The aminoglycosides have a narrow range of safety for intravitreal use during endophthalmitis treatment. Because vancomycin covers gram-positive organisms causing greater than 90% of postoperative endophthalmitis and because aminoglycosides add risk of inadvertent retinal toxicity, the authors recommend intravitreal ceftazidime (instead of amikacin) for coverage of gram-negative organisms when treating clinically diagnosed endophthalmitis (Table 26–9).

Endophthalmitis may also occur following suture removal or late-onset keratitis involving the wound.104–106 The removal of 10-0 nylon sutures may allow entry of organisms in sufficient quantity to cause intraocular infection. With the trend to sutureless cataract surgery, these cases are now becoming less common. However, delayed-onset keratitis associated with a previous cataract wound may be associated with breakdown of the wound allowing entry of organisms. These keratitis-associated cases are often caused by more virulent organisms and generally have a poor visual prognosis.104 Strictly speaking, the EVS results apply only to cataract and secondary IOL surgery, but the EVS antibiotic treatment regimen may be used for other postoperative endophthalmitis categories.

DELAYED-ONSET ENDOPHTHALMITIS

Delayed-onset or chronic postoperative endophthalmitis occurs weeks to months after cataract surgery and is not specific to phacoemulsification. These patients present with progressive intraocular inflammation and a chronic indolent course. The most frequent reported organisms include Propionibacterium acnes, Staphylococcus epidermidis, and fungi.

The clinical features of delayed-onset endophthalmitis observed on slit-lamp examination will usually help to distinguish between these causative organisms. P. acnes cases are characterized by the presence of a large white intracapsular plaque associated with chronic granulomatous inflammation (Fig. 26–9).107 These eyes may have large keratic precipitates on the corneal endothelium and beaded fibrin strands in the anterior chamber. One author (L.J.) has recently encountered a bilateral case, with earlieronset iritis, eventually mimicking granulomatous uveitis, occurring 1 year after cataract surgery. In cases caused by S. epidermidis, chronic progressive vitritis is a typical feature with no white intracapsular plaque. In cases caused by fungi, the anterior chamber may often be relatively quiet, but linear, white strands resembling “a string of pearls” may be present in the anterior vitreous indicating the presence of Candida organisms (Fig. 26–10). Because these organisms generally replicate more slowly, they are often resistant to medical therapy alone.79

FIGURE 26–9 Delayed-onset endophthalmitis caused by Propionibacterium acnes occurring 4 months after cataract surgery and showing a white intracapsular plaque with moderate intraocular inflammation. (From Regillo CD, Brown GC, Flynn HW Jr. Vitreoretinal Disease: The Essentials. New York: Thieme; 1999:564, Fig. 35–2.)

In delayed-onset endophthalmitis, pars plana vitrectomy is commonly recommended to establish the correct diagnosis by culture, remove offending organisms, and remove areas of localized white intracapsular plaque when present. Recurrent or resistant infection despite vitrectomy may require removal of the entire capsular bag and the intraocular lens.105,106

FIGURE 26–10 Delayed-onset endophthalmitis caused by Candida parapsilosis occurring 6 weeks after cataract surgery and characterized by a string of pearls and white infiltrates in the anterior vitreous. (From Regillo CD, Brown GC, Flynn HW Jr. Vitreoretinal Disease: The Essentials. New York: Thieme; 1999:564, Fig. 35–3.)

SUPRACHOROIDAL

EFFUSION/HEMORRHAGE

(ALSO SEE CHAPTER 8)

Suprachoroidal effusion/hemorrhage (SCH) may occur during or after any form of intraocular surgery. Transient hypotony is a common feature during or after all intraocular surgery that may lead to a choroidal effusion followed by rupture of long or short posterior ciliary arteries with subsequent frank hemorrhage.108 Obstruction of vortex veins during scleral buckling procedure is another mechanism that may predispose to choroidal effusion and/or SCH.109 Suprachoroidal hemorrhage may be limited to one or two quadrants or can be massive (360degree suprachoroidal hemorrhage), resulting in extrusion of intraocular contents or forcing retinal surfaces centrally into apposition. Reported risk factors for SCH include glaucoma, aphakia, myopia, advanced age, arteriosclerotic cardiovascular disease, hypertension, and intraoperative tachycardia.110–117

MANAGEMENT AND COURSE OF SCH

Intraoperative management strategies are controversial. Most authors recommend immediate closure of ocular incisions, removal of vitreous prolapse into the wound if possible, and drainage of SCH if continued high pressure is present.110–113 Intraoperative SCH drainage is almost never complete but is usually successful in lowering IOP and creating a scleral opening for continued postoperative drainage.

In cases of suprachoroidal effusion due to hypotony, the hypotony must be managed to prevent continued effusion. If the effusions enlarge and touch, the retina may stick together, causing significant damage. The effusions should therefore be drained when the effusions begin to “kiss.” The timing of the secondary surgical intervention for SCH remains a controversial area, but most surgeons recommend observation for 7 to 14 days to allow liquefaction of the SCH. There are no randomized prospective clinical trials addressing this timing issue because of the multiple ocular diseases in these patients and the complex variables present prior to the occurrence of massive SCH. The surgical goals of secondary surgical intervention for massive SCH include drainage of liquefied SCH, removal of prolapsed vitreous by vitrectomy, and management of rhegmatogenous retinal detachment if present using a scleral buckle and/or intraocular gas tamponade (Fig. 26–11).110–115 The use of perfluorocarbon liquids has also been advocated.118 Likewise some authors have recommended high-dose systemic and topical corticosteroids during the immediate postoperative

period.113 Risk factors for poor visual outcome include concurrent retinal detachment and more than two quadrants of SCH involvement.112

One author (L.J.) has a strong preference for nonintervention in SCH, and follows patients closely, offering surgery when resolution is slow (>3 weeks) or when complications such as glaucoma, traction, rhegmatogenous retinal detachment, or vitreous hemorrhage occur.

