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Bilateral surgically induced necrotising scleritis with secondary superinfection
  1. M R Vagefi1,
  2. D A Hollander1,
  3. G D Seitzman2,
  4. T P Margolis2
  1. 1Department of Ophthalmology, University of California, San Francisco, CA, USA
  2. 2Department of Ophthalmology and The Francis I Proctor Foundation, University of California, San Francisco, CA, USA
  1. Correspondence to: Todd P Margolis MD The Francis I Proctor Foundation, 95 Kirkham Street, Room 305, University of California at San Francisco, San Francisco, CA 94143–0944, USA;

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Surgically induced necrotising scleritis (SINS) is a rare complication of ocular surgery that has been described after pterygium excision, cataract extraction, trabeculectomy, penetrating keratoplasty, strabismus surgery, and retinal detachment repair.1–3 We describe a rare case of bilateral necrotising scleritis complicated by a secondary polymicrobial infection following uncomplicated phacoemulsification and pterygia excision.

Case report

A 66 year old Samoan male, with type II diabetes, end stage renal disease, coronary artery disease, and gout underwent uncomplicated combined phacoemulsification and bare sclera pterygium excision (without antimetabolites) in the right eye, followed 1 month later by the same combined procedure in the left eye. Three weeks later, the patient developed severe right sided eye pain. An erythrocyte sedimentation rate was 98 mm in the first hour, and oral prednisone (80 mg/day) was initiated. A temporal artery biopsy was negative and prednisone was discontinued after 4 days of treatment. One week later, the patient developed left sided eye pain as well as a productive cough. Corneoscleral necrosis developed in the left eye and rapidly progressed to perforation.

On examination, the visual acuity was 20/40 right eye and light perception left eye. In the left eye (fig 1), there was ischaemic scleral necrosis with thinning, perforation, and iris prolapse at the nasal limbus. On the right, there was a hypopyon and a 4 mm×3.5 mm area of necrotic, ischaemic sclera with thinning at the limbus. Fundus examination of the right eye demonstrated moderate non-proliferative diabetic retinopathy. B-scan ultrasound revealed choroidal thickening right eye and haemorrhagic choroidals left eye.

Figure 1

 (A) Right eye demonstrating a local area of scleral necrosis at the nasal limbus and a hypopyon. (B) Left eye demonstrating scleral necrosis with thinning, perforation, and iris prolapse at the nasal limbus.

Scleral cultures were taken, and the patient’s corneoscleral perforation was emergently closed with cyanoacrylate glue. An extensive laboratory evaluation for systemic aetiologies of scleral necrosis was unrevealing except for a mildly elevated rheumatoid factor of 62 IU/ml (normal <40 IU/ml.) Culture results demonstrated a bilateral polymicrobial infection, with Streptococcus pneumoniae and Streptococcus viridans in the right eye, and Streptococcus pneumoniae, Streptococcus viridans, and Haemophilus influenzae in the left eye.

The patient was treated with topical (gatifloxacin and vancomycin), intravenous (ciprofloxacin), and subconjunctival (vancomycin) antibiotics. In addition, oral anticollagenase therapy (tetracycline and vitamin C) was employed. Repeat cultures taken on day 3 were negative. By day 4, however, the vision in the right eye had decreased to 20/200, the area of necrosis had enlarged and the pupil began to peak nasally. Systemic immune suppression was initiated with an intravenous pulse of 1 g of both cyclophosphamide and methylprednisolone. Within 48 hours of initiating immune suppression, granulation tissue began to fill the areas of necrosis and ocular pain subsided. Two months following presentation, while on a prednisone taper, the patient’s best corrected visual acuity was 20/40 right eye. He remained at light perception in the left eye.


We believe this complicated case of bilateral, rapidly progressing, necrotising scleritis in a post-surgical patient represents a case of bilateral surgically induced necrotising scleritis (SINS) complicated by secondary polymicrobial infection. SINS has been reported following bare sclera pterygia excision, though it is more commonly associated with adjunctive β irradiation, thiotepa, and mitomycin C.4–6 The time course of events, as well as the response to immune suppression supports a primary autoimmune aetiology complicated, secondly, by a polymicrobial infection. Immune suppression, however, was initiated only after aggressive antimicrobial therapy.

The necrotising nature of the scleritis in our patient is consistent with the series by O’Donoghue et al in which a fourfold greater rate of necrosis occurred in post-surgical patients compared to a non-surgically induced scleritis population.2 In their series, the majority of patients (75%) had two or more surgical procedures before the onset of scleritis, and systemic immune suppression was necessary in 93% of patients. Our case similarly illustrates the need to consider immunosuppressive therapy in patients with postoperative necrosis.


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