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Peripheral ulcerative keratitis after clear corneal cataract extraction1
Peripheral ulcerative keratitis after clear corneal cataract extraction Esen Karamursel Akpek, MD, Anna-Maria Demetriades, John D. Gottsch, MD ABSTRACT A previously healthy 80-year-old man had uneventful clear corneal cataract extraction. An extensive peripheral corneal infiltrate with overlying epithelial defect at the incision site was noted at the regular follow-up visit 1 week after surgery. Corneal cultures showed no evidence of infectious keratitis. A systemic evaluation uncovered early-stage, active rheumatoid arthritis. This case illustrates that peripheral ulcerative keratitis may occur with a small clear corneal incision and may be the presenting sign of a previously undiagnosed rheumatoid disease. J Cataract Refract Surg 2000; 26:1424 –1427 © 2000 ASCRS and ESCRS
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eripheral ulcerative keratitis associated with collagen vascular disease may be difficult to distinguish clinically from local or systemic infectious causes. Thus, any patient presenting with peripheral ulcerative keratitis requires a thorough evaluation to exclude a collagen vascular etiology resulting from the ocular and systemic morbidity these disorders may carry.1 The occurrence of necrotizing scleritis, sterile corneal ulcers, or both after cataract surgery in patients with known collagen vascular disease has been well documented in the literature.2–5 Rarely, ocular manifestations may be the presenting sign of an underlying vasculitic disorder. We describe a patient presenting with fulminant peripheral ulcerative keratitis within 1 week of uneventful clear corneal cataract surgery. Laboratory investigaAccepted for publication January 14, 2000. From the Cornea and External Diseases Service, The Wilmer Eye Institute, Johns Hopkins Hospital, Baltimore, Maryland, USA. None of the authors has a financial or proprietary interest in any material or method mentioned. Reprint requests to John D. Gottsch, MD, The Wilmer Eye Institute, Johns Hopkins Hospital, 600 North Wolfe Street, Maumenee Building # 317, Baltimore, Maryland 21287, USA. E-mail: [email protected]. © 2000 ASCRS and ESCRS Published by Elsevier Science Inc.
tions of an infectious etiology were negative. A systemic evaluation disclosed moderately active rheumatoid arthritis with only subtle joint findings. Because of the temporal relationship and rapid response of the ocular as well as joint findings to the systemic treatment with prednisone and sulfasalazine, this unusually early-onset postsurgical peripheral ulcerative keratitis was most likely caused by the underlying active rheumatoid disease. A detailed preoperative evaluation based on patients’ signs and symptoms may prevent such rare yet potentially serious complications.
Case Report In December 1998, an 80-year-old man was referred to the Cornea and External Disease Service of the Wilmer Eye Institute for a peripheral corneal ulcer that developed 1 week after uneventful cataract surgery. The patient was electively admitted for cataract surgery in his left eye, performed elsewhere. Preoperative evaluations disclosed a best spectacle-corrected visual acuity (BSCVA) of 20/60. Slitlamp examination demonstrated a 3⫹ senile nuclear cataract, compatible with patient’s age, and unremarkable fundus findings. The patient’s medical history was significant only for hypertension, which was controlled with medical treatment of angiotensin converting enzyme inhibitors once a day. His ocular history revealed no previous sur0886-3350/00/$–see front matter PII S0886-3350(00)00359-X
CASE REPORTS: AKPEK
Figure 1. (Akpek) Slitlamp photograph of the patient’s left eye. Note the intense conjunctival injection and a peripheral corneal ulcer extending between 1 and 6 o’clock positions. Insert: Dense inflammatory cell infiltrate at the clear corneal incision.
Figure 2. (Akpek) Slitlamp photograph of the patient’s left eye. Arrow demonstrates the infiltrate at the paracentesis site.