NEEDLE PENETRATION OF THE GLOBE

In recent years, cataract surgery under topical anesthesia has become more popular. This anesthesia obviates the concern about needle penetration during administration of retrobulbar or peribulbar anesthesia. However, many surgeons prefer traditional anesthesia, which may result in this rare complication.

The Atkinson retrobulbar block employs an elevated and adducted eye position to place the needle tip into the muscle cone adjacent to the optic nerve. Because of the risk of needle entry into either the globe or the optic nerve, many ophthalmologists switched to using a peribulbar block with the eye position straight ahead and larger volumes of anesthetic to fill the orbit.119

Factors predisposing to needle penetration of the globe include axial high myopia, posterior staphyloma, previous scleral buckling surgery, and poor patient cooperation with the injection.120–122 Another more recent risk factor is injection of the anesthetic by nonophthalmologists (anesthesiologists and nurse anesthetists) who may have limited experience in providing this method of anesthesia.

When needle entry is suspected, indirect ophthalmoscopy is recommended to evaluate the posterior segment. The visual acuity and IOP should be documented. If marked IOP elevation occurs, one should consider anterior chamber paracentesis. Ocular hypotony may also indicate that penetration has occurred.

Early management of posterior segment needle entry wounds is controversial. Most authors recommend prompt laser treatment or cryopexy to visible retinal perforation sites, but blood or lens opacities may preclude a satisfactory view of the area. The patient can be followed with serial echography examination until clearing of vitreous hemorrhage occurs. If retinal detachment occurs, early intervention is recommended. Any elective surgery should be postponed.

The visual prognosis is usually dependent on the presence or absence of retinal detachment and damage inflicted initially to the posterior pole. In one report, retinal breaks without retinal detachment had a much better visual prognosis than eyes complicated by retinal detachment. In the former category, seven

A

C

of nine cases without retinal detachment achieved 20/50 or better visual acuity, whereas in the latter category only 2 of 14 retinal detachment cases achieved 20/400 or better visual acuity.120

ROLE OF THE POSTERIOR

SEGMENT SURGEON

B

FIGURE 26–11 Management of massive suprachoroidal hemorrhage. (A) Needle infusion into anterior chamber and scleral drainage of suprachoroidal hemorrhage. (B) Anterior vitrectomy and continued scleral drainage. (C) Posterior vitrectomy and continued scleral drainage. (From Regillo CD, Brown GC, Flynn HW Jr. Vitreoretinal Disease: The Essentials. New York: Thieme; 1999:565, Figs. 35–4A,B,C.)

outcome is highly dependent on their judgment and surgical skills. A sympathetic and cooperative team approach with the anterior segment surgeon will help alleviate patient anxiety during this phase of management.

CONCLUSION

Retina-vitreous specialists have a critical role in the management of many of the complications of phacoemulsification and cataract surgery. Final visual

The anterior segment surgeon should have a good working relationship with the retinal specialist. If serious intraoperative or postoperative complications

occur, and the posterior segment has been violated, a retinal consult will add valued management options. Early referral and management may prevent sightthreatening outcomes.

ACKNOWLEDGMENTS

The first author (L.J.) acknowledges the remarkable work of his coauthors (H.W.F. and W.E.S.) in the publication of many original articles and several chapters in this field. They graciously permitted the reorientation of their published materials for this chapter under combined authorship.

REFERENCES

1.Prevent Blindness America. Vision problems in the US. In: Prevent Blindness America. New York: Prevent Blindness America Publishers; 1994:8–10.

2.Leaming DV. Practice styles and preferences of ASCRS members: 1994 survey. J Cataract Refract Surg 1995;21:378–385.

3.Weinstein GW, Charlton JF, Esmer E. The “lost lens”: a new surgical technique using the Machemer lens. Ophthalmic Surg 1995;26:156–159.

4.Aaberg TM Jr, Rubsamen PE, Flynn HW Jr, Chang S, Mieler WF, Smiddy WE. Dropped nuclei and giant retinal tears as a complication of cataract surgery. Am J Ophthalmol 1997;124:222–226.

5.Irvine SR, Irvine AR. Lens-induced uveitis and glaucoma. Arch Ophthalmol 1958;60:829–840.

6.Epstein DL. Diagnosis and management of lensinduced glaucoma. Ophthalmology 1982;89:227–230.

7.Blodi BA, Flynn HW Jr, Blodi CF, et al. Retained nuclei after cataract surgery. Ophthalmology 1992;99: 41–44.

8.Vilar N, Flynn HW Jr, Smiddy WE, Murray TG, Davis JL, Rubsamen PE. Removal of retained lens fragments after phacoemulsification reverses secondary glaucoma and restores visual acuity. Ophthalmology 1997;104:787–792.

9.Borne MJ, Tasman W, Regillo C, et al. Outcomes of vitrectomy for retained lens fragments. Ophthalmology 1996;103:971–976.

