Treatment of retinopathy of prematurity
Release time : 06/07/2025 09:30:01
Retinopathy of prematurity is a disease caused by the abnormal proliferation of baby's retinal blood vessels and is related to factors such as receiving oxygen therapy.
The key to treatment is early detection, seizing the optimal period for treatment, which lasts about one month. This period is referred to in medical terms as the "window of opportunity."
The key to the early treatment of retinopathy of preterm infants is early detection. Medical personnel from obstetrics and gynecology, neonatology, ophthalmology, and other departments should pay great attention to this issue and work closely together. Additionally, it is necessary to establish a comprehensive eye examination system for preterm infants.
If the iris anterior and posterior adhesion has been formed, and is relatively extensive, then anti-glaucoma surgery may be considered.
ROP is not invariably progressing from Stage I to Stage V; the majority of lesions will regress without further progression once they reach a certain stage, and only about 10% of cases experience complete retinal detachment. Therefore, for lesions in Stages I and II, observation is sufficient and treatment is not necessary; however, if the lesion reaches a threshold stage, it must be treated immediately. Thus, early detection and timely treatment of threshold ROP are the principles of this disease. Currently, surgical treatment remains the primary method, with recent years also seeing the development of some pharmacological treatments targeting its potential pathogenesis.
1. Surgical Treatment (1) Cryotherapy: Continuous cryotherapy on the retinal periphery of the non-vascular area around the threshold ROP can prevent 50% of cases from developing severe consequences such as macular folds, posterior pole retinal detachment, and lens posterior fibrosis that significantly affect vision. Cryotherapy is typically performed under local anesthesia, but it can also be conducted under general anesthesia. General anesthesia may lead to bradycardia, apnea, and cyanosis. Complications associated with cryotherapy include corneal edema, hemorrhage, tearing, vitreous hemorrhage, central retinal artery occlusion, and retinal hemorrhage. Currently, the short-term efficacy of ROP cryotherapy has been confirmed, but its long-term effectiveness remains to be further determined.
(2) Laser photocoagulation therapy: In recent years, with the advent of indirect ophthalmoscope laser output devices, early use of ROP in photocoagulation therapy has achieved good results. Compared with cryotherapy, photocoagulation has a better effect on ROP in zone I, similar effect on zone II lesions, and is more precise. It can reduce vitreous hemorrhage, postoperative bulbar conjunctival edema and intraocular inflammation. At present, it is believed that photocoagulation is the first choice for threshold ROP. Most foreign countries advocate diode laser treatment. Diode laser is red or infrared light, has strong penetration, is not easily absorbed by refractive matrix, and has few complications. Some authors also tried to use transscleral 810nm laser instead of freezing, and the complications were significantly reduced.
(3) Scleral cerclage: If the threshold ROP is not controlled and develops to stage IV or stage V ROP where the fundus can still be clearly seen, scleral cerclage may achieve good results. Scleral cerclage for the treatment of ROP is to relieve retinal traction, promote subretinal fluid absorption and retinal reattachment, and prevent the disease from progressing to stage V. However, some scholars believe that some children can heal themselves without surgery.
(4) Vitrectomy: Patients with failed scleral cerclage and stage V can only undergo complex vitrectomy. The best surgical effect is that the retinal detachment is wide funnel shape, about 40% of the retina can be reattached, and the narrow funnel shape is the worst., only 20%. After vitrectomy, the retina is partially or completely anatomically restored, but the final recovery of the child's visual function is extremely limited, and useful vision is rarely restored.
2. Medical treatment (1) Oxygen supplementation treatment for pre-threshold ROP: Because oxygen therapy can induce the occurrence of ROP, it was once forbidden to give oxygen to premature infants for a period of time, but this is not the fundamental solution, and it also increases the mortality rate of premature infants. With the establishment of the role of vascular growth factors in the formation of ROP, it has been found that hypoxia can induce the synthesis of vascular growth factors. Oxygen supplementation therapy is proposed to inhibit the growth of new blood vessels and inhibit the occurrence and development of ROP, but further research is needed.
(2) Neovascular inhibitors: Still under development and animal testing.
Symptoms of retinopathy of prematurity are common in 3 to 6 weeks after birth and are clinically divided into active period and fibrous membrane formation period.
1. The active period is divided into five stages: (1) Vascular change stage: seen in the early stages of the disease.
The arteries and veins are tortuous and dilated.
The diameter of the vein is sometimes 3 to 4 times larger than the normal diameter.
Brush-like capillaries can be seen at the peripheral blood vessel terminals of the retina.
