Corneal perforation and its repair, and re-perforation, and re-repair in a
Sjogren’s syndrome patient
Mary E. Kutch, OD
Indiana University School of Optometry resident- Guanajuato, Mexico 2008-9
PUCO resident- Johnathan M. Wainwright Memorial VAMC, Walla Walla, WA 2007-8
Abstract:
A report of the spontaneous corneal perforation in a rheumatoid arthritis patient with
secondary Sjögren’s syndrome, detailing its repair, re-perforation, re-repair, complications, and
co-management throughout, as well as alternative repair strategies.
A 78yo Caucasian male with rheumatoid arthritis and secondary Sjögren’s syndrome presented
to our clinic reporting a “blurry, leaky, red, itchy,” severely light-sensitive right eye and crusting
discharge for 3 days- without any associated trauma. His current systemic medications included 200mg
of Hydroxychloroquine taken twice a day and 20mg of Leflunomide for his Rheumatoid arthritis, as well
as treatment for hypertension, hypothyroidism, depression, and atrial fibrillation. His ocular history
includes bilateral inferior punctal cautery for keratoconjunctivitis sicca and sterile peripheral corneal
ulcer of the left eye five years prior. Current ocular medications are limited to Refresh Plus unit dose,
prescribed 5+ times per day- but patient commenting that he is using it every morning, and, “my wife
says I should use it more often.”
Uncorrected visual acuities measured 20/150 in the right eye, improving with pinhole to 20/60
and left eye at 20/40. Previously, vision was correctible to 20/20 in both eyes. The right pupil was
miotic, with a marked consensual pain response. Slit lamp examination of the right eye revealed 3+
conjunctival injection, a shallow anterior chamber, and 2x1.8mm ulcerated area with a 0.3mm centrally
eroded area inferior to the line of sight. Fluorescein stain confirmed a positive Seidel’s sign, and
Goldmann Tonometry measured the intraocular pressures at 0 and 11mmHg OD/OS.
The nearest corneal specialist, 50 miles away, was consulted, with emergency surgical referral
available in 2 hours to repair the perforated corneal ulcer. One drop of Homatropine 5.0% was instilled
in-office in the right eye, as well as Ciprofloxacin HCl 0.3%, to be used every 15 minutes until corneal
consult. The patient was also instructed to increase his dosing of Refresh Plus to at least four times per
day in the other eye.
Without trauma, what led to the perforation of this cornea? The cornea is an avascular tissue, made
up of stratified squamous non-keratinized epithelium, with microplicae extending at its surface.4 A
glycocalyx clings closely to these microplicae and helps maintain a moist, translucent, and resilient
window to the world. 4 Its hydrophilic glycosylated extracellular domain attracts the liquid tearfilm as
well as repels pathogens, and allows the lids to glide past.4 The tearfilm plays a crucial role in
maintaining the health and transparency of the cornea, with its major components flowing from the
Meibomian glands and lacrimal gland, minor contributions from the accessory glands of Krause and
Wolfring, and conjectured assistance from the sebaceous glands of Zeiss and sweat glands of Moll.4 In
secondary Sjögren’s syndrome, the almond-sized lacrimal gland is attacked by CD4, B and T
lymphocytes due to an autoimmune disease, such as rheumatoid arthritis (RA.) Additionally, with RA,
due to the induced androgen-deficient state- it is thought that there is decreased anti-inflammatory
cytokine and transforming growth factor-β (TGF- β) released. 4 In general, immune-mediated
inflammation is thought to play a part in keratoconjunctivitis sicca- with unstable corneal epithelium and
infection exacerbated by deficient surface immunity- as well as the upregulation of degrading
collagenases and matrix metalloproteases in the corneal epithelium. Additionally, deposition of immune
complexes in the limbal vessels result in activation of complement and chemotaxis of inflammatory cells
further worsening the condition.12 Topical NSAIDs also induce this process, increasing the expression of
proteases, such as MMP-1 and -8, which degrade the corneal epithelium and can result in ulcerative
keratolysis, as has been reported in the literature following cataract surgery in a Stevens Johnson
syndrome patient8.