10.Gilliland GD, Hutton WL, Fuller DG. Retained intravitreal lens fragments after cataract surgery. Ophthalmology 1992;99:1263–1269.

11.Kim JE, Flynn HW Jr, Smiddy WE, et al. Retained lens fragments after phacoemulsification. Ophthalmology 1994;101:1827–1832.

12.Hutton WL, Snyder WB, Vaiser A. Management of surgically dislocated intravitreal lens fragments by pars plana vitrectomy. Ophthalmology 1978;85:176– 189.

13.Lambrou FH Jr, Steward MW. Management of dislocated lens fragments after cataract surgery. Ophthalmology 1992;99:1260–1262.

14.Fastenberg DM, Schwartz PL, Shakin JL, et al. Management of dislocated nuclear fragments after phacoemulsification. Am J Ophthalmol 1991;112:535–539.

15.Kapusta MA, Chen JC, Lam WC. Outcomes of dropped nucleus during phacoemulsification. Ophthalmology 1996;103:1184–1187.

16.Liu KR, Peyman GA, Chen MS, Chang KB. Use of high-density vitreous substitutes in the removal of posteriorly dislocated lenses or intraocular lenses. Ophthalmic Surg 1991;22:503–507.

17.Greve MDJ, Peyman GA, Mehta NJ, Millsap CM. Use of perfluoroperhydrophenanthrene in the management of posteriorly dislocated crystalline and intraocular lenses. Ophthalmic Surg 1993;24:593–597.

18.Lewis H, Blumenkranz MS, Chang S. Treatment of dislocated crystalline lens and retinal detachment with perfluorocarbon liquids. Retina 1992;12;299–305.

19.Brod RD, Flynn HW Jr, Clarkson JC, Blankenship GW. Management options for retinal detachment in the presence of a posteriorly dislocated intraocular lens. Retina 1990;10:50–56.

20.Smiddy WE, Flynn HW Jr, Kim JE. Retinal detachment in patients with retained lens fragments or dislocated posterior chamber intraocular lenses. Ophthalmic Surg Lasers 1996;27:856–861.

21.Malbran ES, Malbran E Jr, Negri I. Lens guide suture for transport and fixation in secondary IOL implantation after intracapsular extraction. Ophthalmology 1986;9:151–160.

22.Lindquist TD, Agapitos PJ, Lindstrom RL, Lane SS, Spigelman AV. Transscleral fixation of posterior chamber intraocular lenses in the absence of capsular support. Ophthalmic Surg 1989;20:769–775.

23.Smiddy WE, Sawusch MR, O’Brien TP, Scott DR, Huang SS. Implantation of scleral-fixated posterior chamber intraocular lenses. J Cataract Refract Surg 1990;16:691–696.

24.Grehn F, Sundmacher R. Fixation of posterior chamber lenses by transscleral sutures: techniques and preliminary results [letter]. Arch Ophthalmol 1989; 107:954–955.

25.Lewis JS. Sulcus fixation without flaps. Ophthalmology 1993;100:1346–1350.

26.McCluskey P, Harrisberg B. Long-term results using scleral-fixated posterior chamber intraocular lenses. J Cataract Refract Surg 1994;20:34–39.

27.Teichmann KD. Pars plana fixation of posterior chamber intraocular lenses. Ophthalmic Surg 1994; 25:549–553.

28.Tomikawa S, Hara A. Simple approach to secondary posterior chamber intraocular lens implantation in patients without a complete posterior lens capsule support. Ophthalmic Surg 1995;26:160–163.

29.Vajpayee RB, Angra SK, Sandramouli S, Rewari R. Direct scleral fixation of posterior chamber intraocular lenses using a special needle-holder. Ophthalmic Surg 1992;23:383–387.

30.Mittelviefhaus H, Wiek J. A refined technique of transscleral suture fixation of posterior chamber

lenses developed for cases of complicated cataract surgery with vitreous loss. Ophthalmic Surg 1993;24: 698–701.

31.Lyle WA, Jin JC. Secondary intraocular lens implantation: anterior chamber vs posterior chamber lenses. Ophthalmic Surg 1993;24:375–381.

32.Regillo CD, Tidwell J. A small-incision technique for suturing a posterior chamber intraocular lens. Ophthalmic Surg Lasers 1996;27:473–475.

33.Smiddy WE, Flynn HW Jr. Managing retained lens fragments and dislocated posterior chamber IOL’s after cataract surgery. Focal Points 1996;14:1–14.

34.Ross WH. Management of dislocated lens fragments after phacoemulsification surgery. Can J Ophthalmol 1996;31:234–240.

35.Stark WJ, Worthen DM, Holladay JT, et al. The FDA report on intraocular lenses. Ophthalmology 1983;90: 311–317.

36.Smith SG, Lindstrom RL. Malpositioned posterior chamber lenses: etiology, prevention and management. Am Intraocular Implant Soc J 1985;11:584–591.

37.Murphy GE. Traumatic dislocation of a shearing lens 31 months after implantation. Ophthalmic Surg 1983;14:53–54.

38.Smiddy WE, Flynn HW Jr. Management of dislocated posterior chamber intraocular lenses. Ophthalmology 1991;98:889–894.

39.Flynn HW Jr, Buus D, Culbertson WW. Management of subluxated and posteriorly dislocated intraocular lenses using pars plana vitrectomy instrumentation. J Cataract Refract Surg 1990;16:51–56.

