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

Introduction

Despite the availability of efficacious treatments for the management of diabetes, and the widespread use of laser photocoagulation in diabetic retinopathy, there are still a large number of patients that progress to advanced proliferative diabetic retinopathy. Modern vitreoretinal surgery techniques allow us to change the natural course of vision loss in advanced diabetic retinopathy, whether it may be proliferative diabetic retinopathy or macular edema. In the recent past, two developments have allowed us to consider earlier surgical intervention in progressive diabetic retinopathy:

1.Minimally invasive sutureless vitrectomy and

2.Pharmacological agents that block vascular endothelial growth factor (anti-VEGF). These tools have decreased the risk and discomfort associated to surgery while at the same time improving the surgical benefits. We must now view vitrectomy surgery

as another option in the management of diabetic retinopathy and not just as a last resort in patients facing blindness.

We will first review general concepts of patient selection and management in the different clinical scenarios that require vitrectomy in diabetes. In the latter part of this chapter we will discuss specific surgical techniques to be used in these pathologies.

Proliferative Diabetic

Retinopathy

The two most common indications for vitrectomy surgery in the setting of proliferative diabetic retinopathy are vitreous hemorrhages and tractional retinal detachments.

a) Vitreous Hemorrhage

The Diabetic Retinopathy Vitrectomy Study (DRVS)1 concluded that patients with vitreous hemorrhages that did not clear after

observation over the course of 6-12 months had better outcomes with vitrectomy than those observed without vitrectomy. As alluded to in the introduction, modern vitreoretinal surgery techniques allow us to recommend earlier vitrectomy than what the DRVS study concluded.

The goals of vitrectomy in diabetic vitreous hemorrhage are two fold:

1.To treat the underlying proliferative diabetic retinopathy and,

2.To clear the visual axis. Observation of a vitreous hemorrhage without treating the underlying disease can lead to unchecked progression of the retinopathy. Whenever a patient with diabetic vitreous hemorrhage is seen in the office, we first attempt to perform pan-retinal photocoagulation if the media permits it. Often younger patients will present with dense preretinal hemorrhages covering the posterior pole but with clear view of the retina beyond the vascular arcades (Figure 1). Since these hemorrhages may quickly disperse through the vitreous in the course of days to weeks, the opportunity provided by the clear view of the retina should allow adequate panretinal photocoagulation at the time of presentation.

When patients are seen with diffuse vitreous hemorrhages, two clinical questions should be answered:

1.Is the underlying retina attached? and,

2.Is proliferative diabetic retinopathy the cause of the vitreous hemorrhage? Binocular indirect ophthalmoscopy can often be per-

Figure 1: Acute subhyaloid hemorrhage in diabetic patient. These patients often present with acute central vision loss. The ophthalmologist should proceed with panretinal photocoagulation within the week of diagnosis. These subhyaloid hemorrhages often progress to diffuse vitreous hemorrhages, which preclude adequate laser therapy. Early laser therapy allows treatment of the underlying retinopathy before the media opacities impede it.

formed through dense vitreous hemorrhages to determine if the retina is attached or not, even if no subtle retinal details are seen. Often the view of the preequatorial retina is better than the view of the posterior pole, and that may be enough to determine the status of retinal attachment. If the view simply does not permit ophthalmoscopy, B-scanultrasonographyshouldbeperformed to determine retinal status. A patient with an underlying retinal detachment with vitreous hemorrhage requires early vitrectomy instead of observation.

The clinician should always think of the differential diagnosis of vitreous hemorrhage, even in diabetic patients. If the fellow eye

does not have proliferative retinopathy, one should consider the possibility of a different etiology for the vitreous hemorrhage. Whereas some causes of vitreous hemorrhages can be managed by clinical observation with the same timeline as diabetes (eg vein occlusions or sickle cell retinopathy), the possibility of a retinal tear with vitreous hemorrhage may push us into recommending a diagnostic and therapeutic vitrectomy within 1-2 weeks to prevent the development of a rhegmatogenous retinal detachment.

If proliferative diabetic retinopathy is the cause of the vitreous hemorrhage, and the media opacity prevents laser photocoagulation, a newoptionfortherapyisintravitrealanti-VEGF therapy (ie: bevacizumab or ramibizumab). Anti-VEGT will cause regression of the diabetic neovascularization in most patients in the course of 1-2 weeks.2 This medications is a competitive antagonist of VEGF, and as such it does not stop the synthesis of VEGF. In other words, even if anti-VEGF allows early regression of the neovascularization, the neovascularization will recur if no further treatment to the underlying disease is undertaken. Recurrence of neovascularization after anti-VEGF therapy occurs approximately 3-4 months post treatment. During this period, the clinician must either perform panretinal photocoagulation in the office or proceed to vitrectomy and endolaser if the hemorrhage does not clear adequately for office laser treatment. Anti-VEGF, therefore, allows the surgeon to decide on the merits vitrectomy based on the patient’s vision loss, and it’s impact to the patient’s daily life. Given the success of sutureless vitrectomy, most younger and active patients agree with vitrectomy after an observation period of 4-6 weeks.