Rheumatoid arthritis (RA) is a common chronic disease, affecting about 1% of the population
worldwide.7 However, it remains unknown what sparks the start of inflammation and continues it within
the joints- or extra-articularly in those testing positive for Rheumatoid Factor (RF,) but not all.7 Some
theories pinpoint the origin as a mesenchymal disorder. Diagnosis includes four or more of the
following: morning joint stiffness lasting at least an hour, arthritis of three or more joints, arthritis of the
proximal interphalangeal, metacarpophalangeal or wrist joints, symmetric arthritis, subcutaneous
nodules, positive test for rheumatoid factor (RF) and radiographic erosions or perarticular osteopenia in
hand or wrist joints7. RA presents with extra-articular complications in only 25% of its sufferers,
manifesting rheumatoid nodules (found on the sclera), fistulas, hematological abnormalities, vasculitis,
renal disease, pulmonary disease, and cardiac complications12. When RA expresses itself in the lacrimal
and salivary glands, with resulting keratoconjunctivitis sicca and decreased salivary gland flow, with
presence of autoantibodies, it is then termed “Sjögren Syndrome.”
Sjögren’s Syndrome (SS,) as described originally by Henrik Sjögren in 1933, is a chronic
autoimmune inflammatory disorder characterized by lymphocytic infiltration of lacrimal and salivary
glands, leading to dry eye and mouth.5 “The exact etiology is unknown, but involves genetic and
environmental features- The lacrimal and salivary glands become infiltrated with CD4+ T helper and
some B cells, salivary epithelial cells express high levels of HLA-DR, antibodies made within the gland
are directed against rheumatoid factor (Fc region of IgG) and antinuclear antigens (SS-A, SS-B), which
are not specific to salivary or lacrimal glands.” 5 Interestingly, genetic predisposition in Caucasians is
linked to HLA-DR3 and to heterozygosity of HLA-DQ, but different genetic markers in other ethnic
groups. 5
Sjögren syndrome can occur alone or secondary to rheumatoid arthritis, systemic lupus
erythematosus, or progressive systemic sclerosis. Patients with SS suffer from decreased production of
the aqueous portion of tears due to the destruction of the serous glands as well as interruption of their
neurovascular innervation. 5 The imbalance in aqueous and mucinous tear secretions leads to a relative
increase in tenacious secretions and decreased tear breakup time as well as increased debris in the tears,
which lead to decreased visual acuity, discomfort, filamentary keratitis, blepharitis (due to Meibomian
gland abnormalities,) foreign body sensation, red eye, or painful eye, but not commonly photophobia.5
The treatment goals of SS are to decrease symptoms and slow progression. This is done topically with
artificial tears, environmental changes (directing air vents away from the face, a humidifier in the home,
or even moisture chamber goggles,) as well as systemic immunomodulators when the erythrocyte
sedimentation rate (ESR) is elevated. In patients with arthralgias, treatment with antimalarial drugs is
helpful, as well as steroids, nonsteroidal anti-inflammatory drugs (NSAIDs,) azathioprine, and
chlorambucil.5
By the time our patient presented to the referral center, notes indicated the ulcerated area had
increased to 1.7mm vertically x 4mm horizontally, with 0.5mm area of perforation. No infiltrates were
seen, but the cornea had 1+ diffuse stromal edema. The anterior chamber was still described as flat,
without hypopyon. A same-day corneal lamellar patch graft was recommended with probable
tarsorrhaphy and/or conjunctival graft.
Surgical repair consisted of anesthetizing the right eye, making a paracentesis in the cornea
opposite the wound, filling the anterior chamber with viscoelastic (thus deepening it,) and an 8mm
trephine was used to mark off the ulcerated section of cornea. The marked area was dissected with a
diamond blade, and lamellar dissection performed with additional use of a crescent blade. A ½ disc of
lamellar donor cornea, shaped to match the defect, was secured over the area using 10-0 nylon, with
multiple interrupted sutures, carefully sparing central vision. The inferior conjunctiva was then
dissected free of Tenon’s capsule and a bucket-handle of conjunctiva was made and glued to the corneal
graft using Tisseel fibrin glue. Additionally, a small amount of 2% Xylocaine was injected into the
superior punctal area, followed by hot-point cautery to the superior punctum. Lastly, 2% Xylocaine was
also injected into the middle of the grey line of the upper and lower eyelids. 5-0 Dacron suture was
passed in a double-armed fashion over silicone dams and tied on the upper eyelid to create a temporary
tarsorrhaphy.
