Ординатура / Офтальмология / Английские материалы / Retinal Vascular Disease_Joussen, Gardner, Kirchhof_2007

for surgery. However, the individual decision for surgery is commonly not as easy. On the one hand, the surgical risk in a “simple” vitreous hemorrhage is low. On the other hand, the blood may clear spontaneously. As long as there is no retinal detachment, iris rubeosis or macular edema, no irreversible damage will occur when surgery is postponed. Therefore

19 III it is not possible to give a clear general recommendation of how long to wait for surgery. In a very dense or recurrent hemorrhage it may be prudent to operate within a few days. Other patients may benefit from waiting many months for the hemorrhage to clear. It is left to the surgeon’s and patient’s combined judgement to estimate which hemorrhage may clear rapidly enough to wait.

Vitreous hemorrhage occurs if neovascularizations tear. This commonly happens in eyes which undergo partial vitreous detachment or contraction of the fibrovascular membranes. These vitreous

a

changes may occur spontaneously but may be accelerated after scatter laser treatment of the retina. Retinal photocoagulation induces fibrotic transformation, contraction of neovascular membranes, and partial vitreous detachment. Thus, scatter photocoagulation may eventually trigger vitreous hemorrhage shortly after treatment before neovascularizations become atrophic.

In eyes with known traction on the central retina or evidence of traction in ultrasound echography [6], delaying surgery may cause irreversible damage to the macula. In this situation surgery should not be delayed. Figure 19.2.1.1a shows an example of a vitreous hemorrhage which can be observed. The hemorrhage is not very dense and no traction on the retina is present. In contrast, in Figure 19.2.1.1b tractional membranes are visible and surgery is recommended. Iris neovascularizations are an indirect sign of severe retinal ischemia requiring retinal coagulation treatment. Eyes with iris rubeosis and vitreous hemorrhage therefore need vitreous surgery to allow adequate photocoagulation, before irreversible obstruction of the chamber angle occurs.

19.2.1.2.3 Extrafoveal Tractional Detachment

Not all eyes with extrafoveolar tractional retinal detachment need surgery. In many cases the situation may remain stable for many years and a detached retina may even spontaneously reattach. Risk factors for visual loss have been the presence of active neovascularizations, progression of the detachment and the occurrence of vitreous hemorrhage [8].

Before advanced vitreous surgery was available, retinal photocoagulation was considered to be dan-

a

b

Fig. 19.2.1.3. a Fibrovascular membranes along the major vascular arcades without traction to the fovea but with retrohyaloidal hemorrhage. Visual acuity was 20/60. b One year after scatter laser treatment the membranes became atrophic, the blood had reabsorbed and no significant traction to the fovea developed. Vision remained stable at 20/60

Fig. 19.2.1.4. a Severe proliferative diabetic retinopathy with active fibrovascular membranes. Visual acuity was 20/60. b Three months after supplementary scatter laser treatment the membranes became atrophic but traction on the fovea developed and vision dropped to 20/400. c One year later, after vitrectomy and removal of the membranes, vision had improved to 20/60. Note the thickened arterial walls with narrowing of the vessel lumen

gerous in eyes with tractional detachment and active neovascularizations[46]. Laser induced fibrotic transformation of the neovascularizations may possibly increase traction on the retina and the tractional detachment may progress. Without surgery the visual prognosis of these eyes was poor. Today we recommend performing scatter treatment to induce atrophic regression of the new vessels. It is important, however, in this situation that eyes with extrafo-

III 19

a

b

c

veal tractional detachment must be carefully watched after laser treatment. If the detachment progresses and the fovea is threatened, immediate surgery should be performed. With a detached fovea the

19 III

a

b

a

b

Fig. 19.2.1.6. a Fibrovascular membranes along the major vascular arcades with traction to the fovea and with vitreous hemorrhage despite dense scatter laser treatment. Visual acuity was 20/400. b One year after vitrectomy and removal of the membranes the eye became stable and vision improved to 20/40

c

Fig. 19.2.1.5. a Severe non-proliferative diabetic retinopathy, vision 20/30. b One year later severe progressive proliferative diabetic retinopathy with traction to the macula and vitreous hemorrhage had developed despite scatter laser treatment. Vision had dropped to 20/400. c Three weeks after vitrectomy, endolaser and removal of the membranes, the retina is flat. Vision later improved to 20/60. c One year later, slow resolution of exudates and edema was observed, and vision had improved to 20/80.

