic Mitogen Activated Protein Kinase Control; Proliferative balancing function.

The advanced gestation of the retinal blood vessels starts at the 15th week of the optic disc from the hyaloid artery to the peripheral nasal and temporal development. Gebeliin 32-36. Nazal or serrataya in the week, 40-42. At the weekend, the temporal area is serrataya. For this reason, retinal vasculature of the prematuum in the infants is not complete and the larynx has not been completed yet.

Blood saturation in the mother’s womb was 70% and partial oxygen pressure was 30-35 mmHg. If the blood saturation is 100% Pao2 in room conditions, it is 60-100 mmHg. Prematuem, re-born baby, this condition creates a recurrent hyperoxia. Retinal blood flow is less than that of choroidal blood. In the oxygenated retinas and other dietary needs, it is choroidal and nematic. In the past, the perfusion of the retinal blood flow and choroidal blood flow will be kept constant at a wide range. In prematum and newborns, retinal blood flow and choroidal blood flow are almost absent. In prematuum re-infants, in addition to mechanical ventilation therapy applied due to respiratory problems, high oxygen pressure, honey choroid and retinal blood flow are increased and autoregulation is impaired. This situation is caused by vasoobliteration. This doum is called moisture phase I. The proliferative phase of the hypoxia honey neovascularization secondary to vasooblitization is termed Phase II.

Phase I (hyperoxic phase): Prematum, retinopathy, balangccedil; It is a stage. Approximately 30-32. It takes place between weeks. VEGF, erythropoietin, and hypoxia inducible factor (HIF) release in hyperoxic media. Hyperoxia causes free oxygen radicals to increase thromboxane A2, platelet-activating factor (PAF) and lysophosphatidic acid (LPA). In addition, antioxidant effects such as steroid vitamin C, vitamin E, hemoxygenase-1, Cu-Zn, suumin, peroxide dismutase and glutadione peroxidase cause endothelial damage resulting in vasoobliteration and vasculitis resulting in apoptosis of endothelial cells. In the vasoconstriction and vasooblitization tissue, the hypotaxis comes to the fore.

Prematum, retinopathy is secondary to hypoxia, rumen, rumen, rumen; Oxygen induced indomitable vasospasm and suicide; VEGF is increased in the retina following hypoxia. Recurrent apnea, bronchopulmonary dysplasia, anemia, etc. are caused by retinal hypoxia. This increases secondary VEGF release. This artificial retina in VEGF rarely provides normal vascularity. It is often the case that unusual new veins start to develop. If the vascularity is normal, retinopathy relapses. Abnormal vascularization is progressive retinopathy. In PR, first phase VEGF or Placental stimulation; (PIGF-1), vasculature, endothelial bulb; (VEGFR-1) -specific ligand can be administered in small doses.

Phase II (Hypoxic Phase): It is the case that VEGF is re-vascularized with art. Hypoxia bam1 this phase 32-34. Week in balar. VEGF is a cytokine that secretes hypoxia bam, and vasculature is endothelial humin, creat mitogen. Although the role of VEGF and oxygen in the development of retinal blood vessels is important, biochemical mediators of pathogenesis have also been shown to be effective. Deg; nsuuml; lin similar to buuml; yuuml; me faktouml; ruuml; (IGF-1) plays a role as the most important moist mediator after VEGF. In mouse PR model, both phase I and phase II of IGF-1 have been shown to be effective. IGF-1 is a source of in vitro placenta and amnion sv and is fetal in pregnant mucinous phase and is nemlidic in males and gynecomastia. Gebeli’in uuml; uuml; uuml; ncuuml; In the trimester, the serum is taken from the infant’s liver only after the IGF-1 concentration is elevated to the blood level. Proliferation of IGF-1, which is required for stable proliferation of vascular endothelial growth factor (VEGF), is closely related to proliferation.

