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

irrigation can be maintained safely through an anterior chamber cannula or bent needle placed through the limbus and in front of the IOL. Fibrin membranes can then be peeled anteriorly using a cystotome, intraocular forceps, or the vitreous cutter. Opaque debris in the anterior vitreous can also be removed safely by placing the vitreous cutter through the pars plana and behind the IOL, while illumination is provided by the microscope (Figure 5).

Dry vitrectomy is performed to obtain a specimen for culture before infusion is initiated. A small syringe is connected by a short piece of tubing to the outflow port of the vitreous cutter. The surgical assistant is asked to aspirate a small sample, typically 0.3 cc, while the cutter is active at high speed and maintained in the central cavity.

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If the infection is severe enough to opacify the cornea, a central button may be removed with a trephine. One may pre-place a Flieringa ring and proceed with an open-sky vitrectomy to remove the central vitreous debris; alternatively, a temporary keratoprosthesis can be placed for closed vitrectomy. If the irrigating cannula cannot be visualized, one safe alternative is to place an end-irrigating light pipe into the mid-vitreous cavity. When switching from a limbal to pars plana irrigation system, it is desirable to have dual sources of fluid to avoid hypotony with chamber collapse and possible hemorrhage. A gentle vitrectomy is then performed from anterior to posterior, with attempts to remove pockets of loculated, purulent matter but without efforts to shave to the vitreous base or remove all the peripheral cortical vitreous. The inflamed posterior hyaloid can be tightly adherent to

the posterior retina, and we do not recommend attempts to force its separation because of the high risk of retinal tears.

Although the classic teaching has been to do a controlled central core vitrectomy due to concerns about creating peripheral breaks in inflamed retina and also the media not being so clear, more and more people are now advocating a more aggressive approach to vitrectomy for endophthalmitis. Extensive central and peripheral vitrectomy is done followed by a silicon oil tamponade which would prevent fluid collection through any hidden break till the time the Inflammation settles and allows good visibility to treat further. Despite the poor visual prognosis of endophthalmitis surgery, more radical intervention can increase the chance of surgical success and decrease the number of additional procedures in eyes with postoperative endophthalmitis. The silicon oil also compartmentalizes the infection and being inert has less chances of causing any reaction to itself. However, though EVS advocated only 50% vitrectomy for endophthalmitis but the EVS reports that 10.5% of cases required an additional procedure within 7 days of entry into the study. In 25% of patients, a late additional procedure was required and was performed more than 7 days after study entry. At the final examination, 3% had phthisis. During the entire study, additional surgery was performed in 34% of patients. However, despite the relatively poor visual prognosis of endophthalmitis surgery, total PPV with buckling surgery, silicone tamponade, and endolaser increases the chance of surgical success and decreases the number of additional procedures in eyes with severe postoperative endophthalmitis.

In the setting of trauma, a more thorough exploration is warranted to remove any intraocular foreign bodies. If the crystalline lens has been violated, then complete removal is recommended using the vitreous cutter or fragmatome from a pars plana approach. Depending on the clinical circumstances, prophylactic intraocular antibiotics, typically in half the usual therapeutic dose, may be administered. Because of possible break down of the blood-retinal barrier, systemic antibiotics may have a role in this situation.

Bibliography

1.Alfaro DV, Pastor JC, Meredith “Post traumatic endophthalmitis” in Vitreoretinal Surgery of the injuried eye. Lippincott-Rave Publishers, 1999 pp 339-348.

2.Bernard H. Doft. The Endophthalmitis Vitrectomy Study. Clinical Trials in Ophthalmology - A Summary and Practice Guide. Peter J. Kertes and Mandi Conway. PP 97 - 112. Williams and Wilkins, 1998.

3.Brod RD, Flynn HW “Endophthalmitis management” in Retina –Vitreous-Macula. W.B. Saunders Company 1999, pp 1466-1478.

4.Chapter 123. Endophthalmitis Management by Roy D. Brod and Harry W. Flynn, Jr. In Retina, Vitreous, Macula. Edited by David R. Guyer, Lawerence A. Yannuzzi, Stanley Chang, Jerry A. Shields, W. Richard Green.

5.Ciulla TA et al. Belbitis, Early Endophthalmitis, and Late Endophthalmitis after Glaucoma-Filtering Surgery. Ophthalmology 1997;104:996-995.

6.CiullaTA, Beck AD “Blebitis, early and late endophthalmitis after glaucoma filtering surgery, Ophthalmology,104(6):986-95, 1997.

7.Cohen SM, Flynn HW, Murray TG, Smiddy WE et al. Endophthalmitis After Pars Plana Vitrectomy. Ophthalmology 1995;102:705-712.