visual acuity drops and even after anatomically successful surgery the visual prognosis is guarded in eyes with diabetic retinopathy [17]. On the other hand, many eyes may be stabilized by laser treatment alone, not requiring surgery. Even if surgery may later become necessary, laser induces partial transformation of active new vessels into atrophic fibrotic membranes and partial vitreous detachment. This will make surgery technically easier and may reduce the risk of postoperative hemorrhages.

Figure 19.2.1.1c shows an example of a tractional retinal detachment nasally to the fovea, not threatening the fovea. Scatter laser treatment has already been performed, the membrane is atrophic and the situation appears to be stable without further therapy. Figures 19.2.1.2 and 19.2.1.3 show the course of the disease in eyes where active fibrovascular membranes without foveal traction could be stabilized

with scatter laser treatment. In the eyes shown in Figs. 19.2.1.4 – 19.2.1.6, laser treatment did not stabilize the retinopathy and traction on the fovea developed. In these cases vitreous surgery was necessary to stabilize vision.

In some cases traction on the fovea may cause tractive macular edema, even if the fovea itself is not detached. Focal laser treatment is not helpful and not recommended in this situation. The best therapy for tractional edema is to remove the traction surgically to allow resolution of the macula edema. Figure 19.2.1.7 shows the slow reabsorption of tractional macular edema after surgical removal of the membranes.

19.2.1.2.4 Tractional Detachment of the Fovea

If the fovea itself is tractively elevated, vision is usually very poor. For this situation surgery is the only

therapeutic option. However, even after anatomically successful surgery, functional results are usually disappointing and much worse than after surgery for a non-diabetic rhegmatogenous retinal detachment. Often, eyes with tractional detachment of the macula have advanced macular ischemia, which is limiting visual recovery. Risk factors for poor visual outcome are extension of the retinal detachment, duration of macular detachment and iris rubeosis (indicating severe retinal ischemia) [17]. In eyes with this combination of risk factors, we have to consider not performing any surgery, especially if the fellow eye is good and general health is poor. Patients with advanced diabetic eye disease usually suffer from other severe manifestations of the microvascular and macrovascular diabetic complications. Extended and repeated surgery may be a serious stress factor for patients with impaired general health. Life expec-

tancy is also limited with advanced diabetic complications, and is not much better than in patients with malignomas [18]. These non-ocular factors have to be considered if a decision to perform surgery is made in a situation with a reduced prognosis quo ad visum. If both eyes have reduced vision, surgical attempts will nevertheless have to be performed despite the poor prognosis. Figure 19.2.1.8 shows a patient with long-standing tractional detachment of the macula in his only eye. After vision had dropped to LP, surgery was performed but vision did not improve despite anatomically successful surgery. Figure 19.2.1.9 shows the fundus of an eye with recent tractional detachment of the fovea and a vision of HM. The fellow eye had good vision. Fluorescein angiography showed severe retinal ischemia. Therefore no surgery was recommended.

19.2.1.2.5Tractional Rhegmatogenous Retinal Detachment

Diabetic fibrovascular membranes may not only elevate the retina, but in rare cases also create tears in the retina. A rhegmatogenous retinal detachment may develop. Clinically these tears may be difficult to identify, because they can be small and hidden behind membranes or blood. On the other hand, circumscribed thinning of the retina, e.g., in areas of former photocoagulation, can mimic retinal tears. For the diagnosis of a rhegmatogenous detachment one should look for a bullous and mobile retinal detachment, in contrast to a concave, immobile, tentlike shape of a tractive detachment. Diabetic trac- tional-rhegmatogenous detachment in most cases progresses rapidly and therefore has to be operated