40.Capone A Jr, Mandell BA, Aaberg TM Sr, Sternberg P Jr, Lambert HM, Lopez PF. Contemporary vitreoretinal surgical management of posteriorly dislocated intraocular lenses. Proceedings of the Symposium on Retina and Vitreous, New Orleans Academy of Ophthalmology, 1993:271–281.

41.Panton RW, Sulewski ME, Parker JS, Panton PJ, Stark WJ. Surgical management of subluxed posteriorchamber intraocular lenses. Arch Ophthalmol 1993; 111:919–926.

42.Smiddy WE, Flynn HW Jr. Management options for posteriorly dislocated intraocular lenses. Ophthalmic Pract 1994;12:72–77.

43.Shakin EP, Carty JB Jr. Clinical management of posterior chamber intraocular lens implants dislocated in the vitreous cavity. Ophthalmic Surg Lasers 1995;26: 529–534.

44.Smiddy WE, Ibanez GV, Alfonso E, Flynn HW Jr. Surgical management of dislocated intraocular lenses. J Cataract Refract Surg 1995;21:64–69.

45.Mello MO Jr, Scott IU, Smiddy WE, Flynn HW Jr, Feuer W. Surgical management and outcomes of dislocated intraocular lenses. Ophthalmology 2000;107: 62–67.

46.Batlan SJ, Dodick JM. Explanation of a foldable silicone intraocular lens. Am J Ophthalmol 1996;122: 270–272.

47.Schneiderman TE, Johnson MW, Smiddy WE, Flynn HW Jr, Bennett SR, Central HL. Surgical management of dislocated plate haptic silicone posterior chamber intraocular lenses. Am J Ophthalmol 1997;123:629– 635.

48.Ellerton CR, Rattigan SM, Chapman FM, Chitkara DK, Smerdon DL. Secondary implantation of openloop, flexible, anterior chamber intraocular lenses. J Cataract Refract Surg 1996;22:951–954.

49.Jacobi KW, Krey H. Surgical management of intraocular lens dislocation into the vitreous: case report. Am Intraocular Implant Soc J 1983;9:58–59.

50.Brockman EB, Franklin RM, Kaufman HE. Visual disability resulting from a dislocated intraocular lens. J Cataract Refract Surg 1993;19:312–313.

51.Sinskey RM. Posterior chamber implant removal with or without replacement. Cataract 1983;1:8–10.

52.Stark WJ, Bruner WE, Martin NF. Management of subluxed posterior-chamber intraocular lenses. Ophthalmic Surg 1982;13:130–133.

53.Eifrig DE. Two principles for repositioning intraocular lenses. Ophthalmic Surg 1986;17:486–489.

54.Allara RD, Weinstein GW. A new surgical technique for managing sunset syndrome. Ophthalmic Surg 1987;18:811–814.

55.McCannel MA. A retrievable suture idea for anterior uveal problems. Ophthalmic Surg 1976;7:98–103.

56.Sternberg P Jr, Michels RG. Treatment of dislocated posterior chamber intraocular lenses. Arch Ophthalmol 1986;104:1391–1393.

57.Lyons CJ, Steele AD. Report of a repositioned posteriorly dislocated intraocular lens via pars plicata sclerotomy. J Cataract Refract Surg 1990;16:509–511.

58.Moretsky SL. Suture fixation technique for subluxated posterior chamber IOL through stab wound incision. Am Intraocular Implant Soc J 1984;10:477–480.

59.Insler MS, Mani H, Peyman GA. A new surgical technique for dislocated posterior chamber intraocular lenses. Ophthalmic Surg 1988;19:480–481.

60.Girard LJ, Nino N, Wesson M, Maghraby A. Scleral fixation of a subluxated posterior chamber intraocular lens. J Cataract Refract Surg 1988;14:326–327.

61.Chan CK. An improved technique for management of dislocated posterior chamber implants. Ophthalmology 1992;99:51–57.

62.Campo RV, Chung KD, Oyakawa RT. Pars plana vitrectomy in the management of dislocated posterior chamber lenses. Am J Ophthalmol 1989;108:529–534.

63.Smiddy WE. Dislocated posterior chamber intraocular lens: a new technique of management. Arch Ophthalmol 1989;107:1678–1680.

64.Koch DD. New optic hole configuration for iris fixation of posterior chamber lenses. Arch Ophthalmol 1988;106:163–164.

65.Nabors G, Varley MP, Charles S. Ciliary sulcus suturing of a posterior chamber intraocular lens. Ophthalmic Surg 1990;21:263–265.

66.Friedberg MA, Pilkerton AR. A new technique for repositioning and fixating a dislocated intraocular lens. Arch Ophthalmol 1992;110:413–415.

67.Maguire AM, Blumenkranz MS, Ward TG, Winkelman JZ. Scleral loop fixation for posteriorly dislocated intraocular lenses. Arch Ophthalmol 1991;109: 1754–1758.

68.Lawrence FC II, Hubbard WA. “Lens lasso” repositioning of dislocated posterior chamber intraocular lenses. Retina 1994;14:47–50.

69.Bloom SM, Wyszynski RE, Brucker AJ. Scleral fixation suture for dislocated posterior chamber intraocular lens. Ophthalmic Surg 1990;21:851–854.

70.Anand R, Bowman RW. Simplified technique for suturing dislocated posterior chamber intraocular lens to the ciliary sulcus. Arch Ophthalmol 1990;108: 1205–1206.

71.Chang S, Coll GE. Surgical techniques for repositioning a dislocated intraocular lens, repair of iridodialysis, and secondary intraocular lens implantation using innovative 25-gauge forceps. Am J Ophthalmol 1995;119:165–174.

