Ординатура / Офтальмология / Английские материалы / Retinal and Vitreoretinal Diseases and Surgery_Boyd, Cortez, Sabates_2010

anatomic location, and may be damaged when attempting to create a surgical access. The other risk, even if there is a quadrant or quadrants without SCH, is to damage the retina contralateral to the sclerotomy if the SCH is very large.

It is not uncommon when creating a pars plana access, that the SCH starts draining through this sclerotomy, even if it is this anterior. In cases where blood (and not vitreous) comes out of the wound, it is usually difficult to insert the cannula in the vitreous cavity, adding the risk of suprachoroidal infusion of BSS, which will make the problem even worse. To overcome this problem, a light pipe may be used (an endolight probe coupled with infusion).

Once the vitreous cavity is pressurized, either by an anterior chamber or pars plana infusion, the pressure forces the SCH out through the posterior sclerotomy. It is sometimes necessary to depress one lip of the wound to facilitate the egress of blood, and sometimes of tiny blood clots. The drainage should be continued as much as possible, until no more blood is observed to come out of the sclerotomy. At this time it is important to examine the fundus with indirect ophthalmoscopy, to assess the size of the remaining hemorrhage. If a substantial hemorrhage remains, it is advisable to create a new drainage sclerotomy or sclerotomies, until most of the hemorrhage has been drained. It is important to note that most of the times a complete drainage cannot be achieved, and small “islands” of suprachoroidal blood remain, that later will reabsorb spontaneously in the matter of weeks.

Once the suprachoroidal blood has been drained, a standard three-port pars plana vitrectomy procedure can be performed in order to address the rest of the vitreoretinal pathology. Depending on the surgical findings, other procedures such as endophotocoagulation,endodiathermy,theuseofperfluorocarbon liquids, removal of intraocular foreign body, retinotomy, retinectomy, air/fluid exchange, and/or internal tamponade with gas or silicone may be needed.(68)

It is important to note that when silicone oil is used as tamponade, most of the times there will be a remaining inferior fluid meniscus after a few weeks in the postoperative period, even though the silicone fill in the immediate postoperative period is complete. The explanation for this is, as mentioned above, that after SCH drainage there is always remaining blood in the suprachoroidal space, that will reabsorb during the following weeks, leaving room in the vitreous cavity for the fluid meniscus.

Prognosis

Despite modern vitreoretinal surgical techniques, visual outcomes of eyes with traumatic SCH are modest at best. It is difficult to assess the prognosis of traumatic SCH since most publications group it with intraoperative and postoperative SCH. Reynolds et al reported 106 patients with SCH, out of which 35 were due to trauma. Factors for bad prognosis included the presence of retinal detachment and SCH affecting the four quadrants. Thirty four percent of the patients undergoing a surgical procedure

achieved visual acuity of 20/200 or better.(57) Wirostko et al reported a study on 48 eyes with SCH, 16 of which were secondary to trauma. They classified SCH in four categories: 1) Non-appositional choroidal hemorrhage without vitreous or retinal incarceration; 2) Centrally appositional choroidal hemorrhage without vitreous or retinal incarceration; 3) SCH with associated vitreous incarceration in the wound, and 4) SCH with retinal incarceration in the wound. They found a higher probability of no light perception vision, persistent hypotony and irreparable retinal detachment with increasing SCH complexity, especially when retinal incarceration was present.(69) Other authors have published results about non-traumatic SCH, finding that predictors of poor final visual acuity were vitreous incarceration in the wound, retinal detachment, afferent pupillary defect, longer duration of apposition, and extension of the SCH to the posterior pole.(65,66,67,70,71,72)

Conclusion

The presence of either traumatic subretinal hemorrhage or suprachoroidal hemorrhage means that severe damage has been done to the eye. Even with modern management and vitreoretinal surgical techniques at our disposal, visual prognosis in these cases is very limited, due to the delicate nature of the structures involved. The complex management of these pathologies requires skilled and experienced surgeons, and surgical facilities with the necessary vitreoretinal surgical tools at their disposal.