Fig. 19.2.1.10. a Tractional rhegmatogenous retinal detachment, visual acuity HM. b After vitrectomy with gas tamponade and endolaser, the retina is attached and vision improved to 20/100. Eight weeks after surgery the patient noted metamorphopsia. Proliferative vitreoretinopathy with epiretinal membranes and wrinkling of the retina was observed. c Two weeks later the retina was completely detached

on immediately like other rhegmatogenous detachments. Technically it may be difficult to remove all tractive tissue tightly adhering to the mobile detached retina. Therefore the rate of intraoperatively created holes was relatively high [58]. Reproliferations after surgery are unfortunately not too rare and constitute a combination of diabetic fibrovascular membranes and the typical proliferative vitreoretinopathy (PVR) after rhegmatogenous retinal detachment. Figure 19.2.1.10 shows such an eye with tractional rhegmatogenous retinal detachment which developed severe reproliferations 2 months after primarily successful surgery.

19.2.1.2.6 Macular Edema

Treatment of macular edema is described in detail in the next chapter. Here only tractional macular edema is mentioned. Traction by atrophic fibrovascular membranes may present with distortion of the central retina, creating a picture similar to macular pucker. A typical example is shown in Fig. 19.2.1.11. Traction of fibrovascular membranes may also cause a type of macular edema with typical hard exudates. Tractional edema has a good chance to resolve after vitrectomy (see Fig. 19.2.1.7). Visual recovery is dependent on the degree of macular ischemia.

19.2.1.2.7 Surgery for Neovascular Glaucoma

Neovascular glaucoma is a severe complication of advanced proliferative diabetic retinopathy. Patho-

c

physiologically it is assumed that the ischemic retina is the source of production of vasoproliferative growth factors, which can diffuse to the anterior segment of the eye, especially in aphakic and vitrectomized eyes. Growth of fibrovascular membranes in the chamber angle obstructs aqueous outflow and intraocular pressure rises, often to very high levels. Therapy should be directed first to the cause of the neovascular stimulus. Extensive photocoagulation of the retina or cryotherapy to the peripheral retina should be applied [47]. This treatment can induce regression of neovascularizations; however, intraocular pressure commonly remains elevated because the vascular membranes in the chamber angle do not completely disappear. They may undergo fibrotic transformation and still obstruct the aqueous outflow. Therefore treatment to lower intraocular pressure is usually necessary. Conventional glaucoma surgery has poor success rates in these eyes. They have a disrupted blood aqueous barrier and intraocular fluids contain high concentrations of cytokines stimulating fibrosis. Rapid obstruction of the trabe-

between the sites of adhesion to the retina (“segmentation” technique [43]). The remaining stumps are trimmed with the vitreous cutter. Other approaches involve severing the membrane from the retina in a single piece by cutting the adhesions with horizontally cutting scissors (“delamination” [42] or “en bloc” [40] technique).

Diabetic neovascular membranes primarily grow from retinal vessels. To remove them, a vessel has to be cut or torn off. This creates an opening of the vessel lumen and a potential source for a vitreous hemorrhage. Visible bleeding stumps may be coagulated intraoperatively using endodiathermia depending on the localization. If the source of hemorrhage is a large vessel or the optic disk, this may not be possible. The bleeding often stops spontaneously or after increasing the infusion pressure. These tiny tears in retinal vessels, however, may cause postoperative hemorrhages in the early postoperative phase.

19.2.1.3.2Application of Endolaser Whenever Possible

One of the most important steps in diabetic vitreous surgery is coagulation treatment of the retina [13, 15, 30, 55]. Complications requiring vitreous surgery are almost always an indicator for an active and unstable retinopathy. Therefore almost all eyes undergoing vitreous surgery require endolaser treatment of the ischemic retina. Moreover, the surgery itself may even worsen some aspects of the retinopathy. Preretinal neovascularizations participate in oxygen and nutrient supply to the retina; this is the biologic function of the new vessels. If active neovascularizations are removed from the retinal surface, this may further reduce the vascular supply to the inner retina. Thus, vitrectomy may even worsen retinal ischemia and stimulate the production of vasoproliferative growth factors. Moreover, after removal of the vitreous, these growth factors may more easily reach the anterior segment [56]. Progression of iris rubeosis is a severe complication of vitreous surgery [51]. This complication, however, may be significantly reduced by intraoperative endolaser treatment to the retina [20].