Prematurity Retinopathy Risk Factor

Prematurity is a risk factor for retinopathy, which is to be emphasized by research and research. CRYO-ROP is considered to be a risk factor for the development of children with premature rheumatoid arthritis, such as white rum, duodenal, duodenal, duodenal, gestational or oesophageal females [5 ]. (Vitamin E, magnesium, selenium, and baker’s), and the other side of the body, which is followed by an APGAR score, oxygen scavenger, metabolic acidosis, hypercarbia, RDS, blood transfuum, Serum iron, serum zinc, sepsis, methyl xanthine treatment, beta-blocker use, intraventricular hemorrhage, space renal insufficiency, necrotizing enterocolitis, chorioamnionitis, total parenteral nutrition, maternal hemorrhage-eclampsia risk factors , the outer flange. [6, 7]

Doum Haftas and Doum Arl: Gestational and inexperienced people are increasingly at risk for PR. In the CRYO-ROP group, 47% of infants between 1000-1250 g, more than 750 gr, 90% of newborn infants with arthritis, and premature rheumatoid arthritis were found to have retinopathy . The similar situation is that the gestational age in the village is too late. PR was detected in 83% of babies born 28 weeks earlier and 30% of newborn babies 31 weeks old. [5] Uuml is reported to have a PR incidence of 95% in infants who are prematurely born prematurely at 28 weeks of gestation.

Oxygen Impact: A significant risk factor for the development of PR; It is very common. Repeated oxygen changes can lead to anomalies in the retinal vessels. [1, 9] In addition, hypoxia and hypercarbia are accentuated in the sulcus, cerebral and retinal perfumed in the forehead, and in the lower respiratory tract, oxygen is administered at a lower concentration. Reduction in the risk of PR has been shown to increase the risk of development. [10] For this reason, the monitoum together with the doum must be connected to the riff, and the cocaine must be discharged from the oxygen and carbon dioxide waves.

Periventricu- lar ventilation (bleeding) (VH): Since retinas are histologically nasal in nature and have a circulatory system similar to that of the central nervous system, intraventricular hemorrhage may be effective on retinal vein development ; nuuml; lmektedir.uuml;

Vitamin water: allergens are present at weekly intervals in newborn infants; The incidence of PR of 10.000 IU intramu- mum, squamous, and vitamins was decreased. [11th]

Prematuum was detected as plasma in the reels and vitamin E was detected in the plasma as normal, and under the olive. The antioxidant effect is also taken into consideration, and the E vitamin therapy administered at varying doses has reduced serious development of PR. [12]

Transfu- sion: The blood used in blood-altered and transfu- sion-bound blood is more likely to flow into the tissues due to the presence of the hemoglobin-type of hemoglobin, which in turn promotes the development of PR by impairing the retinal vessels.

Ik Impact: You can see that the phototoxic activity of your qualities leads to the development of PR by generating free oxygen radicals.

Suuml; rfaktan Therapy: Suuml, rfan treatment is a significant increase in the proportion of babies with healthy, well-behaved babies. However, there has been an increase in the PR of treatment of rheumatoid arthritis.

Corticosteroid therapy: Prevention of doum- ing and steroid use in humid eyes has significantly reduced the severity of psychosis and severity. [14]

Genetics Factor rler: a genetically distinct risk factor; But the black rkta lesser gruml; ruuml; lduuml; uuml; It is bildirilmit. Prematurity re-retinopathy is different in different societies and has been associated with persistent genetic defects, such as rheumatoid arthritis and rheumatoid arthritis.

Erythropoietin (EPO): In the Newborn, EPO from the bovine, brekler in the liver of the liver affects retinal vein development independently of VEGF. During hypoxia, the secreted protein induced by salmon hypoxia stimulates the r-1 alpha (HIF-1 alpha) EPO release. In mouse experiments, administration of EPO in Phase 1 has protective effect whereas in Phase 2, administration of EPO causes neovascular lysis to increase.

Initial Inspection Timing

The PR examination schedule should be found in the postmenstrual period, in the case of the postmenstrual period. At the postmenstruel 31 th week in infants with gestational or 26 weeks’ Gestation was performed for 26 weeks, and for infants on the fourth week after birth.