8.Doft BH et al. Additional Procedures after the Initial Vitrectomy or Tap-Biopsy in the Endophthalmitis Vitrectomy Study. Ophthalmology 1998;105:707716.

9.Doft BH et al. Diabetes in Post-operative Endophthalmitis in the Endophthalmitis Vitrectomy Study. Arch Ophthalmol 2001;119:650-656.

10.Endogenous Fungal Infections of the Retina and Choroid. Gary and Holland. Chapter 96. In Stephen J. Ryan, Editor-in-Chief. Retina Vol. 2, 2001. Mosby.

11.Greenfield DS, “Late complications of glaucoma filtration surgery” Ophthalmology Clinics of North America (13)3,2000.

12.Greenfield DS. Late complications of Glaucoma Filtration Surgery. Ophthalmol. Clin North Am 2000;13(3).

13.Hamza HS, Loewenstein A and Haller JA. Ocular Infections: Update on therapy. Fungal Retinitis and Endophthalmitis. Ophthalmol Clin North Am 1999;12(1):89-106.

14.Infections:Updateontherapy.PeterA.Campochiaro. Ophthalmol Clin North Am 1999;12(1):83-88.

15.Johnson MW et al. The Endophthalmitis Vitrectomy Study: Relationship Between Clinical Presentation and Microbiologic Spectrum. Ophthalmology 1997;104:261-272.

16.Kattan HM, Flynn HW, Pflugfelder SC, Robertson C and Forster RK. Nosocomial Endophthalmitis Survey. Current Incidence of Infection after Intra Ocular Surgery. Ophthalmology 1991;98:227-238.

17. Kresloff MS, Castellarin AA, Zarbin MA “Endophthalmitis” Surv Ophthalmol, 43:193-224,1998.

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21.Mandelbaum S, Forster RK, “Exogenous Endophthalmitis” in Ocular infection and immunity, Mosby 1996, pp1298-1320.

22.Meredith TA, Posttraumatic Endophthalmitis, Arch Ophthalmol 117:520-521,1999.

23.Mittra RA and Miller WF. Diagnostic and Surgical Techniques Controversies in the Management of Open Globe Injuries Involving the Posterior Segment. Surv Ophthalmol 1999;44(3):215-225.

24.Mittra RA, Mieler WF, Controversies in the management of Open –Globe injuries involving the posterior segment, Surv Ophthalmol 44:215-225, 1999.

25.Mohmann CP, Heeb M, et al. Diagnosis of Infectious Endophthalmitis after Cataract by Polymerase Chain Reaction. J Catar Refrac Surg 1998;24:821826.

26.Montan PG et al. Endophthalmitis After Cataract Surgery: Risk Factors Relating to Technique and Events of the Operation and Patient History. Ophthalmology 1998; 105:2171-2177.

27.Nelson PT, Marcus DA and Vovino JA. Retinal Detachment Following Endophthalmitis. Ophthalmology 1985;92:1112-1117.

28.O’Day DM, Jones DB, Patrinely J and Elliott JH. Staphylococcus Epidermidis Endophthalmitis Visual Outcomes Following Non-invasive Therapy. Ophthalmology 1982;89:354-360.

29.Ocular Infection and Immunity. Editors: J. S. Pepose, Garry N. Holland and Kirk R. Wilhelmus. Mosby 1996. Chapter 91. Endogenous Fungal Endophthalmitis. Author: Thomas H. Petttit, John E. Edwards, Jr., Eric P. Purdy and John D. Bullock.

Guyer, Lawrence A. Yannuzzi, Stanley Chang, Jerry A. Shields, W. Richard Green. Chapter 64. Fungal Diseases by Neal D. Brourman and Mark

S. Blumenkranz.

33.Roth DB and Flynn HW, Jr. Antibiotic Selection in the Treatment of Endophthalmitis: The Significance of Drug Combinations and Synergy. Surv Ophthalmol 1997; 41 (5): 395-401.

34.Shields MB, “Filtering Surgery” in Text book of

Glaucoma, Williams and Wilkins, 504-537,1998.

35.Sternberg P, Jr. and Martin DF. Management of Endophthalmitis in the Post Endophthalmitis Vitrectomy Study Era. Arch Ophthalmol 2001;119(5):754-5.

36.Sternberg P, Martin DF, “Management of endophthalmitis in the post-endophthalmitis vitrectomy study era” Arch ophthalmol 199:754-755,2001.

37.The Endophthalmitis Vitrectomy Study Group. Microbiologic factors and visual in the endophthalmitis vitrectomy study. Am J Ophthalmol 1996;122(6):830-46.

38.The Endophthalmitis Vitrectomy Study Group. Results of the Endophthalmitis Vitrectomy Study. A Randomized Trial of Immediate Vitrectomy and of Intravitreous Antibiotics for the Treatment of Post-operative Bacterial Endophthalmitis. Arch Ophthalmol 1995;11.