At the one-day post-op appointment, the pt reported the right eye “felt fine.” Visual acuity was
limited to light perception only in this eye. Slit lamp biomicroscope examination revealed 1+ periorbital
ecchymosis, intact tarsorrhaphy, with a small opening nasally. The conjunctival patch graft flap was
barely visible on left gaze, sutures were intact, and graft in good position. Medications now included
Prednisolone acetate 1.0% four times per day in the right eye, as well as oral Cephalexin (250mg four
times per day for five days,) Percocet as needed for pain and Ciprofloxacin qid OD. No topical steroids
were prescribed initially to allow for maximal corneal healing. Follow-up was indicated for 10 days
later.
However, the patient returned to the clinic earlier than scheduled- 10/16/07 because his suture
had come loose- snagged when he wiped his lid with a tissue. The eye comfort was “okay, but a little
watery” and vision “is pretty good now that the lid opened a little.” Visual acuity was 20/40-3 unaided,
improving to 20/40+2 pinhole. Lids showed trace ecchymosis, intact temporary tarsorrhaphy, 1-2+
conjunctival injection inferiorly. The cornea had a conjunctival flap over the inferior 20% (and covering
80% of patch graft) with the patch graft in excellent position with several interrupted sutures, remaining
cornea clear. No Seidel sign was present, the anterior chamber was deep and quiet, and the iris normal.
The remainder of the temporary tarsorrhaphy was then removed without complication. The medication
schedule was then altered to: discontinue Ciprofloxacin OD, continue PredAcetate 1.0% qid, and use
preservative-free artificial tears every 15 to 30 minutes. Follow-up was revised for two weeks later.
The patient again returned sooner than scheduled, 10/22/07, to our clinic at the Jonathan M.
Wainwright Memorial VA Medical Center. This time, he reported that his vision was blurred in the
right eye and itchy. He was using PredAcetate 1.0% qid as instructed and Refresh Plus unit dose every
30 minutes in both eyes. Visual acuity measured 10/80 (Feinbloom). Slit lamp examination noted Gr
1+ dermatochalasis of both lids without tarsorrhaphy, quiet conjunctivae, and a corneal lamellar patch
graft inferior to the line-of-sight with interrupted sutures and conjunctival flap. The graft was clear,
without infiltrates. Blood staining was present on the endothelium at the top of the crescent of the graft
(see photo 1). The anterior chamber
Photo 1: 13 days post lamellar patch graft
contained pigmented cells and trace white
cells, but no flare. The iris remained flat and
round. The patient was to continue with the
same medication schedule, refrain from
rubbing the eye, and gently clean the outer
corner of right temporal lid with moistened
cotton-tip applicator bid to decrease itching.
No sutures were removed. Follow-up was scheduled at the surgical center for 11/3/07.
The follow-up appointment shifted to 11/21/07, nearly three weeks later, at which time the graft
was doing well, vision had stabilized at 20/25 and all remaining exposed sutures were removed.
One week later, the patient returned to the referral center due to a watery eye- stating, “This is
noteworthy, because I don’t make tears.” Vision had reduced to count fingers at 3 feet in the right eye.
Slit lamp exam was remarkable for a 5x1.2mm epithelial defect on the graft with melting/thinning at the
superior graft-host junction and positive Seidel sign. Same-day surgery was performed with viscoelastic
injected to deepen the anterior chamber, and a Gundersen (conjunctival) flap covered the entire cornea.
Visual acuity was measured as light projection OD and 20/25+ in the left eye.
11/29/07 the patient returned to our care the following morning, at which time the pressure patch
was removed in-office and lids were cleaned with sterile eye wash. Current medications include
Ofloxacin (one drop hourly in the right eye) and oral pain medication. Lids were remarkable only for
dermatochalasis, the right eye cornea was covered by total conjunctival flap, well-apposed, with tissue
glue at the seal inferiorly and 2 interrupted sutures. No Seidel sign was present. The anterior chamber
appeared deep through the conjunctival graft, no hypopyon was seen, and the iris was visible.