72.Lewis H, Sanchez G. The use of perfluorocarbon liquids in the repositioning of posteriorly dislocated intraocular lenses. Ophthalmology 1993;100:1055–1059.

73.Fanous MM, Friedman SM. Ciliary sulcus fixation of a dislocated posterior chamber intraocular lens using liquid perfluorophenanthrene. Ophthalmic Surg 1992;23:551–552.

74.Smiddy WE, Flynn HW Jr. Dislocated IOL repositioning technique [letter]. Arch Ophthalmol 1993;111: 161–162.

75.Murray TG, Abrams GW. Pars plana vitrectomy in the management of dislocated posterior chamber lenses [letter]. Am J Ophthalmol 1990;109:362.

76.Pavlin CJ, Rootman D, Arshinoff S, Harasiewicz K, Foster FS. Determination of haptic position of transsclerally fixated posterior chamber intraocular lenses by ultrasound biomicroscopy. J Cataract Refract Surg 1993;19:573–577.

77.McDermott ML, Puklin JE. Pars plana cicatrization of sewn-in posterior chamber intraocular lens haptics. Ophthalmic Surg Laser 1997;28:239–240.

78.Duffey RJ, Holland EJ, Agapitos PJ, Lindstrom RL. Anatomic study of transsclerally sutured intraocular lens implantation. Am J Ophthalmol 1989;108:300– 309.

79.Flynn HW Jr, Brod RD, Pflugfelder SC, Miller D. Endophthalmitis management. In: Tasman W, Jaeger E, eds. Duane’s Clinical Ophthalmology. Vol. 6. St. Louis: CV Mosby; 1994:1–22.

80.Scott IU, Flynn HW Jr, Feurer W. Endophthalmitis associated with secondary intraocular lenses. Ophthalmology 1995;102:1925–1931.

81.Cohen SM, Flynn HW Jr, Murray TG, Smiddy WE, and the Postvitrectomy Endophthalmitis Study Group. Endophthalmitis after pars plana vitrectomy. Ophthalmology 1995;102:705–712.

82.Kangas TA, Greenfield PS, Flynn HW Jr, Parrish RK, Palmberg PF. Delayed-onset endophthalmitis associated with conjunctival filtering blebs. Ophthalmology 1997;104:746–752.

83.Aaberg TM Jr, Flynn HW Jr, Newton J. Nosocomial endophthalmitis survey: a 10-year review of incidence and outcomes. Ophthalmology 1998;105:1004– 1010.

84.Thompson WS, Rubsamen PE, Flynn HW Jr, Schiffman J, Cousins SW. Endophthalmitis following penetrating trauma: risk factors and visual acuity outcomes. Ophthalmology 1995;102:1696–1701.

85.Barr CC. Prognosis factors in corneoscleral lacerations. Arch Ophthalmol 1983;101:919–924.

86.Boldt HC, Pulido JS, Blodi CF, Folk JC, Weingeist TA. Rural endophthalmitis. Ophthalmology 1989;967: 1722–1726.

87.Donahue SP, Kowalski RP, Jewart BH, Friberg TR. Vitreous cultures in suspected endophthalmitis: biopsy or vitrectomy? Ophthalmology 1993;100:452–455.

88.Joondeph BC, Flynn HW Jr, Miller D, et al. A new culture method for infectious endophthalmitis. Arch Ophthalmol 1989;107:1334–1337.

89.Speaker MG, Milch FA, Shah MK, et al. Role of external bacterial flora and the pathogenesis of acute postoperative endophthalmitis. Ophthalmology 1991;98: 639–650.

90.Bannerman TL, Rhoden DL, McAllister SK, et al. The source of coagulase-negative staphylococci in the Endophthalmitis Vitrectomy Study: a comparison of eyelid and intraocular isolates using pulsed-field gel electrophoresis. Arch Ophthalmol 1997;115:357–361.

91.The Endophthalmitis Vitrectomy Study Group. A randomized trial of immediate vitrectomy and of intravenous antibiotics with treatment of postoperative bacterial endophthalmitis: results of the Endophthalmitis Vitrectomy Study. Arch Ophthalmol 1995; 113:1479–1496.

92.Han DP, Wisniewski SR, Wilson LA, et al. Spectrum and susceptibilities of microbiologic isolates in the Endophthalmitis Vitrectomy Study. Am J Ophthalmol 1996;122:1–17.

93.The Endophthalmitis Vitrectomy Study Group. Microbiologic factors in visual outcomes in the Endophthalmitis Vitrectomy Study. Am J Ophthalmol 1996; 122:830–846.

94.Johnson MW, Doft BH, Kelsey SF, et al. Relationship between clinical presentation and microbiologic spectrum: the Endophthalmitis Vitrectomy Study. Ophthalmology 1997;104:261–272.

95.Mao LK, Flynn HW Jr, Miller D, Pflugfelder SC. Endophthalmitis caused by Staphylococcus aureus. Am J Ophthalmol 1993;116:584–589.

96.Flynn HW Jr, Meredith TA. Interpretation of EVS results [letter]. Arch Ophthalmol 1996;114:1027–1028.

97.Peyman GA. A different point of view [editorial]. The Endophthalmitis Vitrectomy Study. Arch Soc Espanola Oftalmol 1996;3:205–207.

98.Davis JL. Intravenous antibiotics for endophthalmitis [editorial]. Am J Ophthalmol 1996;122:724–726.