The CRYO-ROP table has been created and the table next to it has been created

LK INSPIRATION TIME (WEEK)
GESTATIONAL YEAK (WEEK)	POSTMENSTRUEL YAZ	CHRONOLOGY
22	31	9
23	31	8
24	31	7
25	31	6
26	31	5
27	31	4
28	32	4
29	33	4
30	34	4

Prematum, retinopathicin Snflamas

Retinopathy of prematurity has been classified by the committee as “International Classification of Retinopathy of Prematurity – ICROP” by a committee of 11 ophthalmologists, who had extensive clinical experience with the disease in 1984. International Prematurity Retinopathy The clinical evaluation of Snflamas PR has been repeated in 1987 with the aim of providing standards. This includes classification criteria; Retinal neovascularization describes retinal papilla-centered localization of retinal space, amount of cervical vertebrae from retina to vitreous, stage of aggression, disease activation and progressive progression (plus disease).

yerleždeg; M

Zone1: Central optical disc, optical disc-2 times the distance from the center of the arc to the circular area on the earth to be rescued. On a fundoscopic examination, a 28 D lens can be placed in the temporal zone for 1 second by placing the lateral optic disk on the nasal mount.

Zone2: Central optic disc, where there is serrate, temporal ecovascular is the most circle.

Zone 3: The temporal area between the temporal equator and the oceanic horizon;

EVRE (stage)

Stage 1: Posterior vasculature of the retina and the posterior vasculature of the avasculature is demarcation extending between the retina (fine-white non-curved line).

Stage 2: Ridge (= rising edge = shunt): The demarcation line has become thicker and has become a rising edge. Occasionally, veins can enter the navel, causing the vessel to swell in the retracted cavity and burst into the muscle.

Stage 3: (Ridge + extraretinal (fibrovascular) proliferation of the vitreous): Stage 3 (Extraretinal Fibrovascularum Proliferation): Fibrovascularum extending from the edge to the vitreous is present. Retinal retinal detachment does not make me retinal detachment, but vitreous traction is present.

Stage 4 (Subtotal retinal detachment: a. Extrafoveal b. Foveal involvement)

Stage 4A (Extrafoveal retinal detachment): Percutaneous retinal detachment with tractional type with central cornea. The rear leg has spread, a prognosis is kouml;

Stage 4B (Foveal Retention Subtotal Retinal Detachment): With the involvement of the fovea, the prognosis of the rsel prognosis is worse;

Stage 5: Total tractional retinal detachment (funnel attachment): Dekolmann can be identified with the attached USG. It is named after the n-posterior bifilar, luuml, mucin, acclen, k-capal.

Funnel acclen

Funnel

Rear funnel accedil; k

Rear funnel tight

The decollete is accedil both at the front and back and the chest is followed by a concave donut. An optical disk extension is available. It is observed that both retina and retina are located immediately behind the lens of the retina. The less frequent is the rumulus, the rumen, the nuuml; One type is the type of the funnel and the other side is narrow in the back. The acceddes are narrow in the back, and the least in the rear is the lemur type.

SPREADING DERECESdeg;

Retinal involvement is expressed as a clock.

PLUS (ARTI) DISEASE: International Classification of ROP (ICROP) was first introduced in 1984. [15] Expresses ROP activation. Kouml; tuuml; Prognosis is the main gouml; Degree of enlargement and fullness in the veins of the eye, rigidity in the dilation of the pupils, mainly vitreous bulging in the posterior pole, tortuosity in the retinal artery (tortuosity) and enlargement of the veins. Sometimes resides are also found in the hand anterior tunica vasculosa lentis.

ARTI -NCESdeg; DISEASE (PRE-PLUS): In the posterior pole vessels, normal venous flow is increased and the arterial pressure is increased, but if these are present, the patient’s disease is insufficient.

ORP: Usually in the posterior pole, mostly in the Zon 1 and rarely in the Zon 2 posteriorda plus sickle. ‘Rush disease’ is the other name of this illness. Prematum does not follow the classic stages of retinopathy. If it is not treated, it can progress rapidly to stage 5.