gery in the left eye and an extracapsular cataract extraction in the right eye 7 years previously. Phacoemulsification in the left eye was performed through a small clear corneal incision at the superotemporal aspect using retrobulbar anesthesia. A foldable silicone posterior chamber intraocular lens (IOL) was implanted in the capsular bag. There were no preoperative or intraoperative complications. Visual acuity in the left eye was 20/25 the day after the surgery. Anterior segment findings were unremarkable. At the routine visit 1 week after surgery, a peripheral corneal ulcer in the left eye was noted, and the patient was referred. The patient reported decreased visual acuity but no pain. Intense conjunctival hyperemia was noted. Best spectacle-corrected visual acuity was 20/20 in the right eye and 20/60 in the left. Intraocular pressure was 11 mm Hg in both eyes. Slitlamp examination demonstrated a peripheral corneal ulcer extending between the 1 and 6 o’clock positions with dense infiltration at the clear corneal incision and paracentesis sites (Figures 1 and 2). There were 4⫹ anterior chamber cells and 3⫹ flare with fibrin threads. The right eye was pseudophakic with a well-centered posterior chamber IOL. A bilateral dilated fundus examination was unremarkable. Corneal cultures and scrapings were taken using the blunt end of a surgical blade and topical anesthesia of proparacaine. The smears were stained with hematoxylin and eosin, Giemsa, and Wright stains. The culture media used included blood, chocolate, and Sabouraud’s dextrose agars and Schaedler’s broth. Viral cultures and blood serologies for herpes simplex virus, herpes zoster virus, and hepatitis B and C viruses were also obtained. No infectious etiology was found.
A detailed questionary review of all the systems uncovered mild morning stiffness and pain in both hands. Mild swelling of the metatarsophalengeal joints was noticed without deformities. A blood workup disclosed a normal complete blood count (hemoglobin, 15.4 mg/dL; hematocrit, 42.1%; white blood cells, 8700/mm3), an elevated erythrocyte sedimentation rate (43 mm/hour), an elevated C-reactive protein (1.6 mg/mL), normal complement levels (C3, 142 IU/mL; C4, 29 IU/mL), negative antineutrophil cytoplasmic antibodies, a negative Sjo¨gren’s panel, and a highly positive rheumatoid factor (475 IU/mL). A rheumatology consult revealed mild synovitis of the metacarpophalengeal and proximal interphalengeal joints. The patient was placed on oral prednisone 50 mg a day and sulfasalazine 500 mg 2 times a day. Prednisolone acetate 1% and ciprofloxacin eyedrops were also administered 4 times daily. Two days after initiation of treatment, a trace conjunctival injection remained without further stromal ulceration and with total re-epithelialization of the ulcer. At the 19 month follow-up, BSCVA was 20/20 in the right eye and 20/40 in the left eye with a manifest refraction of –1.75 ⫹2.75 ⫻ 178. Moderate corneal irregular astigmatism and posterior capsule haze were noted. The patient remains on oral prednisone 4 mg 4 times a day and sulfasalazine 500 mg twice a day and has had no recurrence of peripheral corneal ulcerative disease (Figure 3).
Discussion Peripheral ulcerative keratitis, with or without associated necrotizing scleritis, after extracapsular cataract surgery has been documented.2–5 Jones and Maguire2
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CASE REPORTS: AKPEK
Figure 3. (Akpek) Slitlamp photograph of the patient’s left eye 2 months after surgery, demonstrating corneal recovery with residual irregular astigmatism.
studied 70 patients with rheumatoid arthritis who were on systemic treatment and had cataract surgery. Complications were uncommon, and the incidence of sterile corneal ulcers was not higher than in the population in general. Maffett et al.3 describe the clinical and histopathological findings in 11 eyes of 8 patients with a preoperative diagnosis of collagen vascular disease and secondary keratoconjunctivitis sicca that developed sterile corneal ulcers after extracapsular or intracapsular cataract extraction. In 10 eyes, the ulcer was central initially. Peripheral ulcerative keratitis occurred in 1 eye only, 6 weeks postoperatively. This patient had active rheumatoid arthritis, and the ulcerative keratitis responded well to systemic cyclophosphamide therapy. Salamon and coauthors4 and Dı´az-Valle et al.5 also report the occurrence of sterile corneal ulcers with adjacent scleritis in small case series. The ulcers occurred several weeks to months after uneventful cataract surgery through a scleral/corneoscleral incision. Our case is unique in that a fulminant peripheral ulcerative keratitis occurred as the first manifestation of an occult collagen vascular disorder after a small clear corneal incision. There was no associated scleritis, and the infiltrate was confined to the corneal stroma at the incision and the paracentesis sites. The patient was treated with systemic steroids and sulfasalazine and responded well, with rapid re-epithelialization and healing of the ulcer. No recurrence was observed during the 19 month follow-up with the patient on the same therapeutic regimen. 1426