Intraocular pressure was soft and equal to the left eye by palpation. Medications were to be continued as
directed, and then Ofloxacin decreased to four times daily the following day. Fox shield was to be used
at night until follow-up the next week.
However, that evening, the patient presented to the emergency room reporting extreme eye pain.
He was given topical scopolamine and timolol 0.5%, after consultation with the patient’s surgeon. In the
morning, the right eye intraocular pressure measured 57mmHg by Tonopen and angle closure or
retained viscoelastic in the anterior chamber was presumed, since the view of the anterior segment was
obscured by the conjunctival graft and tissue glue. Over the course of the day, the intraocular pressure
slowly decreased to 37mmHg with the use of oral acetazolamide, as well as topical anti-glaucoma
medications in-office.
One week postoperatively, the patient reports a feeling of improved sight OD, no eye pain, but
depth perception problems. Current ocular medications for the right eye included Ofloxacin four times
daily, Refresh Plus (carboxymethylcellulose 0.5%) every 30 minutes, Bimatoprost twice daily,
Brimonidine four times daily, Scopolomine twice daily and Cosopt (timolol 0.5% and dorzolamide
2.0%) four times daily to reduce the intraocular pressure. Visual acuity has improved to hand motion at
6 feet OD, with a pharmacologically dilated pupil. Slit lamp examination reveals the total conjunctival
flap apposed to cornea with 2 sutures, decreased corneal edema, and the original corneal patch graft able
to be visualized inferiorly through the conjunctival graft. The anterior chamber was well-formed and the
iris was visible. (See Photo 2.) Intraocular pressure is now reduced to 8mmHg in the right eye.
Ofloxacin, Brimonidine, and Bimatoprost were then discontinued, with Scopolomine continued twice
daily and Cosopt reduced to twice daily, as well as Refresh Plus q30min.
12/14/07, 1 week later, pt returns to clinic reporting “scratchy feeling” on one occasion, but no
pain. Visual acuity has again improved to 8/600
Photo 2: 7 days post total conjunctival graft
(Feinbloom) in the right eye (with
pharmacological mydriasis). Slit lamp exam is
consistent with the prior visit, no staining with
fluorescein OU, and intraocular pressure 10mmHg
in the right eye. Cosopt and Hyoscine were then
discontinued, with Refresh Plus q30min, warm
compresses qam with non-preserved saline
recommended for “washing” eyes.
While our patient’s corneal perforation was repaired with a corneal lamellar patch graft, then
conjunctival graft, many alternatives exist and there aren’t any clear guidelines for the indications of
surgical procedures or systemic management of rheumatoid corneal perforations2. In the most
traditional sense, a penetrating keratoplasty could be performed to repair a perforation, but due to the
risk of rejection, particularly with inflammatory disease, and the small size of the perforation, it could be
considered overkill. Most successful with small (<1.5mm diameter) perforations, cyanoacrylate glue
with or without a bandage contact lens has been used for acute repair13,15,16,21,22. With the advantage of
in-office application at a slit lamp biomicroscope, glue is inexpensive and readily available16. Several
polymers of cyanoacrylate glue are on the market (N-heptyl, isobutylacryl, methyl-2-, octyl, etc…), with
their main difference being the length of the carbon sidechain16. The longer the sidechain, the longer the
glue takes to polymerize, but less formaldehyde is released and it is less toxic to the corneal tissue16.
Due to optimum combination of these two factors, Adhist (N-butyl-2-cyanoacrylate glue was favored by
Sharma, et al16.
Fibrin glue (Tiseel) is also frequently used for this type of repair, and has been shown as
effective as cyanoacrylate glue, with less inflammatory effects, less corneal vascularization, and more
physiologic healing16. It is made at a local blood bank and is also readily available16. A bandage contact
lens alone would be considered a very conservative approach, and would work better in someone who is
a fast-healer- not an immune-modulated corneal perforation.23
Amniotic membrane is also being used to patch corneal perforations, but is more expensive and
not as readily available. A more novel and non-biological approach, the Neuro Patch is a polyurethane
patch which is used as a dura mater substitute in neurosurgery13. It is biocompatible and allows for
migration of connective tissue without inflammatory cells as found on a histological examination13.
