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Ann. Rev Med 1979. 30:331-38 Copyright © 1979 by Annuol Reviews Inc. All rights reserved

VITRECTOMY SURGERY

.7327

Annu. Rev. Med. 1979.30:331-338. Downloaded from www.annualreviews.org Access provided by Cambridge University on 01/28/15. For personal use only.

FOR DIABETIC RETINOPATHY George H. Bresnick, M.D. and Franklin L. Myers, M.D. Department of Ophthalmology, University of Wisconsin, Madison, Wisconsin 53706

INTRODUCTION The vitrectomy operation is a new ophthalmic surgical procedure for the treatment of diabetic retinopathy. Since vitrectomy is a major intraocular surgical procedure with the potential for serious ocular complications, its use is reserved for certain advanced stages of proliferative diabetic retinopa­ thy (PDR) where safer alternative modes of therapy (e.g. photocoagulation) are ineffective. With this in mind one may consider vitrectomy surgery for two aspects of severe diabetic retinopathy: and

(b)

(a) severe vitreous hemorrhage,

retinal detachment affecting or threatening central vision.

This review article delineates the current techniques, indications, and results of vitrectomy surgery in the treatment of diabetic retinopathy. The natural history and a description of other modes of treatment of diabetic retinopathy introduce the discussion of the surgical procedure. Since new developments in this area of ophthalmic surgery are occurring rapidly, the potential of future advances is also discussed. The medical problems en­ countered in caring for the diabetic patient undergoing vitrectomy may be considerable, and therefore this aspect is also reviewed.

NATURAL HISTORY OF DIABETIC RETINOPATHY Nonproliferative and Proliferative Phases The fundus abnormalities seen in diabetic retinopathy consist of changes within the retina (intraretinal), in front of the retina (preretinal), and within the vitreous cavity (intravitreal). The intraretinal changes comprise the nonproliferative phase of the disease, while the preretinal and intravitreal alterations constitute the proliferative phase. Many of the nonproliferative 331

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Annu. Rev. Med. 1979.30:331-338. Downloaded from www.annualreviews.org Access provided by Cambridge University on 01/28/15. For personal use only.

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changes are manifestations of retinal ischemia due to the occlusion of capillaries and small arterioles within the retina. (The mechanism of retinal vaso-occlusion is poorly understood.) These occlusive changes precede or coincide with the development of retinal neovascularization; the retinal ischemia that results from small-vessel occlusion is thought to stimulate the growth of new vessels and fibrous tissue during the proliferative phase of the disease (1). Abnormally increased permeability of the retinal capillaries is another fundamental aspect of the nonproliferative phase of the disease. Retinal edema and hard exudate deposits are the major consequence of the abnor­ mal retinal vascular permeability. Causes of Visual Loss from Diabetic Retinopathy

Visual loss from the nonproliferative component of the disease may result from macular ischemia or from retinal edema and hard exudates involving the macula. No treatment is available for macular ischemia; retinal photocoagulation directed at abnormally permeable capillaries and mi­ croaneurysms may be of benefit, however, in certain cases of macular edema (2, 3). The most severe visual loss from diabetic retinopathy occurs from the proliferative aspects of the disease. Vitreous hemorrhage and tractional detachment of the retina are the two major causes of this severe visual loss; both result from the growth of fibrovascular tissue and the subsequent shrinkage of this tissue and of the vitreous. The fibrovascular tissue originates from the retinal vessels, breaks through the intemal limiting membrane of the retina, and proliferates at the interface between retina and vitreous. The fibrovascular tissue is intimately connected to the cortical (outer) vitreous layer. For unknown reasons the vitreous and fibrovascular tissue contract, pulling the newly formed fibrovascular tissue forward. This traction exerted on the new vessels by the contracting vitreous is a major cause of vitreous hemorrhage in PDR (4,5). Vitreous contraction may also produce traction on the retina itself at sites of adhesion between vitreous, fibrovascular tissue, and retina; tractional detachment of the retina may result. If the retinal detachment involves the macula, severe visual loss may occur. TREATMENT OF PROLIFERATIVE DIABETIC RETINOPATHY Photocoagulation Treatment