The pathogenesis of peripheral ulcerative keratitis in patients with rheumatoid arthritis after cataract surgery is not understood. Studies of necrotizing sclerocorneal ulceration suggest an association between the disruption of episcleral and perforating scleral vessels during surgery as a precipitating factor, leading to entrapment of the immune complexes and thus initiation of an inflammatory response.5 Alternative hypotheses suggest aqueous tear insufficiency, surgical denervation of the cornea, and the use of topically administered medications causing epithelial toxicity.6 These ulcers often begin as clean epithelial defects that appear soon after surgery in the presence of significant keratoconjunctivitis sicca secondary to the underlying disease. They commonly respond to local therapeutic measures, including aggressive artificial tears and bandage contact lens insertion and sometimes to occlusion of the lacrimal puncti. The differentiation between a paracentral sterile corneal ulcer and peripheral ulcerative keratitis (crescent-shaped destructive inflammation of the juxtalimbal corneal stroma associated with epithelial defect, presence of stromal infiltrate, and degradation) may have important implications with regard to treatment and prognosis. The onset of peripheral ulcerative keratitis in the course of a collagen vascular disorder may reflect the presence of a potentially lethal systemic vasculitis.7 The peripheral cornea has distinct morphological and immunological characteristics that predispose to inflammatory diseases, including presence of Langhans cells, and high molecular immunoglobulin M (IgM) and C1 (initial component of complement serving as the recognition unit of classic pathway of complement) leading to immune complex formation.8 Patients with rheumatoid arthritis have circulating IgM antibodies (rheumatoid factor) directed against self immunoglobulin G.9 These antigen–antibody complexes, whether derived from the limbal vasculature, tears, or aqueous humor or formed within the cornea itself, can bind C1, activating the classic complement pathway and leading to corneal destruction.10 In our case, fulminant peripheral ulcerative keratitis was encountered immediately after cataract surgery. We hypothesize that the surgical incision led to the formation of the peripheral ulcerative keratitis by facilitating the direct access of the rheumatoid factor and immune
J CATARACT REFRACT SURG—VOL 26, SEPTEMBER 2000
CASE REPORTS: AKPEK
complexes to the stroma by breaking the immune privilege of the cornea. Because of the multiple and varied etiologies of peripheral ulcerative keratitis, appropriate management requires the establishment of correct diagnosis. Dermatologic, neurologic, traumatic, infectious and postinfectious disorders; abnormalities of the eyelids and eyelashes; and systemic and local autoimmune diseases should be considered in the differential diagnosis of peripheral ulcerative keratitis. Antimicrobial therapy, systemic tetracycline, lid hygiene, correction of anatomic lid and eyelash problems, and lubrication regimens, including punctal occlusion and temporary or permanent tarsorrhaphy, can be helpful. However, in patients with an underlying collagen vascular disorder, systemic therapy with immunosuppressive/immunomodulator agents may decrease the likelihood of ocular morbidity and, in some cases, mortality.1 Our patient was treated with systemic steroids and sulfasalazine as well as topical steroids and prophylactic antibiotics. The corneal ulcer re-epithelialized in 2 days. Topical treatment was tapered and discontinued over 2 weeks. The ulcer did not recur in the 19 month follow-up with the patient on systemic treatment. This case emphasizes that peripheral ulcerative keratitis may occur with a small clear corneal incision as the presenting sign of an occult rheumatoid arthritis.
References 1. Foster CS, Forstot SL, Wilson LA. Mortality rate in rheumatoid arthritis patients developing necrotizing scleritis or peripheral ulcerative keratitis; effects of systemic immunosuppression. Ophthalmology 1984; 91:1253– 1263 2. Jones RR, Maguire LJ. Corneal complications after cataract surgery in patients with rheumatoid arthritis. Cornea 1992; 11:148 –150 3. Maffett MJ, Johns KJ, Parrish CM, et al. Sterile corneal ulceration after cataract extraction in patients with collagen vascular disease. Cornea 1990; 9:279 –285 4. Salamon SM, Mondino BJ, Zaidman GW. Peripheral corneal ulcers, conjunctival ulcers, and scleritis after cataract surgery. Am J Ophthalmol 1982; 93:334 –337 5. Dı´az-Valle D, Benı´tez del Castillo JM, Castillo A, et al. Immunologic and clinical evaluation of postsurgical necrotizing sclerocorneal ulceration. Cornea 1998; 17:371– 375 6. Hemady R, Chu W, Foster CS. Keratoconjunctivitis sicca and corneal ulcers. Cornea 1990; 9:170 –173 7. Messmer EM, Foster CS. Vasculitic peripheral ulcerative keratitis. Surv Ophthalmol 1999; 43:379 –396 8. Pleyer U, Bergmann L, Krause A, Hartmann C. Autoimmunerkrankungen der peripheren Hornhaut; immunpathologie, Klinik und Therapie. Klin Monatsbl Augenheilkd 1996; 208:73– 81 9. Koffler D. The immunology of rheumatoid diseases. Clin Symp 1979; 31:1–36 10. Mondino BJ. Inflammatory diseases of the peripheral cornea. Ophthalmology 1988; 95:463– 472