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Figure 2: Preretinal fibrous contraction in diabetes. The “sphincter” configuration of the preretinal membrane is typical of proliferative diabetic retinopathy. Although the retina is attached, the contraction of the membranes has produced retinal traction with macular striae. Scissors dissection of the epiretinal membrane can release the traction on the fovea.

b) Tractional Retinal Detachments

Tractional retinal detachments constitute one of the most interesting and surgically challenging pathologies in vitreoretinal surgery. Diabetic tractional retinal detachments occur secondary to contractions of vitreous and of epiretinal fibrovascular proliferation in proliferative diabetic retinopathy (Figure 2). Neovascularization usually starts at the optic nerve head and courses along the vascular arcades, often forming a complete ring around the macula after meeting in the temporal raphe. Regression and consequent contraction

of the active neovascularizations leads to two different tractional vectors on the retina: a) Tangential traction along the retinal surface and b) Antero-posterior vitreous traction on the pathological vitreous attachments on the epiretinal fibrovascular tissue. Surgical repair ofdiabetictractionretinaldetachmentsrequires release of all tractional vectors on the retinal surface (Figures 3 a-b, 4).

Indications for vitrectomy surgery in diabetic tractional retinal detachments are detachment of the fovea with central vision loss and extrafoveal retinal detachments with functionally significant scotomas. We will discuss the technical issues regarding tractional retinal detachment repair later in this chapter.

Non-proliferative Diabetic

Retinopathy: Macular Edema

a) Vitreo-Macular Traction Syndrome

The abnormal vitreoretinal interphase in diabetics is often the cause of diabetic macular edema. Optical coherence tomography has allowed us to evaluate the anatomy and relationship of the fovea and vitreous in detail, and can show obvious anteroposterior traction on the fovea and often a localized foveal detachment3 (Figures 5, 6 and 7). Diabetic macular edema can now be understood as having three possible pathogenetic causes: a) Focal leakage from macular

Figure 5: Diabetic traction retinal detachment. The macular area appears detached secondary to preretinal traction and contraction of the fibrovascular “sphincter” that is typical of proliferative diabetic retinopathy.

Figure 7: Chronic diabetic traction retinal detachment. Despite peripheral laser, there is persistent vascular activity of the neovascular tissue. The retina appears atrophic and translucent from chronic traction and ischemia. The retinal vessels beyond the arcades appear occluded. This patient has a poor visual prognosis even with anatomic reattachment of the retina with vitrectomy surgery.

Figure 6: Severe diabetic traction retinal detachment. Massive preretinal proliferation precludes identification of anatomic landmarks. Radial retinal folds extend towards the equator of the globe. Careful observation of the vasculature of the preretinal tissue allows identification of retinal vessels and neovascular proliferative vessels: Retinal vessels exhibit dichotomous branching, whereas abnormal neovessels branch in irregular fronds. Presence of small neovessels indicate activity of the proliferative process.

microaneurysms (best managed with focal laser photocoagulation), b) Diffuse macular edema secondary to breakdown of the macular capillary blood-retinal barrier4 (which is the most difficult form to treat) and c) Tractional macular edema from vitreomacular traction or epiretinal membrane. A particular patient may have components of all three of these mechanisms, which need to be specifically addressed to achieve resolution of the macular edema (Figures 8 a-b and 9). The recent introduction of high resolution OCT allows greater ability to evaluate the vitreo-macular anatomy.

In the presence of foveal traction, release of the traction is often necessary for resolution of the macular edema. To achieve this, we recommend sutureless 25 G vitrectomy with

A

B

Figure 8 a-b: a) Macular traction detachment in type 1 diabetes. 25 year old patient with uncontrolled diabetes. The posterior vitreous was attached temporal to the optic nerve, but remained attached nasal and inferior to the optic nerve. Note the configuration of the neovascular vessels nasal to the nerve, which appear flat against the retinal surface, since the posterior hyaloid is still attached. The papillo-macular bundle is incorporated into the fibrovascular tissue at the optic nerve head, which has caused a localized detachment of the macula with 20/400 vision. b) Postoperative result two weeks following vitrectomy with scissors delamination of epiretinal membranes of the patient in figure 8a. This patient was initially treated with intravitreal bevazicumab and panretinal photocoagulation. Vitrectomy was later performed by the author and all the fibrovascular tissue was successfully removed without complications. After only two weeks following surgery, there is significant improvement in the retinal anatomy, but there is still a small amount of submacular fluid that hasn’t been reabsorbed after the retinal traction was removed. The macula reattached completely one month after vitrectomy, with final visual acuity of 20/100.