The first line of treatment of PDR is photocoagulation. The results of a recent collaborative trial of photocoagulation (6) show that this treatment

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Annu. Rev. Med. 1979.30:331-338. Downloaded from www.annualreviews.org Access provided by Cambridge University on 01/28/15. For personal use only.

can significantly reduce the incidence of severe visual loss from PDR by eliminating or reducing neovascularization and by curtailing the prolifera­ tive process. Nevertheless, some eyes with PDR develop visual loss from vitreous hemorrhage and/or tractional retinal detachment in spite of photocoagulation, and other eyes are considered untreatable with photocoagulation because they already have severe vitreous hemorrhage or severe vitreoretinal traction. It is these two groups of eyes that are potential candidates for vitrectomy surgery. Indications for Vitrectomy Surgery

The indications for vitrectomy surgery in eyes with vitreous hemorrhage depend upon the severity and duration of the hemorrhage. Many of these eyes (especially those with mild to moderate degrees of hemorrhage) will clear spontaneously over a period of a few weeks to several months and will not require surgery. For this reason, most ophthalmic surgeons do not perform vitrectomy surgery for vitreous hem­ orrhage unless the vision is severely reduced «5/200 visual acuity) and, unless the hemorrhage has been present for a least 6-12 months. VITREOUS HEMORRHAGE

Tractional detachment of the retina in PDR usually begins as a small area of retinal elevation located at some distance from the macula. In many eyes the detachment will not progress or will progress only slowly, and unless the detachment ex­ tends to include the macula, good visual acuity will be maintained. For this reason, surgery is not undertaken for tractional retinal detachment unless the macula is detached or imminently threatened. Should vision decrease because of macular detachment, prompt surgical repair is important to restore useful vision. Conventional scleral-buckling surgery may be used in some cases of retinal detachment in PDR (7), but vitrectomy surgery is required if the degree of vitreoretinal traction is severe. TRACTIONAL DETACHMENT OF THE RETINA

HISTORICAL DEVELOPMENTS AND TECHNIQUES OF VITREOUS SURGERY

Traditionally, a surgical approach to diseases involving the vitreous body of the eye was considered too dangerous to undertake because one could easily produce retinal tears and retinal detachment by inadvertent traction on the collagenous vitreous framework. A dramatic breakthrough occurred in 1972 when Machemer et al (8) introduced an instrument called the vitreous infusion suction cutter (VISe) that could cut and remove vitreous with a minimum amount of vitreoretinal traction. The features of the instru� ment were:

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Annu. Rev. Med. 1979.30:331-338. Downloaded from www.annualreviews.org Access provided by Cambridge University on 01/28/15. For personal use only.

1. A small-diameter (2.6 mm) tube with a motor-driven rotating internal cutting device that could safely remove small beads of vitreous. 2. An infusion system that replaced the vitreous with an equivalent amount of normal saline (or other biologically compatible fluid) such that a reason­ ably constant volume and pressure were maintained in the eye. 3. An illuminated operating microscope and corneal contact lens combina­ tion that allowed direct visualization of the vitreous and retina during the procedure. The instrument was introduced into the eye through a small anterior sclerotomy incision located over the pars plana of the ciliary body. The cutting and sucking action of the instrument allowed the removal of blood and vitreous from the vitreous cavity and the severance of vitreoretinal traction bands. In this way the operation could perform two basic functions: (a) removal of vitreous opacities (e.g. hemorrhage) and (b) release of vi­ treoretinal traction to allow settling of tractional retinal detachment. Since the introduction of the VISe a number of similar devices have been designed (9-13) with modifications that attempt to (a) reduce the size of the instrument, (b) improve the cutting capability of the instrument, (c) provide an intraocular fiber optics illumination system, and (d) provide intraocular diathermy and cryocoagulation. These and similar refinements have extended the capabilities of the proce­ dure and reduced some of the complications. Delicate surgical maneuvers such as peeling of opaque membranes from the surface of the retina and intraocular coagulation of intravitreal new vessels are now feasible. RESULTS OF VITRECTOMY SURGERY