19.2.1.3.3Check the Periphery with Wide-Angle Viewing System for Retinal Tears

Preparation of tightly adhering fibrovascular membranes from the retina is often time consuming and requires repeated exchange of instruments in the eye. Moreover, the vitreous is commonly partly attached and may be sticky in diabetic eyes, possibly because it contains blood and fibrin due to a breakdown of the blood-retina barrier. In diabetic vitrec-

tomies iatrogenic retinal holes in the vitreous base may therefore occur more often than with other indications for vitrectomy, leading to retinal detachment if not treated properly [51]. Careful inspection of the retinal periphery, preferably with a wide-angle viewing system [61] under indentation, is therefore man-

datory.

III 19

19.2.1.3.4 Cataract Surgery

If the lens has to be operated on, intracapsular surgery should be avoided, to leave a barrier between the anterior and the posterior segment intact. Intracapsular surgery is associated with an increased risk for neovascular glaucoma [1]. If the capsule of the lens is left in place in extracapsular cataract surgery, diabetic eyes have an increased risk of postoperative fibrin exudation and formation of synechia between the lens capsule and the iris due to an impaired blood-retinal barrier [16, 23, 53]. There is no absolute contraindication for the implantation of an intraocular lens (IOL) in these eyes [3, 4]. Even in eyes with iris rubeosis, an IOL may be implanted [31]; extensive coagulation treatment of the retina, however, is mandatory in these cases [25, 26]. The IOL in diabetic eyes should be implanted safely into the capsular bag and a large opening of the anterior lens capsule should be provided to improve visualization of the fundus. Silicone lenses should be avoided. If later in the course of the disease liquid silicone has to be installed in the vitreous cavity, the liquid silicone may form tight adhesions to the silicone IOL, forming droplets on the IOL which are optically very disturbing, commonly requiring IOL exchange [62]. Combined vitreoretinal and cataract surgery can be successfully performed [32, 52]. The inflammatory response with fibrin in the anterior chamber and the formation of synechia, however, is probably lower in a two step procedure [53]. We therefore prefer to perform cataract surgery in the same procedure as the vitreoretinal procedure only if lens opacities are disturbing posterior segment visualization. Since progression of macular edema is a common complication after cataract surgery, the injection of intravitreal triamcinolone at the end of the surgery may be considered [28, 29, 50]. This supplementary treatment may avoid worsening and even improve macular edema [57] after cataract surgery.

19.2.1.3.5 Silicone

Introduction of liquid silicone has expanded our armamentarium for vitreous surgery in diabetic retinopathy [33, 37 – 39]. Retinal holes may be created during preparation of diabetic fibrovascular membranes, especially if the tractional detachment is

long-standing and the retina itself has become thin and atrophic. In these eyes instillation of liquid silicone may be used as a tamponade for the retinal defects avoiding rhegmatogenous retinal detachment after vitreous surgery. Silicone must not be used in eyes with tractional retinal detachment without completely removing the tractional membranes

19 III [44]. Since water soluble growth factors concentrate in high levels in the thin interface between retina and silicone, a strong stimulus for proliferation of fibrovascular membranes is present leading to reproliferations and retinal redetachment under the silicone. This can be avoided in many cases by complete removal of all fibrovascular tissues before instillation of silicone.

Another indication for liquid silicone is recurrent vitreous hemorrhage after vitrectomy. Since silicone fills the vitreous cavity, a clear optic axis is provided. Visual rehabilitation is improved in these eyes by liquid silicone [22].

A third indication for liquid silicone can be severe anterior segment neovascularization [7, 20, 36]. Filling the vitreous cavity with liquid silicone provides a barrier for diffusion from the posterior to the anterior segment of the eye. In eyes with severe neovascularization of the anterior segment, silicone may reduce the diffusion of vasoproliferative growth factors from the ischemic retina to the iris. Together with retinal coagulation therapy, silicone is a treatment option for severe anterior segment neovascularization.

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