J CATARACT REFRACT SURG—VOL 26, SEPTEMBER 2000
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P
eripheral ulcerative keratitis associated with collagen vascular disease may be difficult to distinguish clinically from local or systemic infectious causes. Thus, any patient presenting with peripheral ulcerative keratitis requires a thorough evaluation to exclude a collagen vascular etiology resulting from the ocular and systemic morbidity these disorders may carry.1 The occurrence of necrotizing scleritis, sterile corneal ulcers, or both after cataract surgery in patients with known collagen vascular disease has been well documented in the literature.2–5 Rarely, ocular manifestations may be the presenting sign of an underlying vasculitic disorder. We describe a patient presenting with fulminant peripheral ulcerative keratitis within 1 week of uneventful clear corneal cataract surgery. Laboratory investigaAccepted for publication January 14, 2000. From the Cornea and External Diseases Service, The Wilmer Eye Institute, Johns Hopkins Hospital, Baltimore, Maryland, USA. None of the authors has a financial or proprietary interest in any material or method mentioned. Reprint requests to John D. Gottsch, MD, The Wilmer Eye Institute, Johns Hopkins Hospital, 600 North Wolfe Street, Maumenee Building # 317, Baltimore, Maryland 21287, USA. E-mail: [email protected]. © 2000 ASCRS and ESCRS Published by Elsevier Science Inc.
tions of an infectious etiology were negative. A systemic evaluation disclosed moderately active rheumatoid arthritis with only subtle joint findings. Because of the temporal relationship and rapid response of the ocular as well as joint findings to the systemic treatment with prednisone and sulfasalazine, this unusually early-onset postsurgical peripheral ulcerative keratitis was most likely caused by the underlying active rheumatoid disease. A detailed preoperative evaluation based on patients’ signs and symptoms may prevent such rare yet potentially serious complications.
Case Report In December 1998, an 80-year-old man was referred to the Cornea and External Disease Service of the Wilmer Eye Institute for a peripheral corneal ulcer that developed 1 week after uneventful cataract surgery. The patient was electively admitted for cataract surgery in his left eye, performed elsewhere. Preoperative evaluations disclosed a best spectacle-corrected visual acuity (BSCVA) of 20/60. Slitlamp examination demonstrated a 3⫹ senile nuclear cataract, compatible with patient’s age, and unremarkable fundus findings. The patient’s medical history was significant only for hypertension, which was controlled with medical treatment of angiotensin converting enzyme inhibitors once a day. His ocular history revealed no previous sur0886-3350/00/$–see front matter PII S0886-3350(00)00359-X
CASE REPORTS: AKPEK
Figure 1. (Akpek) Slitlamp photograph of the patient’s left eye. Note the intense conjunctival injection and a peripheral corneal ulcer extending between 1 and 6 o’clock positions. Insert: Dense inflammatory cell infiltrate at the clear corneal incision.
Figure 2. (Akpek) Slitlamp photograph of the patient’s left eye. Arrow demonstrates the infiltrate at the paracentesis site.
gery in the left eye and an extracapsular cataract extraction in the right eye 7 years previously. Phacoemulsification in the left eye was performed through a small clear corneal incision at the superotemporal aspect using retrobulbar anesthesia. A foldable silicone posterior chamber intraocular lens (IOL) was implanted in the capsular bag. There were no preoperative or intraoperative complications. Visual acuity in the left eye was 20/25 the day after the surgery. Anterior segment findings were unremarkable. At the routine visit 1 week after surgery, a peripheral corneal ulcer in the left eye was noted, and the patient was referred. The patient reported decreased visual acuity but no pain. Intense conjunctival hyperemia was noted. Best spectacle-corrected visual acuity was 20/20 in the right eye and 20/60 in the left. Intraocular pressure was 11 mm Hg in both eyes. Slitlamp examination demonstrated a peripheral corneal ulcer extending between the 1 and 6 o’clock positions with dense infiltration at the clear corneal incision and paracentesis sites (Figures 1 and 2). There were 4⫹ anterior chamber cells and 3⫹ flare with fibrin threads. The right eye was pseudophakic with a well-centered posterior chamber IOL. A bilateral dilated fundus examination was unremarkable. Corneal cultures and scrapings were taken using the blunt end of a surgical blade and topical anesthesia of proparacaine. The smears were stained with hematoxylin and eosin, Giemsa, and Wright stains. The culture media used included blood, chocolate, and Sabouraud’s dextrose agars and Schaedler’s broth. Viral cultures and blood serologies for herpes simplex virus, herpes zoster virus, and hepatitis B and C viruses were also obtained. No infectious etiology was found.