99.El-Massry A, Meredith TA, Aguilar HE, et al. Aminoglycoside levels in the rabbit vitreous cavity after intravenous administration. Am J Ophthalmol 1996; 122:684–689.

100.Meredith TA, Aguilar HE, Shaarawy A, et al. Vancomycin levels in the vitreous cavity after intravenous administration. Am J Ophthalmol 1995;119: 774–778.

101.Stonecipher KG, Ainbinder DI, Maxwell DP, et al. Infectious endophthalmitis: a review of 100 cases. Ann Ophthalmol 1994;26:108–115.

102.Axer-Siegel R, Stiebel-Kalish H, Rosenblatt I, et al. Cystoid macular edema after cataract surgery with intraocular vancomycin. Ophthalmology 1999;106: 1660–1664.

103.Alfonso EC, Flynn HW Jr. Controversies in endophthalmitis prevention: the risk for emerging resistance to vancomycin. Arch Ophthalmol 1995;113:1369– 1370.

104.Gritz DC, Cevallos AV, Smolin G, Whitcher JP. Antibiotic supplementation of intraocular irrigating solutions: an in vitro model of antibacterial action. Ophthalmology 1996;103:1204–1209.

105.Winward KE, Pflugfelder SC, Flynn HW Jr, et al. Postoperative Propionibacterium endophthalmitis: treatment strategies and long-term visual results. Ophthalmology 1993;100:447–451.

106.Fox GM, Joondeph BC, Flynn HW Jr, et al. Delayed onset pseudophakic endophthalmitis. Am J Ophthalmol 1991;111:163–173.

107.Clark WL, Kaiser PK, Flynn HW Jr, et al. Treatment strategies and visual acuity outcomes in chronic postoperative Propionibacterium acnes endophthalmitis. Ophthalmology 1999;106:1665–1670.

108.Maumenee AE, Schwartz MF. Acute intraocular choroidal effusion. Am J Ophthalmol 1985;100:147– 154.

109.Zauberman H. Expulsive choroidal hemorrhage: an experimental study. Br J Ophthalmol 1982;66:43–45.

110.Speaker MG, Guerriero PN, Met JA, et al. A casecontrol study of risk factors for intraoperative suprachoroidal expulsive hemorrhage. Ophthalmology 1991;98:202–210.

111.Welch JC, Spaeth GL, Vincent WE. Massive suprachoroidal hemorrhage: follow-up and outcome of 30 cases. Ophthalmology 1988;95:1202–1206.

112.Reynolds MG, Haimovici R, Flynn HW Jr, et al. Suprachoroidal hemorrhage: clinical features and results of secondary surgical management. Ophthalmology 1993;100:460–465.

113.Lambrou FH, Meredith TA, Kaplan HJ. Secondary surgical management of expulsive choroidal hemorrhage. Arch Ophthalmol 1987;105:1195–1198.

114.Lakhanpal V, Schocket SS, Elman MJ, Dogra MR. Intraoperative massive suprachoroidal hemorrhage during pars plana vitrectomy. Ophthalmology 1990; 97:1114–1119.

115.Lakhanpal V, Schocket SS, Elman MJ, Nirankari VS. A new modified vitreoretinal surgical approach in the management of massive suprachoroidal hemorrhage. Ophthalmology 1989;96:793–800.

116.Ingraham HJ, Donnenfeld ED, Perry HD. Massive suprachoroidal hemorrhage in penetrating keratoplasty. Am J Ophthalmol 1989;108:670–675.

117.Cantor LB, Katz LJ, Spaeth GL. Complications of surgery in glaucoma: suprachoroidal expulsive hemorrhage in glaucoma patients undergoing intraocular surgery. Ophthalmology 1985;92:1266–1270.

118.Desai V, Peyman G. Use of perfluoroperhydrophenathrene in the management of suprachoroidal hemorrhage. Ophthalmology 1992;99:1542–1547.

119.Grizzard WS. Ophthalmic anesthesia. In: Reineke R, ed. Ophthalmology Annual 1989. New York: Raven Press; 1989:265–294.

120.Hay A, Flynn HW Jr, Hoffman JI, River AH. Needle penetration of the globe during retrobulbar and peribulbar injections. Ophthalmology 1991;98:1017– 1024.

121.Duker JS, Belmont JB, Benson WE, et al. Inadvertent globe perforation during retrobulbar and peribulbar anesthesia: patient characteristics, surgical management and visual outcome. Ophthalmology 1991;98: 519–526.

122.Morgan CM, Schatz H, Vine AK, et al. Ocular complications associated with retrobulbar injections. Ophthalmology 1988;95:660–665.

Over the past 30 years there has been a progression from large-incision intracapsular surgery to less invasive small-incision extracapsular surgery. Similarly, glaucoma surgery has progressed from full-thickness fistulizing procedures (Scheie and posterior lip sclerectomy) to guarded fistulizing procedures (trabeculectomy), and then to trabeculectomy with antimetabolite usage, and currently deep sclerectomy and viscocanalostomy (nonpenetrating trabecular surgery). This chapter discusses the complications of phacotrabeculectomy and the new phacoglaucoma procedures with emphasis on the avoidance, recognition, and intervention of potential complications.

