Correspondence been using topical prednisolone acetate drops once daily at presentation. Corneal scraping revealed gram-negative bacilli on smears. Corneal scraping was inoculated in blood agar, chocolate agar, thioglycolate broth, and brain–heart infusion broth. The patient was started on moxifloxacin (0.5%) drops. The bacterial culture yielded a moderate growth of gramnegative bacilli from all inoculated media. The isolate was a lactose nonfermenter and was oxidase negative. Further identification of the isolate was made using the mini-API (Analytical Profile Index; BioMerieux SA, Craponne, France). An ID-23GN strip was inoculated with pure culture of the isolate and incubated as per standard protocol. The API score was 99% for the identification of A. xylosoxidans. The organism was sensitive to gentamicin, amikacin, and ceftazidime, and resistant to chloramphenicol, ciprofloxacin, ofloxacin, gatifloxacin, and moxifloxacin. Thus, moxifloxacin was discontinued and fortified gentamicin, 15 mg/mL (1.5%), was started every half hour for 3 days, followed by every hour for 7 days, and thereafter 6 times a day for 1 month. Topical medication was continued for 10 weeks. The infection resolved with scarring and conjunctivalization. Alcaligenes xylosoxidans is a gram-negative, oxidasenegative, nonlactose-fermenting bacillus. It is closely related to the Bordetella genus and frequently confused with Pseudomonas. Previous reports of A. xylosoxidans keratitis have demonstrated association with prior use of steroid and compromised or traumatized cornea.3 It has also been reported after use of contact lens.4 Majekodunmi5 reported a patient with bacterial keratitis who had Clostridium welchii and Achromobacter growing simultaneously. As in previous cases, our patient had a compromised cornea. Prior use of topical steroid might be another risk factor.
A review of the sensitivity pattern of A. xylosoxidans shows it is consistently sensitive to carbenicillin and trimethoprim-sulfamethoxazole. It is resistant to firstgeneration cephalosporins and to all aminoglycosides.3 It has variable sensitivity to piperacillin, ceftazidime, ciprofloxacin, and chloramphenicol. Contrary to previous reports, the strain of the organism seen in our patient was sensitive to gentamicin. However, it was resistant to fourth-generation fluoroquinolones such as gatifloxacin and moxifloxacin. Alcaligenes xylosoxidans, although rare, should be considered a potential pathogen causing keratitis in eyes with a compromised ocular surface where steroids have been used.
An unusual finding of corneal edema complicating selective laser trabeculoplasty
A description of the patients is presented in Table 1. The indication for SLT in both patients was visual field progression with 3 glaucoma agents. Both patients had had no previous ocular disease. In case 1, 30 minutes after SLT, the cornea was clear with no abrasion, and the IOP was 16 mm Hg. One week after SLT, the patient complained of haloes and decreased vision. On examination, her best-corrected Snellen visual acuity was 20/70. A focal area of central epithelial and stromal edema was noted. The IOP was 15 mm Hg. Visual acuity improved to 20/40 after 2 weeks of topical prednisolone acetate 1% 5 times a day and sodium chloride drops 4 times
C
anadian laser trabeculoplasty rates doubled between 2001 and 2004.1 In this context, an improved knowledge of complications is warranted. Selective laser trabeculoplasty (SLT) is associated with fewer complications (4.5%–11% of cases) than argon laser trabeculoplasty (up to 34%), the most common being a transient elevation of intraocular pressure (IOP) and iritis.2 To our knowledge, corneal edema following SLT has not been described. We report 2 cases of post-SLT corneal edema and its treatment.
REFERENCES 1. Yabuuchi E, Oyama A. Achromobacter xylosoxidans n. sp. from human ear discharge. Jpn J Microbiol 1971;15:477–81. 2. Sangwan VS, Matalia HP, Vemuganti GK, et al. Early results of penetrating keratoplasty after cultivated limbal epithelium transplantation. Arch Ophthalmol 2005;123:334–40. 3. Pan TH, Heidemann DG, Dunn SP, Chow CY, Gossage D. Delayed onset and recurrent Alcaligenes xylosoxidans keratitis. Cornea 2000;19:243–5. 4. Lin A, Driebe WT Jr, Polack P. Alcaligenes xylosoxidans keratitis post penetrating keratoplasty in a rigid gas permeable lens wearer. CLAO J 1998;24:239–41. 5. Majekodunmi S, Odugbemi T. Clostridium welchii corneal ulcer—a case report. Can J Ophthalmol 1975;10:290–2.
Srikant K. Sahu,*† Sujata Das,*† Virender Sachdeva,* Virender S. Sangwan* *L.V. Prasad Eye Institute, Hyderabad, Andhra Pradesh, India; and † L.V. Prasad Eye Institute, Bhubaneswar, Orissa, India Correspondence to Sujata Das, MS:
[email protected] Can J Ophthalmol 2009;44:336–7 doi:10.3129/i09-056
Table 1—Patient description before selective laser trabeculoplasty Case 1 2
Age/sex/eye
Diagnosis
VA (Snellen)
IOP (mm Hg)
SLT settings
Pre-SLT treatment
60/F/OS 54/F/OD
POAG OU NTG OU
20/25 20/20
15 12
50 shots OS, 360°, 0.9–1 mJ 60 shots OD, 360°, 0.8 mJ
Latanoprost and brimonidine-timolol Latanoprost-timolol and brinzolamide
Note: VA, visual acuity; IOP, intraocular pressure; SLT, selective laser trabeculoplasty; F, female; POAG, primary open-angle glaucoma; NTG, normal tension glaucoma.