TAKDEg;

ZON	EVRE	TAKdeg;P SIKLIžI
Zon 1	Evre 1 -2	1 haftadan daha ksa suuml;rede
Zon 2	Evre 1	2 hafta sonra kontrol
	Evre 2	1-2 hafta arasnda
Zone 3	Evre 1-2	2-3 hafta sonra

TEDAVdeg;

Follow-up and treatment protocol in retinopathy of prematurity; It has been proven that the patient is suffering from severe illness. The International Classification of Retinopathy of Prematurity (ICROP) group has created pre-threshold definitions in the definition of illness due to threshold and threshold.Eik hastalk

Zon 1/2

Plus+

Ardk 5 saat kadran/ardk olmayan 8 saat kadran Evre3

Eik ouml;ncesi hastalk

Tip 1 (yuuml;ksek riskli) ve Tip 2 (duuml;uuml;k riskli) olarak iki grupta snflandrr.

tip 1 eik ouml;ncesi hastalk ( yuuml;ksek riskli):

Zon 1	Plus+	Evre 1/2/3
Zon 1	Plus –	Evre2 /3
Zon2	Plus+	Evre2/3

tip 2 eik ouml;ncesi hastalk ( duuml;uuml;k riskli):

Zon 1	Plus –	Evre 1/2
Zone 2	Plus –	Evre3

Tip 1 PR Yuuml;ksek riskli	Tip 2 PR Duuml;uuml;k riskli
Periferik retina ablasyonu -ner	Bekle ve progresyonu takip et
ZON 1 (+) hastalk + Evre 1/2/3 Evre 3 hastalk, (+) yok	ZON 1 (+) hastalk yokken Evre 1/2
ZON 2 (+) hastalk ve Evre 2/3	ZON 2 (+) hastalk yokken Evre 3

Patients with Type 1 PR criteria are at high risk group and should be treated early and moist. Until the 1990s, cryotherapy was the only treatment you needed. However, the readings of cryotherapy are side effects, and it is known that retinal avasculature is passed to laser photocoagulation in field ablation. The CRYO-ROP was taken, the patient was ill, the patient was 72 hours old, the retina was avascularized, and the patient was ablated. [16] The ETROP group was later found to be more successful than the anatomic and emotional outcomes of early-age moisturizing treatments applied to people who suffered from illness. [17]

Guuml; nuuml; muuml; zde treatment youml; as a rule 3 youml; ntem.

1-Laser photocoagulation

2-Anti-VEGF treatment

3-Surgical treatment

LASER PHOTOCHOAGULATION: Vascular endothelial growth factor (VEGF) secretion from the retinal layer; The aim is to reduce the applied argon or diode laser ablation process. The standard treatment is youml; The anatomic and maternal success rate of the treatment in the age group and in the high-risk group of the elderly patients is increased by ETROP. [17]

The cryotherapy method is better than the regression of the laser therapy, the risk of the detachment is lower, the angle of the eye is better, the angle of the sharpness is higher and the side effect is more severe; And the gouml is in the foreground. [18-20]

Chemotherapy after laser treatment, vitreous hemorrhage, iris side, lens sunburn, cataract, posterior sinus can be seen. Laser photocoagulation is done at 3 o’clock and 9 o’clock in the morning. Feeds, uuml; nkuuml; Segmental ischemia can also occur with severe hypotony after laser photocoagulation to be applied to this area.

