Optic pit was described by Wiethe in 1882 and is a rare congenital anomaly. Optic pit is thought to be due to incomplete closure of the optic fissure. It is often located in the inferotemporal region of the optic disc. It is often asymptomatic and does not reduce vision. This anomaly, seen once in 11,000, can be bilateral with a 15% rate. This anomaly, which is often asymptomatic, causes maculopathy clinics such as macular edema, schisis in the outer retinal layers, outer lamellar hole, serous macular detachment, and causes symptoms such as decreased visual acuity and central scotoma (32) (Picture 21).
Optic pitin. It is thought to develop as a result of incomplete closure of the optic fissure during embryonal development. There is also retinal nerve fiber loss in the pit area. Although the pathophysiology of optic pit maculopathy (OPM) is not yet fully understood, many hypotheses have been put forward. One of these is Brown et al. It is the assumption put forward by et al. that subretinal fluid originates from the vitreous cavity. Another hypothesis proposed that subretinal fluid originates from cerebrospinal fluid via the subarachnoid space. Studies conducted with OCT have shown that there is a direct relationship between the subarachnoid space and the subretinal space. There are also hypotheses that suggest that subretinal fluid originates from some leaky vessels or from the orbital space (33).
Treatment:
Similar treatment is generally available for maculopathies that develop due to optic pit or coloboma. strategies are implemented. There is no single accepted method and all applied treatments are controversial. The treatment methods to be described are those applied to both the optic pit and the optic coloboma.
Firstly, the conservative observation approach is recommended by many centers (34). Considering the statistic that 25% of developing maculopathies can resolve spontaneously, 3 months of observation without treatment is appropriate at the first application. However, the final visual acuity is lower in cases of serous macular detachment that resolves spontaneously (35).
In 1969, Gass applied Xenon laser photocoagulation to the temporal edge of the optic disc, creating chorioretinal adhesion at the temporal edge of the optic disc and spreading it from the pit area to the subretinal. He put forward the idea of ​​preventing fluid passage, but could not obtain satisfactory results in his applications (36). For many years, Argon laser photocoagulation has been applied as the first treatment in patients with optic pit/coloboma-related maculopathy that has not improved after 3 months of follow-up.
Intravitreal gas administration with or without argon laser photocoagulation is also one of the treatment methods applied. Lincoff et al. suggested that submacular fluid displacement could be achieved with intravitreal gas tamponade and an increase in visual acuity could be achieved (37).
In recent years, the most commonly used method in the treatment of maculopathy due to optic pit is parsmayan vitrectomy (PPV). It is thought that success in PPV is achieved by removing the vitreous and eliminating the traction forces on the optic pit, thereby reducing passive fluid passage under the macula. The main purpose of PPV is to remove the posterior hyaloid. Some surgeons also perform internal limiting membrane peeling (ILMP) to confirm this. It is necessary to be patient in the post-operative period for the subretinal fluid to drain, as it may take months for the fluid to drain. Various studies have also been carried out to prevent direct fluid passage from the optic pit. Rosenthal et al. They aimed to induce the functioning of coagulation factors by injecting autologous platelets onto the optic pit, thereby closing the passageways of cerebrospinal fluid from the optic pit. Although they achieved anatomical and functional success in their published case report, their long-term results are not yet known (41).
Travassos et al. They tried to close the optic pit by placing approximately 0.5 mm3 scleral tissue taken from the lower nasal quadrant into the optic pit mouth. At the end of PPV, submacular fluid was drained, the optic pit mouth was closed with scleral tissue, and gas tamponade was administered.
Another method proposed to close the optical pit area is to peel off the ILM, turn it into a flap around the OSB without removing it from its place, and turn it over the OSB and close it on the pit. In this technique, the ILM flaps created around the OSB after standard PPV are inverted and closed on the pit (inverted flap technique). In this way, the connection between the subarachnoid space and the subretinal space is prevented. It is planned to be removed.
Another occlusive material is autologous fibrin glue. Autologous fibrin glue can be prepared with special devices in blood banks. 5 ml of autologous fibrin glue can be prepared with approximately 120 ml of blood taken from the patient into a tube with citrate added. Since fibrin glue should not wait in the external environment, it is prepared from the blood taken on the day of the operation and used immediately after the operation. The reaction is accelerated by using a coactivator (pH10 buffer solution) together with autologous fibrin glue (44).
This method is a technique that was used in our clinic and was described for the first time in the world and introduced to the literature (45). We use this technique in cases of persistent macular detachment that recurs despite vitrectomy. In these cases, after liquid-air exchange, first a drop of fibrin and then a drop of coactivator are dripped onto the optic nerve head (ONB), and fibrin formation is observed within seconds. Generally, excess fibrin that extends beyond the OSB is peeled off after the air-liquid exchange and only the part on the OSB is left. Afterwards, the surgery is completed with liquid air exchange. Fibrin material can also be clearly seen in postoperative OSB OCT sections.
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