Early in the development of vitreous surgery most of the cases operated were for long-standing (one year or longer) severe vitreous hemorrhage. Reports indicated that in 60-70% of these cases the visual acuity could be improved by surgery (14, 15). However, the level of visual acuity achieved was often disappointing, with less than 3% recovering 20/40 or better vision (16). Retinal degenerative changes secondary to ischemia, and macu­ lar detachment or fibrosis, accounted for most of the more severe visual loss. As the backlog of cases with long-standing vitreous hemorrhage was gradually reduced, surgeons, hoping to improve the visual outcome, began operating earlier in the course of vitreous hemorrhage. Results of earlier surgery are currently under study (see below). Attention was also turned to surgery in so-called clear media cases in which relief of tractional retinal detachment that involved or threatened the macula was the primary aim. Results in these cases are more difficult to assess, since success is judged

VITRECTOMY SURGERY FOR DIABETIC RETINOPATHY

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partly by the anatomical result as well as by the visual result. The outcome in individual cases can sometimes be excellent, but the overall success rate appears to be no greater than

40-50% (17-19).

Nevertheless, when con­

fronted with the inevitable blindness that results if reattachment of the retina is not attempted, most surgeons and patients are willing to proceed with surgery even if the odds for success appear relatively low.

Annu. Rev. Med. 1979.30:331-338. Downloaded from www.annualreviews.org Access provided by Cambridge University on 01/28/15. For personal use only.

COMPLICATIONS OF VITRECTOMY SURGERY In addition to being influenced by the underlying microvascular and vitre­ ous pathology present (degree of capillary closure, extent and sites of vi­ treoretinal adhesions, status of the macula, etc), the success rate is also considerably influenced by the complication rate. Complications include iatrogenic retinal detachment, corneal dystrophy, cataract, recurrent vitre­ ous hemorrhage, and rubeosis iridis with neovascular glaucoma. Retinal detachment that develops during surgery is usually caused by inadvertent tearing of the retina by the vitrectomy instrument. While repair of the detachment is possible in some cases, large tears may produce irrepa­ rable total retinal detachments. Improved visualization with fiber optic attachments and improved cutting capabilities of newer instruments have reduced this complication. Corneal dystrophy due to corneal endothelial damage during surgery is most common when lensectomy (cataract removal) and vitrectomy are combined. Reduced intraocular operating time and the introduction of newer intraocular irrigating solutions seem to have decreased this complica­ tion (20). Cataract may develop during surgery when the lens is inadvertently hit with the vitrectomy instrument or when a large quantity of irrigating solu­ tion has been used. The lens opacities in the latter instance are usually reversible. However, if lens changes develop during surgery sufficient to impair visualization of the fundus, the lens may have to be removed to allow safe completion of the case. Recurrent vitreous hemorrhage following vitrectomy may result from residual retinal neovascularization or from neovascular ingrowth at the sclerotomy site. Fortunately, most of these hemorrhages will clear sponta­ neously, but occasionally a repeat vitreous washout is required. Ten to twenty percent of diabetic eyes undergoing vitrectomy may de­ velop neovascular glaucoma, usually within six months of surgery. Medical and surgical therapy for neovascular glaucoma is usually unsuccessful; most eyes lose useful vision, and some eventually must be removed for intractable pain. Vitrectomy, therefore is a risky procedure in terms of ocular complica­ tions. These obviously must be taken into consideration and balanced against the potential benefits before undertaking surgery.

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MEDICAL PROBLEMS An additonal risk of vitrectomy in the diabetic patient involves the risk of surgery and anesthesia itself. Most cases are done under general anesthesia because the surgery may be lengthy (2-5 hours), and immobilization of the patient after introduction of the vitrectomy instrument into the eye is critical. Nonetheless some surgeons find anesthesia with a retrobulbar block combined with intravenous sedation under continuous anesthetist surveil­

Annu. Rev. Med. 1979.30:331-338. Downloaded from www.annualreviews.org Access provided by Cambridge University on 01/28/15. For personal use only.