Anti-VEGF TREATMENT:

In the market, the anti-VEGF effect has been taken as an alternative treatment in PR treatment by administering intravitreal injection of Aflibercept (Eylea®), which is effective as steroid Bevacizumab (Avastin®), Ranibizumab (Lucentis®) and VEGF receptor agonist. Anti-VEGF is used in premature infants, and the Food and Drug Administration (FDA) and T.C. The Ministry of Health has not yet ratified it. However, the American Academy of Pediatrics requires doses, prophylactic and efficacious drugs, Bevacizumabn Plus + Zon I states that Stage 3 PR is in the disease state and can be detected. [21]

The possible application of intravenous treatment under local anesthesia is an advantage for laser therapy, although it is advantageous, mainly due to the narrowing effect of the laser on the area of ​​the laser in the presence of PR in Zon I or posterior Zon II; In the case of aggressive PR, it is possible to have a detailed corneal opacity of the retinas or to prevent laser ablation, vitreous haemorrhage, pupillary dilatation difficulty in the presence of tunica vasculosa lentis. [22]

The most important moisturizing factor for the use of anti-VEGF agents is the systemic circulation delay, the systemic VEGF level with melasma, and the side effects. These possible effects may include, but are not limited to, reduced doses of bevacizumab; It is necessary to obtain a very high number of phenomena; Can not be obtained. In this case, cataracts, endophthalmitis, vitreoretinal traction are the most important, damped readings are the side effects.

One thing to note in anti-VEGF administration is the presence of retinopathy, a fibrotic component of stage 3, May improve the vitreoretinal traction of the retinal detachment. [22]

cerrahdeg;

Finally, retinopathy has been reported in 85-90% of patients treated with anti-VEGF therapy or laser therapy. [23-25] However, treatment with 5-10% of patients with rheumatoid arthritis may progress to stage 4-5. At this time retinal detachment and preservation of the eye are required to treat scleral buckling or vitroretinal surgery procedures. The vitreous tissue is used to make retinal structures, which are called zuuml; In this case, you must be shaken. Surgical success in Stage 4b ​​and Stage 5, despite the successful outcome in Stage 4a, which does not retain the macula, is achieved.

sonuccedil ;:

Prematurity retinopathy has become an important public health problem, which has increased with the increase in quality of care services for newborn babies. PR is a clinical condition that has always been successful with anatomical and acquired outcome, with the correct diagnosis and timely treatment. Here, the pediatricians are most likely to eliminate the most important, moist, revive, first of all, the risk of developing PR, as well as of the baby, and then to make sure that the baby is properly examined. Especially when oxygen therapy is needed, the partial oxygen pressure should be adjusted to a balanced level. It should be kept in mind that babies can sometimes be misdiagnosed, and this situation should be questioned with caution in infants born to the lower gestational age for at least 27 weeks.

KAYNAKCcedil;A

1.Chow LC, Wright KW, Sola A: Can changes in clinical practice decrease the incidence of severe retinopathy of prematurity in very low birth weight infants? Pediatrics 2003, 111(2):339-345.

2.Kocur I, Resnikoff S: Visual impairment and blindness in Europe and their prevention. British Journal of Ophthalmology 2002, 86(7):716-722.

3.Garner A: An international classification of retinopathy of prematurity. Archives of ophthalmology 1984, 102(8):1130-1134.

4.Group ETfRoPC: The incidence and course of retinopathy of prematurity: findings from the early treatment for retinopathy of prematurity study. Pediatrics 2005, 116(1):15-23.

5.Group CfRoPC: Multicenter trial of cryotherapy for retinopathy of prematurity: preliminary results. Pediatrics 1988, 81(5):697-706.

6.Clyman R, Heymann M: Pharmacology of the ductus arteriosus. Pediatric Clinics of North America 1981, 28(1):77.

7.Yanovitch TL, Siatkowski RM, McCaffree M, Corff KE: Retinopathy of prematurity in infants with birth weight≥ 1250 grams-incidence, severity, and screening guideline cost-analysis. Journal of American Association for Pediatric Ophthalmology and Strabismus 2006, 10(2):128-134.

8.žahin A, žahin M, Tuuml;rkcuuml; FM, Cinguuml; AK, Yuuml;ksel H, Ccedil;nar Y, Ar ž, Ccedil;accedil;a deg;: Incidence of retinopathy of prematurity in extremely premature infants. ISRN pediatrics 2014, 2014.

9.VanderVeen DK, Mansfield TA, Eichenwald EC: Lower oxygen saturation alarm limits decrease the severity of retinopathy of prematurity. Journal of American Association for Pediatric Ophthalmology and Strabismus 2006, 10(5):445-448.