PREOPERATIVE CONDITIONS THAT

PREDISPOSE TO COMPLICATIONS

There are certain preoperative conditions that predispose to complications in both trabeculectomy and nonpenetrating trabecular surgery (NPTS). Medications that promote bleeding are the nemesis of the glaucoma surgeon (Table 27–1). Specifically, these include Coumadin (warfarin sodium), aspirin and other oral nonsteroidal antiinflammatory drugs (NSAIDs), vitamin E in high doses,1,2 platelet aggregation inhibitors other than NSAIDs including Ticlid (ticlopidine hydrochloride) and Plavix (clopidogrel bisulfate), pilocarpine, and other miotics.

The mechanism of action of Coumadin is inhibition of blood clotting by interference with the hepatic synthesis of the vitamin K–dependent clotting factors (II, VII, IX, and X).3

Aspirin irreversibly inhibits platelet aggregation for the 8- to 10-day lifetime of the affected platelets.4 This causes a prolonged bleeding time that in the clinical experience of this author is more difficult to control than bleeding caused by Coumadin at a therapeutic level.

Oral NSAIDs other than aspirin, such as ibuprofen, naproxen, and ketoprofen, reversibly inhibit platelet aggregation and therefore platelet function returns when most of the drug has been eliminated from the patient’s body.4 A new class of NSAIDs, the cyclooxygenase (COX-2) inhibitors, does not affect platelet function because it mainly inhibits only one isoform of the enzyme COX-2.5 The older NSAIDs inhibit both COX-1, which is found in large amounts in platelets, and COX-2, which is minimally present in platelets, but exists in other tissues.5

Vitamin E may interfere with vitamin K metabolism and platelet function and therefore increase the bleeding tendency.1,2 There is currently a trend toward taking antioxidant vitamins. Therefore, the ophthalmologist should inquire about vitamin E usage during the preoperative planning visit.

Ticlid and Plavix are both platelet aggregation inhibitors that are used for secondary prevention of myocardial infarction, stroke, and other vascular events.6,7 Unlike aspirin that inhibits cyclooxygenase and formation of prothrombotic thromboxane in platelets and antithrombotic prostacyclin in vessel walls, Ticlid and Plavix inhibit platelet aggregation by inhibiting the adenosine diphosphate (ADP) pathway for platelet activation.6,7 Both Ticlid and Plavix prolong the bleeding time similarly to aspirin.6,7

TABLE 27–1 DRUGS THAT PROMOTE BLEEDING

Pilocarpine and other miotics (both direct and indirect acting) promote bleeding by causing vasodilatation in the ocular tissues and breakdown of the blood–aqueous barrier. This causes increased fibrin to be released into the anterior chamber and the ocular tissues increasing the likelihood of failure of the trabeculectomy or the NPTS.

Bleeding is undesirable in glaucoma surgery because it promotes inflammation and scar tissue formation. This can cause the glaucoma procedure to fail. To minimize the risk of bleeding, aspirin should be stopped at least 10 to 14 days prior to surgery.2

Older NSAIDs other than aspirin should be stopped at least 3 to 5 days prior to surgery to allow the platelets to recover. The new NSAIDs, which are COX-2 inhibitors Vioxx (rofecoxib) and Celebrex (celecoxib), do not need to be stopped prior to surgery because they do not inhibit platelet function at therapeutic doses.5

It is reasonable to stop Coumadin 3 to 5 days prior to surgery if this is acceptable to the patient’s primary care physician. If this is not acceptable, or if the patient’s prothrombin time (PT) does not normalize by the day of surgery when off Coumadin, then the patient may be given fresh frozen plasma (FFP) several hours prior to surgery. From a practical standpoint, FFP rarely has to be given because most of the time glaucoma surgery is elective rather than emergent and therefore can be postponed until the PT normalizes.

It also seems prudent to discontinue vitamin E for 10 days to 2 weeks prior to surgery to reverse the vitamin’s effect on platelets,2 especially if a patient is taking 400 to 800 IU a day, which is seven to 14 times as much as the recommended daily allowance for vitamin E.

Ticlid and Plavix should be stopped 10 days to 2 weeks prior to surgery because it takes at least 7 to 10 days and sometimes up to 2 weeks for platelet function to return to normal after stopping these drugs.6,7

It is desirable to discontinue miotics for at least 3 weeks prior to trabeculectomy or NPTS and longer if

possible.8 Usually, by starting Diamox 500 mg sequels po b.i.d., it is possible to discontinue miotics for the 3-week period without having an unacceptable rise in intraocular pressure. This may not be possible based on the severity of a patient’s glaucoma and the clinical response to the discontinuance of the miotic. Frequently, a different topical medication can be substituted for a miotic to allow the discontinuance of the latter prior to surgery.

MIOTIC AND OTHER TOPICAL

EYEDROP USAGE

Not only do miotics cause an increase in bleeding and inflammation at the time of glaucoma surgery, but they and other antiglacuoma medications cause morphologic changes to occur in the conjunctiva, Tenon’s fascia, and episclera. These changes, according to clinical studies, have a negative effect on the outcome of filtration surgery.9,10 They include epithelial metaplasia, a decrease in goblet cells, and an increase in subepithelial fibroblasts and inflammatory cells (macrophages, lymphocytes, and mast cells).10–12 Pilocarpine and epinephrine have been the main offenders but other topical agents may cause conjunctival changes as well. One study revealed that a commercial preparation of 0.5% timolol maleate causes a significant decrease in goblet cells after only 1 month of topical treatment.11 The literature supports the concept that the administration of topical antiglacuoma medication, irrespective of type, for more than 3 years causes significant subclinical inflammation within the conjunctiva and foreshortening of the inferior fornix secondary to conjunctival fibrosis.10,13 It is not known whether it is the actual drug or the preservative, such as benzalkonium chloride, or a combination of both that cause these changes. If a patient is on topical antiglacuoma mediation prior to the performance of a trabeculectomy or NPTS, it would seem reasonable to start topical steroids and topical NSAIDs for 3 to 5 days prior to surgery to attempt to diminish inflammation prior to making the incision. Some glaucoma surgeons advocate the use of oral steroids in the perioperative period but a clinical trial indicating their effectiveness, or a risk analysis, has not yet been done.