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Proliferative Vitreoretinopathy (PVR) is currently the biggest obstacle to successful retinal reattachment surgery, accounting for approximately 75% of all primary surgical failures. PVR is characterized by growth and migration of preretinal or subretinal membranes. Contraction of these membranes causes foreshortening of the retina, leading to stretch holes or traction, which redetaches the retina. As the proliferation matures, the once compliant retinal tissue becomes rigid and immobile, making repair more difficult. In addition, patients with PVR-associated detachments often have extensive levels of visual loss. As technological advances in vitreoretinal surgery continue to move forward, effective new treatments for PVR continue to lag behind. Although anatomic repair is possible in greater than 90% of detachments with associated PVR, primary prevention of PVR remains an obstacle.1

Causes of PVR

The main cause of PVR is the proliferation and contraction of cells in the periretinal surfaces and vitreous gel. First, the cells need to gain access to these locations, and then they need a milieu that will make them grow, proliferate, and contract. This milieu is sometimes created by the disease itself. In cases of retinal tear, pigment epithelial cells can already be dispersed into the vitreous. A retinal detachment also is associated with breakdown of the blood ocular barrier. The surgeon’s attempts at intervention and repair can increase the likelihood of dispersing cells or making the milieu more suitable for these cells to grow and contract.

When the blood ocular barrier is broken, growth factors gain entrance into the eye.

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These include fibronectin, a platelet-derived growth factor, and other growth factors that cause cells in the vitreous cavity or the epiretinal or retroretinal surfaces to proliferate and contract. Retinal pigment epithelial cells can produce collagen, but only in the presence of some growth factors. Like the needed ingredients in a recipe, all these mechanisms together—cells, vitreous gel, growth factors— cause PVR.

Once periretinal proliferative membranes are in the vitreous gel, they exert a tractional force that will either reopen the original retinal break or cause new retinal breaks, with redetachment of the retina. The result will be a complicated, more difficult to repair rhegmatogenous retinal detachment.2

Risk Factors

The eyes most likely to develop PVR after retinal reattachment surgery are those with mild PVR prior to surgery. Other risk factors for PVR include excessive cryoretinopexy (Figure 1), retinal tears with greater than 3 disc diameters of exposed retinal pigment epithelium, previous vitrectomy, and postoperative choroidal detachments. Most rhegmatogenous retinal detachments can be complicated by some degree of proliferative vitreoretinopathy. Some patients with immunodeficiencies such as the acquired immunodeficiency syndrome (AIDS) develop mild PVR. Although one study has explored

risk factors using multivariate analysis, some other possible causes of PVR have not been studied. For example, the number of retinal tears present in an eye has not been studied as a risk factor for PVR.

In general, processes that increase vascular permeability are more likely to increase the probability of PVR formation. Specific risk factors that have been identified include: uveitis; large, giant, or multiple tears; vitreous hemorrhage, preoperative or postoperative choroidal detachments; aphakia; multiple previous surgeries; and large detachments involving greater than 2 quadrants of the eye.3-6

Classification: Anterior and

Posterior Components

The type of surgical treatment indicated depends upon the type of PVR. PVR has two basic components: an anterior and a posterior component (Figure 2). Anterior PVR occurs anterior to the posterior border of the vitreous base. The types of tractional forces present at the vitreous base include anteroposterior, circumferential, and perpendicular. Anteroposterior traction is manifest

as anterior displacement of the posterior border of the vitreous base. With this type of anterior traction the posterior border of the vitreous base is displaced either to the anterior insertion of the vitreous base, or to the ciliary processes, the ciliary body, or, in severe cases, even to the pupillary margin. Anteroposteriortractionisrecognizablebecause the iris is retracted posteriorly and because there is a circumferential trough anteriorly at the vitreous base.

The term “proliferative vitreoretinopathy” was coined in 1983 by the Retina Society Terminology Committee. In 1989, the classification was amended by the Silicone Study Group before being most recently modified in 1991 to its current classification. Currently, PVR is divided into grades A, B, and C. Grade A is limited to the presence of vitreous cells or haze. Grade B is defined by the presence of rolled or irregular edges of a tear or inner retinal surface wrinkling, denoting subclinical contraction. Grade C is recognized by the presence of preretinal or subretinal membranes. Grade C is further delineated as being anterior to the equator (grade Ca) or posterior to the equator (grade Cp) and by the number of clock hours involved (1 to 12).7