39.Vitrectomy for infectious Endophthalmitis. Travis

A.Merredith. Chapter 135. In Stephen J. Ryan, Editor-in-Chief. Retina Vol. 2, 2001. Mosby.

40.Vitreoretinal Surgery of the Injured Eye. Editors:

D.Virgil Alfaro III and Peter E. Liggette. 1999 Lippincott-Raven. Chapter 27 Pathogenesis of Post-Traumatic Bacterial Endophthalmitis. Authors: Eugene W. M. Ng and D. Virgil Alfaro III.

41.Vitreoretinal Surgery of theInjured Eye. Editors:

D.Virgil Alfaro III and Peter E. Liggette. 1999 Lippincott-Raven. Chapter 28 Post Traumatic Endophthalmitis. Authors: D. Virgil Alfaro III, Carlos Pasture, Travis Merideth.

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43.Meisler DM, Palestine AG, Vastine DW, et al. Chronic Propionibacterium endophthalmitis after extracapsular cataract extraction and intraocular lens implantation. Am J Ophthalmol 102:733-739, 1986.

44.Endophthalmitis Study Group, European Society of Cataract & Refractive Surgeons. Prophylaxis of postoperative endophthalmitis following cataract surgery: results of the ESCRS multicenter study and identification of risk factors. J Cataract Refract Surg. 2007 Jun;33(6):978-88.

45.ESCRS study of prophylaxis of postoperative endophthalmitis after cataract surgery: Preliminary report of principal results from a European multicenter study. J Cataract Refract Surg. 2006 Mar;32(3):40710.

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47.EndophthalmitisVitrectomy Study Group. Results of the Endophthalmitis Vitrectomy Study; a randomized trial of immediate vitrectomy and of intravenous antibiotics for the treatment of postoperative bacterial endophthalmitis. Arch Ophthalmol 1995; 113:1479–1496.

48.Su ̈leyman Kaynak, , F. HakanO ̈ner. Surgical management of postoperative endophthalmitis: Comparison of 2 techniques J Cataract Refract Surg 2003; 29:966–969.

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Refractive Surgery Today. April 2007. Kaynak S, Oner F H, Kocak N. et al; J Cataract Refract Surg 2003; 29:966–969 © 2003 ASCRS.

Introduction

Even prior to the invention of the ophthalmoscope in 1851, nutritional deficiencies were known as important causes of vision loss while many case reports and series studies described even by the early part of the 20th century the association of nutritional deficiencies to visual function and eye diseases.1

However, it has only been the last decades that large population-based studies provided significant evidence that nutrition plays an important role to eye health. An association of nutritional factors to variety of retinal diseases has been made suggesting that nutritional supplementation or specific dietary modifications may potentially influence the course of these diseases. According to these studies nutrition seems to play an essential role to age-related macular degeneration (AMD), diabetic retinopathy and retinal vascular diseases.

Evidence concerning the role of nutritional factors for these diseases is assessed in this chapter.

Nutrition and Age-Related

Macular Degeneration

Age-related macular degeneration (AMD) is a leading cause of blindness.2

The prevalence of AMD and its resultant morbidity is likely to increase in the future. Changes in nutritional behavior such as greater intake of dietary antioxidants may contribute to lower future rates of AMD incidence and progression according to forecasting models of incidence of AMD.3

Currently there are three main theories for retinal changes associated with non-exudative stages of AMD: the oxidative stress theory, the choroidal circulation theory and the degeneration of Bruch’s membrane theory. Nutrition factors may play a role in all of these theories.4

The oxidative stress hypothesis for the etiology of AMD is based on the breakdown of protective antioxidant systems within the retina, possibly induced or influenced in some cases by insufficient diet.

The choroidal circulation theory hypothesize that removal of waste materials and the supply of nutritional substances as well as oxygen exchange to the neural retina is impaired due to choroidal vascular alterations that lead to AMD alterations.

Finally, age-dependent changes in Bruch’s membrane are considered to compromise transport of nutrients and metabolic substances from and to the RPE. Consequently it is considered that degeneration and thickening of Bruch’s membrane initiate or at least contribute to AMD.

Several studies have demonstrated that various dietary components may affect retinal degeneration, and are discussed in this section.5, 6

Vitamin C

L-ascorbic acid, or vitamin C, is a watersoluble antioxidant that has been shown to react directly with hydroxyl radicals, superoxide and singlet oxygen. The nutritional supply of vitamin C comes mainly from fruits and uncooked vegetables. Those particularly rich in vitamin C include kiwi, guava, melons, mango, citrus fruits, cabbage and Brussels sprouts7 (Figure 1).