A detailed questionary review of all the systems uncovered mild morning stiffness and pain in both hands. Mild swelling of the metatarsophalengeal joints was noticed without deformities. A blood workup disclosed a normal complete blood count (hemoglobin, 15.4 mg/dL; hematocrit, 42.1%; white blood cells, 8700/mm3), an elevated erythrocyte sedimentation rate (43 mm/hour), an elevated C-reactive protein (1.6 mg/mL), normal complement levels (C3, 142 IU/mL; C4, 29 IU/mL), negative antineutrophil cytoplasmic antibodies, a negative Sjo¨gren’s panel, and a highly positive rheumatoid factor (475 IU/mL). A rheumatology consult revealed mild synovitis of the metacarpophalengeal and proximal interphalengeal joints. The patient was placed on oral prednisone 50 mg a day and sulfasalazine 500 mg 2 times a day. Prednisolone acetate 1% and ciprofloxacin eyedrops were also administered 4 times daily. Two days after initiation of treatment, a trace conjunctival injection remained without further stromal ulceration and with total re-epithelialization of the ulcer. At the 19 month follow-up, BSCVA was 20/20 in the right eye and 20/40 in the left eye with a manifest refraction of –1.75 ⫹2.75 ⫻ 178. Moderate corneal irregular astigmatism and posterior capsule haze were noted. The patient remains on oral prednisone 4 mg 4 times a day and sulfasalazine 500 mg twice a day and has had no recurrence of peripheral corneal ulcerative disease (Figure 3).
Discussion Peripheral ulcerative keratitis, with or without associated necrotizing scleritis, after extracapsular cataract surgery has been documented.2–5 Jones and Maguire2
J CATARACT REFRACT SURG—VOL 26, SEPTEMBER 2000
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CASE REPORTS: AKPEK
Figure 3. (Akpek) Slitlamp photograph of the patient’s left eye 2 months after surgery, demonstrating corneal recovery with residual irregular astigmatism.
studied 70 patients with rheumatoid arthritis who were on systemic treatment and had cataract surgery. Complications were uncommon, and the incidence of sterile corneal ulcers was not higher than in the population in general. Maffett et al.3 describe the clinical and histopathological findings in 11 eyes of 8 patients with a preoperative diagnosis of collagen vascular disease and secondary keratoconjunctivitis sicca that developed sterile corneal ulcers after extracapsular or intracapsular cataract extraction. In 10 eyes, the ulcer was central initially. Peripheral ulcerative keratitis occurred in 1 eye only, 6 weeks postoperatively. This patient had active rheumatoid arthritis, and the ulcerative keratitis responded well to systemic cyclophosphamide therapy. Salamon and coauthors4 and Dı´az-Valle et al.5 also report the occurrence of sterile corneal ulcers with adjacent scleritis in small case series. The ulcers occurred several weeks to months after uneventful cataract surgery through a scleral/corneoscleral incision. Our case is unique in that a fulminant peripheral ulcerative keratitis occurred as the first manifestation of an occult collagen vascular disorder after a small clear corneal incision. There was no associated scleritis, and the infiltrate was confined to the corneal stroma at the incision and the paracentesis sites. The patient was treated with systemic steroids and sulfasalazine and responded well, with rapid re-epithelialization and healing of the ulcer. No recurrence was observed during the 19 month follow-up with the patient on the same therapeutic regimen. 1426
The pathogenesis of peripheral ulcerative keratitis in patients with rheumatoid arthritis after cataract surgery is not understood. Studies of necrotizing sclerocorneal ulceration suggest an association between the disruption of episcleral and perforating scleral vessels during surgery as a precipitating factor, leading to entrapment of the immune complexes and thus initiation of an inflammatory response.5 Alternative hypotheses suggest aqueous tear insufficiency, surgical denervation of the cornea, and the use of topically administered medications causing epithelial toxicity.6 These ulcers often begin as clean epithelial defects that appear soon after surgery in the presence of significant keratoconjunctivitis sicca secondary to the underlying disease. They commonly respond to local therapeutic measures, including aggressive artificial tears and bandage contact lens insertion and sometimes to occlusion of the