(2) Retinopathy stage: The lesion develops further, the vitreous body becomes turbid, and the fundus becomes hazy than before.
The number of new blood vessels in the retina increases, most of which are located near the equator, and can also be seen in front of or behind the equator. The retina in this area is obviously elevated, and there are blood vessels crawling on its surface, often accompanied by retinal hemorrhage of varying sizes.
(3) Early proliferative stage: At the above-mentioned localized optic disc elevation, there appears proliferating vascular bands that extend into the vitreous cavity. This condition leads to a peripheral (most cases) or posterior pole (rare cases) retinal small-area detachment.
(4) Moderate proliferative phase: The separation area extends to more than half of the retina.
(5) Excessively proliferative stage: Retinal detachment.
At times, a large amount of blood can also be seen inside the glass chamber.
The disease is in an active phase, with a disease course of 3 to 5 months.
Not all cases undergo these five stages. About 1/3 of the cases stop in stage one, 1/4 in stage two, and the rest stop in stage three, four or five before fibrous encapsulation occurs.
2. During the fibrotic phase, cases that cannot regress spontaneously during an active period eventually develop a fibrous membrane. Depending on the severity, it is classified from mild to severe, ranging from 1 to 5 degrees.
Ⅰdegree: The retinal blood vessels are narrow, the peripheral part of the retina appears grayish-white and turbid with small irregularly shaped pigment spots, and there is a small piece of turbidity in the vitreous body. This often accompanies myopia.
II. Organizing edema of the peripheral fundus with traction on the disc and retinal vessels towards one side, a pigmentary ring at the edge of the opposite disc, and pallor of the disc.
IIIrd degree: Fibrosis and fibrous membranes pull the retina, forming one or several folds.
Each wrinkle is connected to the peripheral membrane-like neoplastic nodules of the retina.
The wrinkles are located on the temporal side at 905 and on the nasal side at 105.
Those located on the lateral sides of the temporal region are quite rare.
Retinal blood vessels do not distribute along this fold, unlike congenital retinal folds.
Degree IV: The fibrous membrane or part of the retina that is separated from the organization is visible behind the lens, and the pupil collar is obscured.
Upon examination with the spectacle shield, the fundus' red light reflex is visible.
Degree V: Behind the lens, the entire body is covered by the fibrous membrane or the detached organized retina.
During mydriasis examination, a serrated elongated ciliary process was seen around the periphery of the pupil.
The anterior chamber is very shallow and often has anterior and posterior synechia.
It may also be caused by secondary glaucoma or extensive anterior stromal opacity resulting in corneal opacification and a smaller, sunken eyeball.
The etiology of retinopathy of prematurity is still unclear, with risk factors including low birth weight, premature birth, and oxygen therapy.
1. Primary reasons for prematurity and low birth weight: The retina does not mature properly, with a line of gray-white blood vessels that cannot be crossed, blocking the normal growth of blood vessels.
The incidence of ROP is higher and the severity of the condition is greater with lower birth weight and smaller gestational age.
2. Oxygen therapy currently has two prevailing explanations for its effects: (1) the longer the duration of oxygen therapy, the higher the inhaled oxygen concentration, and the higher the arterial blood oxygen partial pressure, leading to an increased risk of Respiratory Organ Protection (ROP) and a more severe condition.
The incidence of ROP is higher in patients using CPAP or mechanical ventilation than in those using nasal cannula.
Patients generally have an excessive oxygen exposure history in the neonatal intensive care unit.
(2) After the concentration oxygenation, it stops quickly to make the tissue relative hypoxia and then promotes ROP. It has nothing to do with the length of oxygenation time.
The fluctuation of arterial blood oxygen partial pressure plays a significant role in the progression of ROP.
3. Other causes include hypoxia, acidosis (pH < 7.25), anemia, transfusion, hyperbilirubinemia, hypernatremia, hypoglycemia, low body temperature (< 35.6°C), patent ductus arteriosus, intraventricular hemorrhage, sepsis, exposure to light, and the use of xanthine drugs.
(2) Beta-blockers: These drugs cross the placental barrier and enter the fetus, increasing vascular tension in the retinal capillaries, promoting the development of Retinopathy of Prematurity (ROP).
(3) Blood Carbon Dioxide Partial Pressure (PaCO2): A low PaCO2 can lead to retinal vascular constriction, resulting in retinal ischemia and ultimately leading to ROP.
Maternal anemia and polyhydramnios.
(5) Race: Whites have a high incidence and severe illness.
