If there is a strong inhusion between the retina and the vitreous, the posterior vitreous detachment can cause a traction on the retina.
If the retina itself is fragile at the particular point this can lead to a retinal tear, which will allow the intraoccular fluids to go through and detach the retina.
A retinal artery occlusion occurs when the central retinal artery or one of the arteries that branch off of it becomes blocked. This blockage is typically caused by a tiny embolus (clot) in the blood stream. The occlusion decreases the oxygen supply to the area of the retina nourished by the affected artery, causing permanent vision loss.
Retinitis pigmentosa is a rare inherited disease which affects the photoreceptors of the retina. These cells (rods and cones) absorb the light energy and transmit the signal to other retinal cells, until the signal reaches special parts of the brain.
This disease affects mostly one type of photoreceptors, which are called rods and are activated at night and at mesopic conditions (low light conditions). Some gene's mutation leads to gradual death of the photosensitive cells and thereby cause loss of the peripheral visual field initially and later on loss of central vision also.
We can distinguish retinitis pigmentosa in two subcategories:
• Type 1: Night blindness early (children at the age of 10), due to rods cells loss and as a result, it leads to peripheral vision loss.
• Type 2: Night blindness appears at the adulthood and is characterized by loss of rods as well as cones sensitivity.
Retinitis Pigmentosa symptoms
At initial stages, retinitis pigmentosa causes nyctalopia (also called night blindness), which is represented as difficulty in low light conditions, since early age. A common symptom is the loss of the peripheral vision, due to destruction of retinal rods. Rods are located mostly in the peripheral retina, so there is a narrowing of the visual fiend. The patients describe this condition as seeing through a tube.
Later, the disease may affect also the other type of photoreceptors, which are called cones. These cells are located mostly in the central retina, in the macula lutea and are responsible for central and color vision. In most cases, patients retain for a long time adequate central vision. However, there is always a big risk of the cones destruction, resulting in reduction of visual acuity.
Retinitis Pigmentosa prevalence in population
The prevalence of the disease in the general population is very rare. In particular, it is reported that there is 1 patient for each 3000 or 4000 persons. The severity of the disease depends on how is inherited to the patient. It can be inherited by autosomal dominant, recessive, as well as X-linked. In case of recessive inheritance the disease progress is faster and the prognosis worse.
Retinitis Pigmentosa Treatment
Unfortunately, retinitis pigmentosa cannot be compensated with glass prescription or contact lenses. There is no certain management of restoring visual field. However, the recognition of genes and their mutations, which lead to the disease gives us hope that retinitis pigmentosa can soon be coped with effectiveness. Nevertheless, there are some studies which show that the disease progression can be slowed down by takin high doses of vitamin A in combination with omega-3 fatty acids. In addition, patients can be benefit from taking a large amount of oxygen to reduce the phenomenon of hypoxia (lower amounts of oxygen) that the disease provokes.
In any case, the optometrist and ophthalmologist should be very precise on the appropriate prescription of any refractive condition the patient may have and give ergonomic advice on how using the appropriate light conditions. Moreover, low vision aids can help patients with tunnel vision.
Surgically, there are many cases in which retinitis pigmentosa has been associated with cataract. Thus, the removal of the dense crystalline lens can improve the low vision that the patient have. The surgeon should be very careful to avoid the appearance of cystoid macular edema which may happen postoperatively.
Retinopathy of prematurity is an acquired abnormality which appears on premature infants (cases that gestation is less than 35 weeks) weighing below 1500gr at birth. In general, when the birth weight is less than 2500gr the infant is at risk of developing retinopathy of prematurity.
In high weight premature (birth weight greater than 1500gr) and more than 32 weeks of gestation the disease’s incidence is rare. The lower the birth weight, the higher risk for this type of retinopathy according to ophthalmologists.
Nowadays, advances and progress at neonatology are very high, both in terms of medical knowledge, but also in terms of equipment as well. Thus, newborns who have premature birth weight of 600gr or 700gr can survive. However, the risk of developing retinopathy of prematurity is greater. Apart from weight and duration of pregnancy, there are also other factors, which play an important role in the appearance of the disease.
The main factor is the oxygen supply. The premature infants are placed in an incubator because they have an immediate need of oxygen to survive. The oxygen supply in these cases avoids any brain damage.
On the other hand, oxygen supply may increase the risk of retinopathy of prematurity. Thus, the main issue is to maintain the oxygen in adequate levels for the infant’s survival, as far as possible without affecting their eyes. Studies have shown that if the pressure of the arterial oxygen is always at 90mmHg or higher, then we may notice contraction of retinal blood vessels, especially those in the region, in which they are not well developed yet, due to prematurity.
The development of technology as well as doctors and nurses’ knowledge and education, in both public and private hospitals in Greece, may achieve a balance that ensures the survival of very low weight premature to have least disturbance in their eyes.
Moreover, the administration of cortisone by the obstetrician in case of imminent birth and the administration of a relatively new drug (surfactant factor) by the neonatologists to premature infants who have respiratory problems in the first days of their life, help to improve their lung function. As a result, this is a way to limit the duration and the level of the administered oxygen, so that we can avoid the disease’s development.
Retinopathy of prematurity predisposing factors
- High levels of oxygen supply at incubators
- Intracranial hemorrhage
Retinopathy of prematurity diagnosis & treatment
Retinopathy of prematurity is characterized by abnormal development of blood vessels (neovascularization) and fibrous tissue in the retina (photosensitive tissue where the image is depicted and the signal is transferred to the brain). These conditions may lead to retinal detachment and blindness.
At initial stages ophthalmologists observe the condition without interfering, because in many cases the disease is self-treated. If the disease does not regress, we can administer vitamin E intramuscularly, although it is not generally accepted that helps to inhibit the disease’s progression.
In advanced stages of the disease the ophthalmologist may diagnose tractions that may appear at eye’s fundus. At this stage there is a high risk of retinal detachment. The ophthalmologist can then intervene surgically or by laser (photocoagulation) or cryotherapy. Each of the surgical treatments has both advantages and disadvantages, so the doctor has to decide which therapy is more appropriate in each case. In general photocoagulation is more preferable because of fewer complications.
Overall we can understand how necessary is the presence and examination of an ophthalmologist in a premature infant in order to prevent serious problems. We have to notice that premature infants have to be examined also after leaving the hospital, even if they don’t have serious ophthalmological problems, because in these cases the risk of strabismus or some refractive errors (such as myopia) is higher, in comparison with full-term children.
Central serous maculopathy is a common condition that affects the central part of the retina, called the macula lutea. The etiology of the disease remains unknown, although we know that it appears after a small tear on the retinal pigment epithelium (RPE), which is a pigmented layer full of melanin, where the retinal photoreceptors are lying on.
What is the vitreous body?
Vitreous body is a gel located in the posterior part of the eye, in the space between the crystalline lens (which is removed in cataract surgery) and the retina (the inner layer in which the image is focused and is transferred to the brain).
The space between the crystalline lens of the eye and the retina is filled with a transparent, dense material, which is called vitreous.
In a newborn baby, the vitreous is compact and firm, like jelly and it is fixedly attached to the retina. However, as someone grows older the vitreous becomes less firm, fluidizes and may be detached from the back of the eye. This phenomenon is called vitreous detachment. It is a very common and usually harmless condition.