lacrimal puncti. The differentiation between a paracentral sterile corneal ulcer and peripheral ulcerative keratitis (crescent-shaped destructive inflammation of the juxtalimbal corneal stroma associated with epithelial defect, presence of stromal infiltrate, and degradation) may have important implications with regard to treatment and prognosis. The onset of peripheral ulcerative keratitis in the course of a collagen vascular disorder may reflect the presence of a potentially lethal systemic vasculitis.7 The peripheral cornea has distinct morphological and immunological characteristics that predispose to inflammatory diseases, including presence of Langhans cells, and high molecular immunoglobulin M (IgM) and C1 (initial component of complement serving as the recognition unit of classic pathway of complement) leading to immune complex formation.8 Patients with rheumatoid arthritis have circulating IgM antibodies (rheumatoid factor) directed against self immunoglobulin G.9 These antigen–antibody complexes, whether derived from the limbal vasculature, tears, or aqueous humor or formed within the cornea itself, can bind C1, activating the classic complement pathway and leading to corneal destruction.10 In our case, fulminant peripheral ulcerative keratitis was encountered immediately after cataract surgery. We hypothesize that the surgical incision led to the formation of the peripheral ulcerative keratitis by facilitating the direct access of the rheumatoid factor and immune
J CATARACT REFRACT SURG—VOL 26, SEPTEMBER 2000
CASE REPORTS: AKPEK
complexes to the stroma by breaking the immune privilege of the cornea. Because of the multiple and varied etiologies of peripheral ulcerative keratitis, appropriate management requires the establishment of correct diagnosis. Dermatologic, neurologic, traumatic, infectious and postinfectious disorders; abnormalities of the eyelids and eyelashes; and systemic and local autoimmune diseases should be considered in the differential diagnosis of peripheral ulcerative keratitis. Antimicrobial therapy, systemic tetracycline, lid hygiene, correction of anatomic lid and eyelash problems, and lubrication regimens, including punctal occlusion and temporary or permanent tarsorrhaphy, can be helpful. However, in patients with an underlying collagen vascular disorder, systemic therapy with immunosuppressive/immunomodulator agents may decrease the likelihood of ocular morbidity and, in some cases, mortality.1 Our patient was treated with systemic steroids and sulfasalazine as well as topical steroids and prophylactic antibiotics. The corneal ulcer re-epithelialized in 2 days. Topical treatment was tapered and discontinued over 2 weeks. The ulcer did not recur in the 19 month follow-up with the patient on systemic treatment. This case emphasizes that peripheral ulcerative keratitis may occur with a small clear corneal incision as the presenting sign of an occult rheumatoid arthritis.
References 1. Foster CS, Forstot SL, Wilson LA. Mortality rate in rheumatoid arthritis patients developing necrotizing scleritis or peripheral ulcerative keratitis; effects of systemic immunosuppression. Ophthalmology 1984; 91:1253– 1263 2. Jones RR, Maguire LJ. Corneal complications after cataract surgery in patients with rheumatoid arthritis. Cornea 1992; 11:148 –150 3. Maffett MJ, Johns KJ, Parrish CM, et al. Sterile corneal ulceration after cataract extraction in patients with collagen vascular disease. Cornea 1990; 9:279 –285 4. Salamon SM, Mondino BJ, Zaidman GW. Peripheral corneal ulcers, conjunctival ulcers, and scleritis after cataract surgery. Am J Ophthalmol 1982; 93:334 –337 5. Dı´az-Valle D, Benı´tez del Castillo JM, Castillo A, et al. Immunologic and clinical evaluation of postsurgical necrotizing sclerocorneal ulceration. Cornea 1998; 17:371– 375 6. Hemady R, Chu W, Foster CS. Keratoconjunctivitis sicca and corneal ulcers. Cornea 1990; 9:170 –173 7. Messmer EM, Foster CS. Vasculitic peripheral ulcerative keratitis. Surv Ophthalmol 1999; 43:379 –396 8. Pleyer U, Bergmann L, Krause A, Hartmann C. Autoimmunerkrankungen der peripheren Hornhaut; immunpathologie, Klinik und Therapie. Klin Monatsbl Augenheilkd 1996; 208:73– 81 9. Koffler D. The immunology of rheumatoid diseases. Clin Symp 1979; 31:1–36 10. Mondino BJ. Inflammatory diseases of the peripheral cornea. Ophthalmology 1988; 95:463– 472
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