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Figure 9: Typical diabetic traction retinal detachment. The configuration of the preretinal fibrovascular tissue follows the growth of neovascularization from the nerve head along the termporal arcades, meeting at the horizontal raphe temporal to the macula. In addition to this obvious component of traction along the retinal surface, the surgeon must recognize and surgically relieve the antero-posterior vector of traction caused by the posterior hyaloid attachment immediately peripheral to the preretinal tissue, which often cannot be discerned until the time of surgery. The sharp circular outline along the preretinal tissue in this picture is likely caused by the premacular posterior vitreous cortex attachment to the neovessels. This premacular vitreous often forms a taut “trampoline” above the retina, and should also be removed at the time of surgery.

complete removal of the posterior hyaloid. Great care must be taken no to create a iatrogenic macular hole while removing foveal traction. To this effect, the surgeon often has to carefully peel all the perifoveal epiretinal membrane or posterior hyaloid, paying attention to the tractional forces on the fovea to determine the direction of highest mechanical resistance, and finish peeling the fovea in this same direction, avoiding unroofing a foveal cyst and creating a secondary lamellar macular hole.

b) Persistent Diffuse Diabetic Macular Edema

Non-tractional macular edema, particularly that associated to diffuse breakdown of the blood-retinal barrier in the macula, may be recalcitrant and resistant to treatment. The medical and laser management of macular edema is not in the scope of this chapter. It will suffice to enumerate different treatment strategies that should be considered before recommending vitrectomy for the management of these patients:

1.Focal and macular grid photocoagulation.

2.Optimization of systemic disease status (hypertension, hyperglycemia, congestive heart failure, proteinuria with hypoalbuminemia, obstructive sleep apnea, etc.).

3.Cessation of systemic medications that may exacerbate macular edema (eg. Rosiglitazone or Niacin).

4.Periocular or intravitreal steroids.

5.Intravitreal anti-VEGF agents. In the absence of foveal traction, vitrectomy should

not be performed until the previous strategies have been considered.

Peeling of the macular internal limiting membrane has been shown to be efficacious in the management of persistent diabetic macular edema in the absence of foveal traction.5 The rationale for this procedure involved removal of any potential non-obvious retinal traction, and decompartamentalization of macular tissue. This could allow macular interstitial fluid to be dissolved in the vitreous cavity and to provide a larger volume of distribution of VEGF with decreased concentrations in the macula.

The work done by Holekamp has demonstrated that the vitreous gel acts as an oxygen sink, and that vitrectomy increases oxygen levels in the vitreous cavity.6 The vitreous likely consumes oxygen through ascorbic acid. The removal of the vitreous gel is associated to significant increase in the partial pressure of oxygen in the vitreous cavity and particularly on the retinal surface. The increased oxygen pressure in post-vitrectomy eyes is directly responsible for the accelerated progression of nuclear sclerotic cataracts after vitrectomy surgery. On the other hand, the increased vitreous oxygenation may have the positive effect of supplying much needed oxygen to the retina in ischemic retinopathies.

No large controlled studies have been performed to determine the most appropriate surgical procedure for persistent diabetic macular edema. It is important to mention that the only common denominator in all surgical strategies proposed for diabetic macular edema is core vitrectomy. Current

surgical strategies other than core vitrectomy include vitrectomy with removal of the posterior hyaloid or vitrectomy with internal limiting membrane peeling. It is difficult to objectively determine at this time if core vitrectomy without any membrane peeling is as effective as vitrectomy with peeling of the ILM or posterior hyaloid. We recommend vitrectomy with posterior hyaloidectomy. Intraoperative triamcinolone can be utilized to demonstrate the presence of the posterior hyaloid attachment, and to guarantee its complete removal. Atraumatic internal limiting membrane peeling can be attempted in most patients. If the ILM peeling is technically difficult, we see no present benefit to risking retinal damage if the vitrectomy and posterior hyaloid have been successfully performed. We anxiously await large controlled surgical studies of vitrectomy for macular edema to further refine these recommendations.