How to prevent retinopathy of prematurity? Strict restrictions on oxygen use for early children are the only effective preventive measure. Unless life-threatening due to cyanosis, oxygen at a concentration of 40% can be given, and the time should not be too long.
In addition, early application of large doses of vitamins may also have a certain preventive effect. Early detection and timely application of condensation or laser photocoagulation have been successfully reported to prevent further deterioration of lesions.
In addition, in order to prevent the occurrence of secondary glaucoma after retinopathy of prematurity, in severe cases of active period, mydriasis must be frequently performed to avoid posterior synechia of the iris.
In short, the complications of retinopathy must also be paid attention to and actively prevent and treat them.
What is the best diet for preterm infants with retinopathy of prematurity? What special dietary requirements does retinopathy of prematurity have, and what should be avoided? Additionally, what does a correct diet do for the condition? What foods are beneficial for preterm infants with retinopathy of prematurity? These are the aspects that everyone needs to pay attention to. 1. * * Food rich in antioxidants**: Some studies have shown that vitamin C and E, as well as beta-carotene, can help protect the retina from oxidative damage. Therefore, it is recommended to increase the intake of these foods, such as citrus fruits, leafy green vegetables, nuts, and seeds. 2. * Vitamin A-rich foods**: Vitamin An is essential for the health of the retina. Carrots, sweet potatoes, spinach, and egg yolks are all good sources. 3. * Omega-3 fatty acids**: Omega-3 fatty acids are very important for the health of the eyes, especially in preventing or slowing down the development of retinopathy. Foods rich in omega-3 fatty acids include fish oil, flaxseeds, and walnuts. 4. * High-fiber foods**: High-fiber foods help maintain gut health, which may indirectly support retinal health. Whole grains, legumes, vegetables, and fruits are good choices. 5. * Limit sugar and processed foods**: Too much sugar and processed food can lead to weight gain and fluctuations in blood sugar levels, which can affect retinal health. Avoid candy, cakes, sugary drinks, etc. 6. * Sufficient hydration**: Ensure that the child drinks enough water daily to keep their eyes moist. 7. * Avoid allergies**: Some foods may cause allergy reactions, leading to discomfort in the eyes. If a certain food has caused problems, avoid eating it. 8. * Regular check-ups**: Work with a doctor to regularly undergo ophthalmic examinations to promptly detect and address any potential issues. In summary, the diet for preterm infants with retinopathy of prematurity should focus on nutritional balance and diversity, while avoiding allergies and excessive sugar. Close cooperation with a doctor is crucial, based on the child's specific situation, to develop an appropriate dietary plan.
I. Feeding: 1. Advocate for early feeding. For those with low body weight or generally poor condition, such as those who have experienced cyanosis, difficulty breathing, or have undergone a cesarean delivery, delayed feeding and intravenous fluid supplementation may be appropriate.
Actions: Shorten the time required for physiological weight loss, or reduce the degree of weight loss, decrease the incidence of hypoglycemia, and relative reduction in serum bilirubin concentration.
Generally, the infant begins to drink sugar water from 6 to 12 hours after birth and starts to feed milk from 24 hours.
2. Breastfeeding Method: For infants with a heavier birth weight and good sucking reflex, breastfeed directly; otherwise, use a syringe or gastric tube for feeding.
3. Maximum Intake: For the first 10 days of life, the volume of breast milk per day (ml) = (the actual number of days since birth + 10) × grams of weight per 100 milliliters.
After 10 days of birth: The daily breastfeeding amount (ml) = 1/5 - 1/4 of the weight (g), premature infants can not finish all, the remaining part can be supplemented by intravenous infusion.
4. Feeding Frequency: For infants weighing less than 1,000 grams, feed every hour.
Weight 100 to 1500 grams: feed once every 1.5 hours.
Weight 150 to 2000g: feed once every 2 hours.
Weight between 2001 to 2500 g, every three hours.
II. Nutritional Needs: 1. Calories: Each kilogram of body weight requires 110-150 kcal daily.
Supply should start at a slightly lower level and gradually increase as appropriate.
2. Amino acids: Premature infants lack relevant converting enzymes and cannot convert methionine into cystine and phenylalanine into tyrosine. Therefore, cystine and tyrosine become essential amino acids and must be ingested from food.
3. Protein: Premature infants consume higher protein than normal infants.
4. Vitamins: Premature infants lack vitamin E and are prone to hemolytic anemia.
Premature infants have a lower absorption rate of fat than mature infants and may lack fat-soluble vitamins and other nutrients.
5. Inorganic salts: More than mature children need.
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