lance an acceptable alternative. The great majority of these patients are suffering from the other small- and large-vessel complications of diabetes mellitus, which involve the renal, cardiac, and peripheral vascular systems. Hypertension and cardiac abnormalities are especially pertinent to anes­ thetic risk and must be carefully evaluated and controlled preoperatively. Renal disease, while certainly not a contraindication to surgery and anes­ thesia, must be evaluated, and if required, dialysis instituted so that the patient is in the best possible condition for surgery. Chronic infection, poor understanding by the patient of his disease, and psychological factors all contribute to poor diabetic control that so many of these patients manifest. Although tight control preoperatively is not absolutely necessary, knowledge of the patient's insulin requirements, elec­ trolyte situation, and previous responses to treatment is required in order to smooth out the postoperative management in a period of time when the patient is inactive, may be vomiting from the effects of anesthesia, or may be in pain and not eating. It is a good practice to admit the patient to the hospital three or four days preoperatively for medical assessment, especially if he comes from a long distance to a medical center and is not being actively managed as an outpatient by the medical consultant. Collection of a 24-hour urine speci­ men starting the day before admission and completed on the day of admis­ sion is helpful in determining current control. The practice of giving the patient one half to two thirds of his usual long-acting insulin dosage on the morning of surgery along with intrave­ nous glucose seems to work well. Scheduling the surgery as early in the day as possible is h�lpful, and monitoring of the blood sugar at intervals during surgery is essential. Fortunately most of these patients have little pain postoperatively, can be ambulated rapidly, and can be returned to their preoperative, long-acting insulin dosage the day after surgery. Occasionally, extensive scleral-buck­ ling surgery for retinal detachment must be done, which will result in more pain, postoperative nausea and vomiting, and a more stormy and protracted course. The so-called rainbow-insulin schedule based on urine sugar is best avoided postoperatively; supplemental regular insulin dosage should be based on additional blood sugar determinations.

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Vitrectomy is an elective procedure, and although the patient may be anxious for surgery since it holds out hope for his vision, he must be made aware that management of his whole person takes precedence. Coordination between surgeon, internist, and anesthetist are vital if the rehabilitation of the eye is to be of lasting value to the patient.

FUTURE DEVELOPMENTS

Annu. Rev. Med. 1979.30:331-338. Downloaded from www.annualreviews.org Access provided by Cambridge University on 01/28/15. For personal use only.

Technical advances in the field have continued since the initial break­ through by Machemer

(8).

Smaller instruments, better cutting action, im­

proved visualization, and refined surgical techniques have all been developed but could be improved. The use of lasers for vaporization of the vitreous and intraocular photocoagulation may add to the surgical ar­ mamentarium. More important, however, are current efforts to refine the indications of surgery and determine the proper timing of surgery. A coop­ erative clinical trial, the Diabetic Retinopathy Vitrectomy Study (DRVS), is currently being sponsored by the National Eye Institute. Now entering its third year of patient recruitment, it seeks to determine whether it is better to do immediate vitrectomy on diabetic eyes with severe vitreous hemor­ rhage (vision . 326-36 16. Diabetic Retinopathy Vitrectomy Study 1976. Manual of operations, Chapter 2. DRVS Coordinating Center. Minneapolis: Univ. Minn. 17. MandeIcorn, M. S., Blankenship, G. W., Machemer, R. 1976. Pars plana vi­ trectomy for the management of severe diabetic retinopathy. Am. J. Ophtha/­ mol. 81:561-70 18. Michels, R. G. 1978. Vitrectomy for complications of diabetic retinopathy. Arch. Ophthalmol 96:237-46 19. Blankenship, G. W., Machemer, R. 1978. Pars plana vitrectomy for man­ agement of severe diabetic retinopathy Am. J. Ophthalmol 85:553-59 20. Edelhauser, H. F., Van Hom, D. L., Aaberg, T. M. 1976. Intraocular irrigat­ ing solutions and their use for vitrec­ tomy. In Advances in Vitreous Surgery, ed. A. R. Irvine, C. O'Malley, pp. 26587. Springfield, Ill: Thomas

Vitrectomy surgery for diabetic retinopathy.

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