A caveat that the physician must remember and inform the patient with diffuse diabetic macular edema is that not uncommonly the visual acuity doesn’t improve after successful treatment and resolution of the macular edema. The limiting factor may be macular ischemia from diabetic microvascular damage of the perifoveal capillaries. In addition, there may be recurrence of the macular edema months after resolution with vitrectomy.

Technical Issues

a) 25 G Sutureless Vitrectomy

Advances in vitreoretinal technology and instrumentation have provided the surgeon the ability to perform sutureless transcon-

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junctival vitrectomy. Sutureless vitrectomy has many significant benefits over standard 20 gauge vitrectomy. The preservation of the ocular surface and the conjunctival integrity significantly decreases postoperative patient discomfort and pain, as well as hastens visual recovery. Glaucoma is a frequent comorbidity, and sutureless vitrectomy doesn’t scar the conjunctiva in case of a future trabeculectomy and can avoid completely a previous glaucoma surgery site, decreasing the likelihood of failure or leak from a filtration or seton surgery. The fluidics and anterior location of the port in the vitreous cutter allow safer vitrectomy and permits epiretinal membrane delamination with the cutter itself. At the time of this writing, the main controversies regarding sutureless vitrectomy are whether to use 23 gauge or 25 gauge vitrectomy for sutureless vitrectomy. Many surgeons believe that sutureless vitrectomy is only amenable for simple surgical cases and that complex cases require 20 gauge instrumentation. We use 25 gauge vitrectomy for all our cases, simple and complex.

As mentioned in the discussion of vitreous hemorrhages, preoperative intravitreal anti-VEGF has become a tool in the surgical management of proliferative diabetic retinopathy. Anti-VEGF causes regression of retinal neovascularization within one to two weeks, and decreases postoperative vitreous hemorrhage, which otherwise can occur in up to a third of patients following vitrectomy for proliferative diabetic retinopathy. In patients with large active neovascularizations, worsening of retinal traction can occur after anti-VEGF therapy.7 Due to this, we proced with the intravitreal anti-VEGF injection four

Figure 10: Technique for scissors delamination of epimacular membranes. This picture demonstrates various important anatomic considerations that should guide the surgical dissection of diabetic traction retinal detachments. 1. Epiretinal membranes often have multiple discrete attachment points to the retina that can be cut with scissors in the correct dissection plane. 2. The posterior vitreous cortex usually remains attached at the sites of neovascular proliferation. 3. Vitreous contraction occurs in two planes: a peripheral cone that attaches to the vitreous base, and a horizontal plane above the macula. The surgeon must remove all vectors of traction for complete reattachment of the retina. (Courtesy of Vitreous Microsurgery book, Fourth Edition, by Steve Charles, Jorge Calzada and Byron Wood. L).

to seven days prior to vitrectomy, instead of waiting for complete contraction of the retinal membranes after the anti-VEGF injection. In addition, at the end of diabetic vitrectomy surgery, we inject anti-VEGF into the vitreous cavity, to maintain the inhibition of VEGF during the early postoperative period.

In the presence of dense vitreous hemorrhage that precludes visualization of the retinal surface, great care must be taken to avoid creating an inadvertent retinal tear with the vitreous cutter. We recommend performing a

central vitrectomy and “tunneling” vertically towards the optic nerve or nasal retina, rather than extending the core vitrectomy peripherally without retinal visibility. Once the optic nerve is recognized the surrounding retinal anatomy will become easier to identify, and the core vitrectomy can be extended peripherally (Figure 10).

Following core vitrectomy, attention is directed to the posterior vitreous cortex. In diabetic traction retinal detachments, there is usually a persistent vitreous attachment along the arcades or other areas of retinal neovascularization. The vitreous can then take the configuration of a truncated cone as the peripheral vitreous detaches from the retinal surface, but maintains attachments at the vitreous base and vascular arcades. The vitreous cutter is used to transect the posterior hyaloid 360 degrees along the surface of the cone, resolving the anteroposterior traction on the retina. Intraoperative intravitreal triamcinolone can be used for vitreous visualization during surgery. Although not necessary in all patients, triamcinolone does facilitate completeness of the truncation of the posterior hyaloid.

b) Posterior Hyaloid Dissection

The posterior hyaloid is the common site of pathology that has to be addressed during diabetic vitrectomy. In proliferative diabetic retinopathy, the hyaloid is the substrate for growth of retinal neovascularization and for creation of retinal traction. The surgical dissection of epiretinal tissue (discussed below) removes the posterior hyaloid simultaneously.