Introduction
The integrity of the cornea can be compromised by both inflammatory and noninflammatory conditions, which may lead to stromal thinning, melting, and perforation. Progression may be slow over months to years, or may be rapid over hours to days. Rapid, proper recognition and management of these conditions is crucial to restore vision and to re-establish the integrity of the eye.
Corneal Thinning From Noninflammatory Disorders
Noninflammatory corneal thinning disorders cause progressive ectasia caused by thinning of the stroma. The most common of these disorders include keratoconus, pellucid marginal degeneration, keratoglobus, and posterior keratoconus. Progressive corneal thinning (ectasia) is a rare but serious complication after laser refractive surgery. These conditions generally are slowly progressive. The primary goal, therefore, is to maintain functional vision (see Chapter 4.18 for more information).
Corneal Thinning and Melting From Inflammatory Disorders
Inflammatory corneal disorders can cause thinning with stromal melting. These conditions are often associated with pain, epithelial defects, corneal neovascularization, and other inflammatory changes. Progression is fast and emergent treatment is warranted upon diagnosis.
Noninfectious inflammatory causes include peripheral ulcerative keratitis (PUK), Mooren’s ulcer, Terrien’s marginal degeneration, and collagen vascular disorders. Infectious inflammatory causes include viral herpetic keratitis, bacterial keratitis, and fungal keratitis.
PUK suggests an autoimmune-mediated process and often is associated with rheumatoid arthritis. PUK (see Chapter 4.16 ) is seen with Wegener’s granulomatosis, systemic lupus erythematosus, polyarteritis nodosa, ulcerative colitis, and relapsing polychondritis.
Medical treatment is directed both locally at the cornea and systemically to address the underlying systemic inflammatory process. The goals of local (ocular) treatment are to (1) provide local supportive therapy to decrease corneal melting; and (2) promote re-epithelization of the corneal surface. These goals are accomplished using the following modalities: aggressive lubrication with preservative-free eyedrops and ointments, punctal occlusion, placement of a bandage contact lens, patching, oral doxycycline (or equivalent), and tarsorrhaphy. Topical collagenase inhibitors and corticosteroids are of some value, but may delay healing and cause perforation by initiating stromal melting. The goal of systemic therapy is to suppress the underlying systemic disorder with immunosuppressive or immunomodulatory therapy. If the underlying autoimmune disease is not treated, the corneal pathology will not improve.
Inflammatory corneal disorders caused by infectious organisms (viral, bacterial, or fungal) also cause thinning and melting of the corneal stroma. Treating the pathogen aggressively with both topical and oral medications is most important to reduce further destruction of stromal tissue. Some advocate the use of concomitant corticosteroid drops once the infection is controlled, but this is controversial. If, despite aggressive therapy, stromal keratolysis progresses with development of descemetocele, impending perforation, or frank perforation, the goal becomes maintaining the eye’s integrity.
Surgical Treatment of Corneal Perforations
Tissue Adhesives
Descemetoceles or impending perforations can be stabilized or temporized by application of tissue adhesive and placement of a bandage contact lens with close follow-up. Studies have shown this procedure arrests the process of ulceration in noninfectious eyes. Application of tissue adhesive is much easier to perform in impending perforations than in frank perforations. Frank corneal perforations, however, can be treated successfully with application of tissue adhesives. Although perforations measuring 1–2 mm are most successfully treated, those measuring up to 3 mm have been closed. Cyanoacrylate tissue adhesive traditionally has been used ( Fig. 4.31.1 ). Its use to seal corneal perforations was first reported in 1968. Cyanoacrylate adhesive prevents re-epithelization into the zone of damaged stroma and prevents collagenase production, which leads to stromal melting.