OTHER CONDITIONS THAT

PREDISPOSE TO COMPLICATIONS

Patients who have had previous ocular surgery in which the conjunctiva, episclera, and sclera have been violated are at increased risk of complications from trabeculectomy and NPTS. Having knowledge of the patient’s previous surgery helps the surgeon

formulate a plan of action. When possible, it is desirable to choose a location on the conjunctiva that has not been scarred by previous surgery. This is sometimes not possible after previous intracapsular, planned extracapsular surgery, or glaucoma surgery, where 10 to 14 mm of conjunctiva has been disturbed. This situation would demand that the surgery be performed in the inferior bulbar location with the attendant increased risk of endophthalmitis that exists when a bleb forms. Because a bleb usually doesn’t form after a viscocanalostomy, the inferior bulbar location is theoretically no riskier than a superior location for this operation. However, it is more difficult to operate in the inferior location from an ergonomic standpoint. If the surgeon is forced to operate in nonvirgin conjunctiva, then preoperative evaluation at the slit lamp should include assessment of the conjunctiva with a cotton-tipped applicator to see what clock hours of conjunctiva are the least adherent to the underlying episclera and sclera. This should be noted so that the proposed surgical site is easy to find at the time of surgery.

Patients who are darkly pigmented or young in age have a greater tendency to scar after trabeculectomy. Recording these traits may influence the surgical plan. For example, the surgeon may choose to order 0.4 mg/mL instead of 0.2 mg/mL of mito- mycin-C, as well as perform a more aggressive trabeculectomy by making a larger sclerectomy.

Other factors to consider are additional unique characteristics about the patient’s anatomy that may influence the surgical plan, such as a prominent brow, which may necessitate a temporal approach, or a small palpebral fissure, which may require a lateral canthotomy.

SPECTRUM OF GLAUCOMA

PROCEDURES

Before entering into a discussion of complications it is first necessary to review the current spectrum of glaucoma surgery as well as the details of the newer procedures. Prior to 1968 when Cairns14 introduced the trabeculectomy operation, full-thickness filtering surgery was the procedure of choice for medically uncontrolled open angle glaucoma. Full-thickness procedures were to a great extent supplanted by trabeculectomy procedures especially when mito- mycin-C usage enabled intraocular pressure (IOP) reduction down to the higher end of the range achieved with full-thickness operations. Even though trabeculectomy is currently considered the standard filtration procedure for glaucoma, it is still fraught with some early postoperative complications including hyphema, surgically induced iritis, and excessive

filtration leading to a shallow or flat anterior chamber, suprachoroidal effusions, hypotonous maculopathy, and endophthalmitis.15–17 This has prompted the development of several NPTSs, deep sclerec- tomy,18–21 and viscocanalostomy,22 which seem to reduce the incidence of most of the early complications experienced with trabeculectomy. Another penetrating glaucoma surgery, trabeculotomy, has been utilized for decades primarily in infantile glaucoma. There has been renewed interest in trabeculotomy in conjunction with phacoemulsification and intraocular lens implantation in adults.23 Trabeculotomy does help to minimize certain early postoperative complications of trabeculectomy including shallowing of the anterior chamber, suprachoroidal effusion, and malignant glaucoma, but other complications may be more frequent, such as postoperative IOP spikes.24,25 According to a study by Tanihara et al,23 trabeculotomy success rates were significantly lower when the initial IOP level was greater than 30 mm Hg, and the procedure seemed to be more effective in controlling IOP in eyes with pseudoexfoliation syndrome than in eyes with primary open angle glaucoma. In contrast, the viscocanalostomy operation works in all types of glaucoma except for neovascular. Stegman et al22 report excellent results (<22 mm in 82.7% of blacks without medications) in patients who present with an initial mean IOP level of 47.4 mm. Stegman et al22,26 performed hundreds of trabeculotomies prior to creating the viscocanalostomy operation. These trabeculotomies were performed by several different techniques. The first technique used by Stegman et al was called a trabeculoviscotomy, in which Schlemm’s canal was injected with Healon to rupture the wall of the canal and the trabecular meshwork.26 A subsequent technique involved cutting the canal and meshwork with a very fine pair of scissors.26 Even though their results were fairly good (61% success— IOP <21 in technique 1 and 76% success in technique 2),26 if the operation failed, the significant damage done to Schlemm’s canal and the collector channels precluded a NPTS from being performed in the 160degree area of sclera involved in the trabeculotomy. It is for these reasons, as well as the fact that NPTS is less invasive with no entrance into the anterior chamber, that this author chooses not to discuss trabeculotomy and its complications in this chapter.

DEEP SCLERECTOMY PROCEDURE

The deep sclerectomy operation proceeds as follows. A limbusor fornix-based conjunctival flap can be used. The fornix-based flap probably allows for an easier dissection of a superficial scleral flap anteriorly into the clear cornea. This is the second step of