Autologous lamellar scleral patching has been used when glue failed- the superior conjunctiva is
dissected, a small circle of sclera is then cut with a trephine, sewn to fit over the corneal defect with 10-0
nylon sutures, and covered with a bandage lens14. Within 1 month in the study by Prydal, it was
transparent. The transparency of scleral tissue can be explained by various theories- including the
corneal collagen fibers replaced the scleral fibers, or that sclera needs an epithelium covering it, or it
will thin. The advantage to using one’s own sclera is that it is readily available, there is no risk of
rejection, and it has high tensile strength14.
Deep lamellar keratoplasty is also being used to “plug the hole from the back” without the higher
risk of rejection and induced irregular astigmatism like a penetrating keratoplasty, but still requiring a
fresh donor cornea and is a technically more difficult surgery17.
Tectonic keratoplasty, also known as a “covering graft,” works well for larger perforations or
melted corneas11,20. A 360’ periotomy of the conjunctiva is performed, and the entire donor graft is sewn
on top11. The donor graft has been stored in glycerin and is white opaque11. While not optimal for visual
results, it preserves the integrity of the globe while waiting for a transplant or may degrade, exposing a
healed cornea11,20.
Returning to our patient, he returned in January for a follow-up visit, three months after the first
onset of perforation. At this time, he has no complaints or reported changes in his vision and ocular
comfort, feels he has usable vision for mobility/peripheral awareness OD. Current ocular medications
are limited to faithful Refresh Plus use hourly OU. His visual acuity is slightly reduced at 6/600 OD, but
pupils react normally. Upon slit lamp exam, there is a transparent, bulbous, fluid-filled avascular lesion
at the nasal limbus, near the site of the patch graft which does not stain with fluorescein dye, no Seidel
sign was present, and intraocular pressure was normal. (See Photos 3 & 4) While concerns include a
second anterior chamber forming from re-perforation and leakage under the conjunctival graft, same-day
consultation with the patient’s surgeon identified the lesion as an epithelial inclusion cyst, with biannual
observation recommended and no negative effect toward prognosis expected.
Epithelial inclusion cysts are typically avascular, pearly, white
masses in the cornea, which do not stain with fluorescein dye and
present on the cornea or limbus9,10. They are created by residual
conjunctival epithelial cells that remain under the graft, proliferate
in the anterior stroma and goblet cells secrete mucus into a central
cavity10. They are most frequently found following corneal surgery
or minor trauma, but have also been reported with pterygia, vernal
catarrh, pyogenic granuloma, following scleral buckling, radial
keratotomy, and trabeculectomy3,6,9. Mitomycin-C is used in an
effort to prevent their formation10. In examining said lesion,
differential diagnoses include bullous keratopathy, neoplasm,
abscess, dermoid cyst, and iris prolapse3. While our patient was
Photos 3&4: 3 months post total
conjunctival graft with epithelial inclusion
cyst, without (above) and with NaFl stain
and cobalt filter (below.)
not bothered by his cyst, surgical criteria for excision would
include a symptomatic patient, a cyst inducing high amounts of
irregular astigmatism, lagopthalmos, or decreasing vision3,9.
Management options include observation, peeling the lesion off
with blunt dissection, a Yag laser, cryotherapy, or chemical
cautery with trichloroacetic acid9.
Additional management ideas for our patient include
protective eyewear, increased viscosity artificial tears to lengthen
the duration on the ocular surface, oral tetracyclines, a humidifier
in the home, and flaxseed oil (1 gram orally, once daily) which is
thought to yield additional benefits for his macular degeneration. Due to his history of cardiac disease,
Salagen (pilocarpine) is contraindicated or used with caution. Concerning the loss of binocular vision,
additional management included a discussion of driving requirements and general sensibilities if the
patient were to resume driving, such as increased head movement and scanning, and cognizance of his
reduced depth perception. The option of a Fresnel segment add-on or Eli Pelli lens to increase right-side
visual field was discussed, but the patient declined. Finally, there is the option to trephine a window in
the Gundersen flap, providing clear central vision. However, the surgeon advised against this option
until a minimum of 6 months post-operatively, stating that the prognosis will worsen and repair will be
more difficult if the “window” were to perforate. In Sjögren’s and other extreme dry eye patients, the
risk of this happening is higher.