A common technique is described below, although several other excellent techniques exist. A thorough examination of the eye prior to application of the glue must be performed, with attention to the extent of perforation, possible lenticular damage, and possible uveal prolapse at the perforation site. Placing the patient in the supine position under an operating microscope is easier than examining the patient at the slit lamp. A topical anesthetic and lid speculum should be placed in the eye. Debridement of necrotic tissue from the ulcer crater is performed. This removed material is plated onto culture media to identify a possible infectious cause. The tissue adhesive adheres best to basement membrane so debridement of 1–2 mm of normal epithelium surrounding the ulcer allows for proper adhesion of the glue. A methylcellulose spear is used to dry the site. The tissue adhesive is then placed in microaliquots on the site of perforation with an applicator. The applicator can be a needle from a tuberculin syringe, a 23-gauge Angiocath catheter (with the needle removed), or a micropipette. Alternatively, a polyethylene disc can be made and attached to a sterile wooden stick with ophthalmic ointment, and glue placed on the disc. Both are applied directly to the site of perforation ( Fig. 4.31.2 ). The disc can then be removed or left in place. The goal is to create a controlled method of placement of the smallest amount of glue to seal the perforation. The glue will solidify via polymerization over the next few minutes. A large, heaped mound over the crater is not necessary and can cause irritation and discomfort for the patient after the procedure.
The eye should be checked for evidence of leakage. If secure, then a bandage contact lens is applied, and the patient is checked at the slit lamp to confirm that the anterior chamber is forming and the glue is in place.
Application of tissue adhesive in frank corneal perforations is more challenging, as preparation of the site is more difficult secondary to the constant flow of aqueous from the perforation. Unless contraindicated, an air bubble can be placed into the anterior chamber to temporarily occlude the perforation by surface tension. Larger air bubbles risk pupillary block and increased intraocular pressure (IOP), so caution must be exercised. In eyes with flat anterior chambers, to avoid incarceration of uveal tissue or the lens, viscoelastic material may be injected into the anterior chamber.
Postoperatively, the patient may be placed on an aqueous suppressant, if medically tolerated. Patients with noninfectious perforations should receive a prophylactic broad-spectrum antibiotic four times daily. A protective shield should be kept in place at all times. Preservative-free artificial tears applied frequently will aid in lubrication with a bandage lens in place. Patients also benefit from oral doxycycline because of its ability to inhibit collagenase. Depending on the cause, infected perforations are treated with frequent fortified antibacterial, antiviral, or antifungal therapy. Initially, patients should be examined daily, and any complaints of decreased vision, pain, tearing, or photophobia should be attended to immediately. If the bandage lens falls out, it must be replaced. If the glue becomes dislodged, reapplication is often necessary.
Corneal glue remains in place for weeks to months. It is recommended to leave it in place until it loosens and dislodges on its own, leaving behind a more healthy-appearing stromal tissue.
The reported potential complications for corneal tissue adhesive application include cataract formation, corneal infiltrates, increased IOP, giant papillary conjunctivitis, retinal toxicity, keratitis, and iridocorneal and iridolenticular adhesions.
Studies have shown that fibrin glue causes less neovascularization; however, a longer time is required for the adhesive plug to form. Application of fibrin glue has been shown to be successful with the additional placement of amniotic membrane grafts for structural support of a perforated cornea.
Penetrating Keratoplasty
If the corneal perforation is not amenable to treatment with corneal glue, then tectonic grafting is indicated (either a full-thickness or lamellar graft). The smallest trephination capable of incorporating the site of perforation is chosen. Trephination of a soft eye is very difficult but is aided by the judicious use of viscoelastic materials. Alternatively, the temporary application of cyanoacrylate adhesive and sodium hyaluronate to create a normotensive eye has been described. A customized hard contact lens applied with tissue adhesive to the corneal perforation has been reported to stabilize the eye and allow for trephination. In some cases, handheld trephination may be needed. Care must be taken to avoid protrusion of ocular contents or damaging the iris or lens. The donor cornea should be secured with interrupted 10-0 nylon sutures.
Several case reports and case series have demonstrated the promising use of tectonic Descemet’s stripping automated endothelial (DSAEK) in managing both impending and sterile corneal perforations.
Postoperative care is challenging. A balance between reducing inflammation and the possibility of graft rejection, without significantly reducing the host’s immunity, must be reached. Topical corticosteroids four times daily usually are required. Aggressive antibiotic, antiviral, or antifungal treatment is continued as indicated for infectious cases. For noninfectious cases, a broad-spectrum antibiotic is used four times daily.
Patch Graft
If the perforation is too large for a tissue adhesive, but too small for a full-sized penetrating keratoplasty (PKP) procedure, then a corneal patch graft can be helpful ( Fig. 4.31.3 ). These procedures can temporarily stabilize a perforation or descemetocele or may be a permanent treatment. It is ideal for peripheral pathology. Care should be taken when used for central pathology because it can interfere with visual outcome.
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