10.Shohat M, Reisner SH, Krikler R, Nissenkorn I, Yassur Y, Ben-Sira I: Retinopathy of prematurity: incidence and risk factors. Pediatrics 1983, 72(2):159-163.

11.Lin H-J, Lin C-C, Tsai S-W, Lin H-C, Su B-H: Risk factors for retinopathy of prematurity in very low birth-weight infants. Journal of the Chinese Medical Association: JCMA 2003, 66(11):662-668.

12.Ambalavanan N, Wu T-J, Tyson JE, Kennedy KA, Roane C, Carlo WA: A comparison of three vitamin A dosing regimens in extremely-low-birth-weight infants. The Journal of pediatrics 2003, 142(6):656-661.

13.Finer N, Grant G, Schindler R, Hill G, Peters K: Effect of intramuscular vitamin E on frequency and severity of retrolental fibroplasia: a controlled trial. The Lancet 1982, 319(8281):1087-1091.

14.Higgins RD, Mendelsohn AL, DeFeo MJ, Ucsel R, Hendricks-Munoz KD: Antenatal dexamethasone and decreased severity of retinopathy of prematurity. Archives of Ophthalmology 1998, 116(5):601-605.

15.An international classification of retinopathy of prematurity. The Committee for the Classification of Retinopathy of Prematurity. Archives of ophthalmology 1984, 102(8):1130-1134.

16.Good WV, Hardy RJ: The multicenter study of Early Treatment for Retinopathy of Prematurity (ETROP). Ophthalmology 2001, 108(6):1013-1014.

17.Group ETfRoPC: Revised indications for the treatment of retinopathy of prematurity: Results of the early treatment for retinopathy of prematurity randomized trial. Archives of ophthalmology (Chicago, Ill: 1960) 2003, 121(12):1684-1694.

18.Paysse EA, Lindsey JL, Coats DK, Contant CF, Steinkuller PG: Therapeutic outcomes of cryotherapy versus transpupillary diode laser photocoagulation for threshold retinopathy of prematurity. Journal of American Association for Pediatric Ophthalmology and Strabismus 1999, 3(4):234-240.

19.White JE, Repka MX: Randomized comparison of diode laser photocoagulation versus cryotherapy for threshold retinopathy of prematurity: 3-year outcome. Journal of pediatric ophthalmology and strabismus 1997, 34(2):83-87.

20.McGregor M, Wherley A, Fellows R, Bremer D, Rogers G, Letson A: A comparison of cryotherapy versus diode laser retinopexy in 100 consecutive infants treated for threshold retinopathy of prematurity. Journal of American Association for Pediatric Ophthalmology and Strabismus 1998, 2(6):360-364.

21.Pediatrics SoOAAo: American Academy of Ophthalmology; American Association for Pediatric Ophthalmology and Strabismus. Screening examination of premature infants for retinopathy of prematurity. Pediatrics 2006, 117(2):572-576.

22.žahin A, žahin M, Cinguuml; AK, Ccedil;nar Y, Tuuml;rkcuuml; FM, Yuuml;ksel H, Kaya S, Ar ž, Ccedil;accedil;a deg;: Intravitreal bevacizumab monotherapy for retinopathy of prematurity. Pediatrics International 2013, 55(5):599-603.

23.Coats DK, Miller AM, McCreery KMB, Holz ER, Paysse EA: Involution of threshold retinopathy of prematurity after diode laser photocoagulation. Ophthalmology 2004, 111(10):1894-1898.

24.Mintz-Hittner HA, Kennedy KA, Chuang AZ: Efficacy of intravitreal bevacizumab for stage 3+ retinopathy of prematurity. New England Journal of Medicine 2011, 364(7):603-615.

25.McNamara JA, Tasman W, Vander JF, Brown GC: Diode laser photocoagulation for retinopathy of prematurity: preliminary results. Archives of Ophthalmology 1992, 110(12):1714-1716.