In other comparative studies of Rheumatoid arthritis (RA,) the most common ocular
manifestations include keratoconjunctivitis sicca, scleritis, and sterile corneal ulceration2, 12. Lamellar
patch grafts, in particular, were preferred in one study of RA perforations because host endothelium is
used, decreasing rejection rate in patients with autoimmune disease. However, Malik et. al. noted
penetrating keratoplasty, glue, conjunctival recession, and lamellar keratoplasty were the most popular
methods. Additionally, systemic immunosuppression was found to be most effective than steroids
merely perioperatively2. This included, but was not limited to: prednisone, cyclophosphamide,
methotrexate, cyclosporine, and azathioprine2. While associated with undesirable ocular side effects,
long-term topical steroid use was not linked to a higher rate of keratolysis12. Despite treatment efforts,
32% of RA grafts still failed at 2 years’ time in the study by Malik et. al. and 37% of penetrating
keratoplasties had failed by one year’s time in rheumatoid patients in Bernauer’s study12,13,2.
In conclusion, the treatment of Sjögren’s patients is an ongoing journey of management
including lubrication, immunosuppression, ocular surface and visual rehabilitation. Care should be
taken to thoroughly evaluate any patient suspected of a tear deficiency disorder before refractive surgery
or long-term topical NSAID use is recommended to prevent unpleasant post-operative surprises19. Good
communication with these patients’ primary care physician and rheumatologist should also be
maintained for optimum systemic and ocular care, because as said by Tan, “Approximately 50% of
noninfectious peripheral ulcerative keratitis is associated with a systemic autoimmune disease, such as
rheumatoid arthritis…and the identification of systemic disease is important because there may be a high
mortality rate if not appropriately managed.20”
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foundations and clinical practice. Philadelphia: Lippincott, Williams & Wilkins, 2005.
5. Fox, R and H. Kang. “Sjögren’s Syndrome.” Textbook of Rheumatology, 4th ed. 1993:931-942.
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11. Lifshitz, Tova and Tzafrir Oshry. Tectonic Epikeratoplasty: A Surgical Procedure for Corneal
Melting. Ophthalmic Surgery and Lasers; Jul/August 2001; 32, 305.
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13. Nuyts, et. al. Use of a Polyurethane Patch for Temporary Closure of a Sterile Corneal Perforation.
Arch Ophthalmol 1999:117:1427-1429
14. Prydal, J.I. Use of autologous lamellar scleral patch graft to repair a corneal perforation. British
Journal of Ophthalmology. 2006;900;924
15. Setlik, et. al. The Effectiveness of Isobutyl Cyanoacrylate Tissue Adhesive for the Treatment of
Corneal Perforations. American Journal of Ophthalmology. 2005; 920-921.
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2003;110(2):291-8.
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Perforation. American Journal of Ophthalmology. 2003 Jun; 135(6):896-7
18. Symes, et al. Corneal Perforation Associated With Pellucid Marginal Degeneration and Treatment
With Crescentic Lamellar Keratoplasty: Two Case Reports. Cornea. 2007;26(5):625-8.
19. Ou, J and E Manche. Corneal Perforation After Conductive Keratoplasty in a Patient With
Previously Undiagnosed Sjögren Syndrome. Archives of Ophthalmology. 2007 Aug;125(8):1131-2
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Cornea 2006 Jun;25(5):628-30.
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Corneal Perforations. American Journal of Ophthalmology Nov 2005:920-921.
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Perforation. Cornea 2001 Mar;20(2):220-1.
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autoimmune polyendocrinopathy-Candidiasis-Ectodermal dystrophy. Cornea. 2007 Aug; 26(7):880-2