It has been hypothesized that vitamin C has an important role as a retinal antioxidant due to is high concentration in the retina. However, epidemiological studies did not provide any clear evidence of relation between vitamin C consumption and AMD consumption.

Data from the first National Health and Nutrition Examination Survey did not demonstrate clearly an inverse association of vitamin C with AMD.8

Figure 1: Many fruits like kiwi, guava, melons, mango, citrus fruits, cabbage and brussels sprouts are particularly rich in vitamin C.

In the Eye Disease Case-Control Study Group vitamin C consumption was not associated with a statistically significant reduced risk for AMD, although a possibly lower risk for AMD was suggested among those with higher intake of vitamin C, particularly from foods.9

The Beaver Dam Eye Study found no associations between vitamin C intake and the 5-year incidence of early AMD.10

In the Blue Mountains Eye Study authors reported that increasing total vitamin C intake from diet and supplements, was associated with an increased risk of incident early AMD after the 5-year follow-up,11 however this association could not be confirmed after the 10-year follow-up.12

Some studies found that combination of all antioxidant nutrients that include vitamin C might have a protective effect towards AMD.

A protective effect regarding incidence and progression of AMD by combination of anti-

oxidant nutrients that include vitamin C was found in the Age Related Eye Disease Study (AREDS)13 and Rotterdam Study.14 However, the Blue Mountains Eye Study12 was unable to confirm the protective effect shown on the above-mentioned studies.

Vitamin E

In 1922, vitamin E was first discovered as an essential dietary factor for the reproduction in rats.15 After the isolation of pure vitamin E from cottonseed oil, the name tocopherol was proposed,fromtheGreek,tokos(offspring)and pherein (to bear).16 The richest food sources of vitamin E are certain oils, such as wheat germ oil, sunflower oil and sunflower seeds, almonds, peanut butter, wheat germ and margarine (Figure 2). Vitamin E is essential for maintaining a healthy retina. Patients with inherited abetalipoproteinemia, a disorder in whichfat-solublevitamins,includingvitaminE, cannot be sufficiently absorbed, develop retinal

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degeneration. Supplementation of vitamin E, however, can prevent retinal degeneration in this pathological condition.17, 18

Vitamin E is thought to function as an antioxidant and appears to protect polyunsaturated fatty acids from oxidative damage. A-tocopherol is the dominant variant of vitamin E in human retina with highest concentration in the retinal pigment epithelium (RPE).19 Photoreceptor outer segments are rich in polyunsaturated fatty acids, and therefore it has been hypothesized that α-tocopherol might play a significant role as an antioxidant in the retina. Several animal studies have demonstrated the antioxidant effect of vitamin E in retina.20-22 However, the current findings of the epidemiological studies on a possible association between increasing total vitamin E intake and AMD risk also are inconsistent with studies that have reported a protective effect on AMD progression13 or development,10,14 no effect9,11,23-26 or a negative effect.12 More precisely, Taylor et al in a large

study on the role of vitamin E that included about 1000 participants concluded that daily supplement with vitamin E does not prevent the development or progression of early or later stages of age related macular degeneration.26 This is probably the only large-scale study that investigated the role of vitamin E on AMD as a sole supplement without combining other antioxidants.

In the Blue Mountains Eye Study at 10 years follow-up higher intakes of total vitamin E predicted late AMD.12 This is the only study reporting a harmful effect of dietary vitamin E on AMD risk.

The multicenter Eye Disease Case-Control Study vitamin E consumption was not associated with a statistically significant reduced risk for AMD.9

In the in the Rotterdam Study intake of vitamin E was associated with a substantially reduced risk of AMD in elderly persons.14

The AREDS study demonstrated reduction for the development of advanced AMD with a combination of antioxidants containing vitamin E.13 However, no conclusion, can be drawn for the effect of vitamin E alone.

Carotenoids

Thereisincreasingevidencethatantioxidant properties of carotenoids have a protective role in the retina. The three major carotenoids that have been related to AMD are lutein, zeaxanthin and β-carotene.

β-Carotene

β-Carotene,ahydrocarboncarotenoid,isone of the major carotenoid precursors of vitamin A and it has been shown to be an effective antioxidant.27,28 Beta-carotene is a quencher of singlet oxygen radicals, in contrast to vitamin A, which has only a very small capacity to scavenge free radicals. In the eye it is mostly found in the retinal pigment epithelium/ choroid and not in the overlying retina.29

Dietary sources of β-Carotene are principally marigold flowers, dark green vegetables and colored fruit. Typical examples include carrots, pumpkins, spinach, beans, apricots and peaches 30,31 (Figure 3).

Its been advocated that low serum levels of carotenoids are related to a higher risk of AMD32 and higher serum levels to a lower risk of different stages of AMD.33,34