CAN J OPHTHALMOL—VOL. 44, NO. 3, 2009
337
Correspondence a day. Although the edema resolved, a subepithelial haze remained. The patient had a history of herpes labialis. A presumed diagnosis of herpes simplex stromal keratitis was made by the Cornea Service. The patient continued her steroid drops and started valacyclovir 500 mg orally twice daily. Four months later, the stromal keratitis had resolved, and the visual acuity was 20/25. In case 2, 30 minutes after SLT, there was no IOP spike and the cornea was free of abrasions. One week after SLT, the patient complained of haloes in the right eye. Visual acuity was 20/20 with much hesitancy, and the IOP was 9 mm Hg. Slit-lamp examination revealed mild central stromal edema in the right eye (Fig. 1). Topical prednisolone acetate 1% 4 times daily was started. The patient’s symptoms and edema resolved within 2 months. Stromal edema from epithelial damage is a rare finding following SLT. Preoperative facial preparation with chlorhexidine gluconate can result in stromal edema,3 although this solution was not used in our cases. Lingering alcohol on the lens, although unlikely, might have also resulted in toxic epithelial keratopathy and corneal swelling.4 Brinzolamide may also facilitate the development of corneal edema by attenuating bicarbonate efflux through inhibition of carbonic anhydrase type II in the corneal endothelium.5 However, corneal edema did not develop in any of our other patients using brinzolamide. Direct endothelial damage from misdirected laser is highly unlikely because of the peripheral use of the laser and the central appearance of the edema. The immediate ocular response to SLT may include a release of chemotactic and vasoactive agents, such as the cytokines interleukin-1D, interleukin-1E, and tumour necrosis factor-D.2 This inflammatory cascade may contribute towards herpes simplex virus reactivation.6 Another contributory factor to the development of stromal keratitis in both
patients may have been the post-SLT continued topical use of latanoprost, which can increase the number and severity of recurrences of HSV stromal keratitis.7 The patients did not receive any anti-inflammatory drops after SLT. Topical corticosteroids after laser therapy reduce inflammation and ocular discomfort.8 After these 2 cases, topical anti-inflammatory agents have been used regularly for 4 days after SLT, and there have been no further cases of corneal edema. In previous studies, less immune modulation with less potent anti-inflammatory agents (nonsteroidal compared with steroid agents) has shown a trend toward better reduction of IOP.9 However, the follow-up times were unequal, making direct comparisons difficult. SLT may be complicated by corneal edema, which responds to topical steroids. HSV keratitis should be considered, and antiviral therapy initiated as necessary. REFERENCES 1. Campbell R, Trope G, Rachmiel R, Buys YM. Glaucoma laser and surgical procedure rates in Canada: a long-term profile. Can J Ophthalmol 2008;43:449–53. 2. Latina MA, de Leon JM. Selective laser trabeculoplasty. Ophthalmol Clin North Am 2005;18:409–19. 3. Phinney RB, Mondino BJ, Hofbauer JD, et al. Corneal edema related to accidental Hibiclens exposure. Am J Ophthalmol 1988;106:210–5. 4. Brooks AM, Grant G, Gillies WE. Reversible corneal endothelial cell changes in diseases of the anterior segment. Aust N Z J Ophthalmol 1987;15:283–9. 5. Tanimura H, Minamoto A, Narai A, Hirayama T, Suzuki M, Mishima HK. Corneal edema in glaucoma patients after the addition of brinzolamide 1% ophthalmic suspension. Jpn J Ophthalmol 2005;49:332–3. 6. Kaye S, Choudhary A. Herpes simplex keratitis. Prog Retin Eye Res 2006;25:355–80. 7. Wand M, Gilbert CM, Liesegang TJ. Latanoprost and herpes simplex keratitis. Am J Ophthalmol 1999;127:602–4. 8. Kim YY, Glover BK, Shin DH, Lee D, Frenkel RE, Abreu MM. Effect of topical anti-inflammatory treatment on the long-term outcome of laser trabeculoplasty. Fluorometholone-Laser Trabeculoplasty Study Group. Am J Ophthalmol 1998;126:721–3. 9. Latina MA, Gulati V. Selective laser trabeculoplasty: stimulating the meshwork to mend its ways. Int Ophthalmol Clin 2004;44:93–103.
Sami P. Moubayed,* Mohammad Hamid,* Johanna Choremis,† Gisèle Li† *Université de Montréal and †Maisonneuve-Rosemont Hospital, Montreal, Que. Correspondence to Gisèle Li, MD:
[email protected] Fig. 1—Case 2: mild central stromal edema on slit-lamp examination of the patient’s right eye.
338
CAN J OPHTHALMOL—VOL. 44, NO. 3, 2009
Can J Ophthalmol 2009;44:337–8 doi:10.3129/i09-025
