Dr. Gerald R Schultz, G03079
Corneal melts with the threat of perforation following anterior segment surgery is an unwelcome surprise following otherwise uncomplicated surgery in supposedly healthy patients. This is a report of four of our patients who developed a corneal melt soon after uneventful cataract surgery, and how they were treated. Also included is a young woman who developed a spontaneous corneal perforation after removal of a cerebellar tumor which involved the 5th nerve.
Corneal melts following surgery can be associated with collagen auto-immune disease, i.e. rheumatoid arthritis. It can occur in severe ocular surface disease, such as ocular cicatricial pemphigoid and chemical burns, long-term use of topical steroids and systemic disorders, i.e. diabetes.
It is also seen in neurotrophic conditions, i.e. herpes keratitis and damage to the 5th cranial nerve, where the corneal epithelium and stroma do not get the necessary nutrition from the damaged nerve fibers, and in severe dry eye diseases, i.e. Sjorgen’s Syndrome. Post-operative patients receiving the non-steroidals , nepafenac and ketorolac have developed corneal melts Following is a discussion on the pathophysiology of this complication, methods of identifying patients pre-operatively that may have a proclivity for it following surgery, and its treatment.
Summary of Cases
First Case – 68 year old female with a history of arthritis and Cirrhosis from Hepatitis A. The patient had patches of punctate epithelial erosions (PEEs) post-operatively in the other eye; the phakic eye with cataract was unaffected. The day after surgery she developed microcystic edema and punctate epithelial erosions. Ocular pressure was normal. She was placed on Acuvail and topical steroids. One week following cataract extraction in the second eye the epithelium was clear, but the stroma was hazy. At the three week visit she had a central epithelial defect and a stromal melt. A penetrating keratoplasty was performed, the puncta were plugged and Restasis and lubricants were prescribed. The epithelium of the donor tissue developed significant patches of geographic PEES, but subsequently cleared. Current vision is 20/50.
econd Case – 72 year old male with absence of tears, dry mouth, Sjogren’s Syndrome suspect and PEEs. Pre-cataract extraction he was treated with Restasis and tear supplements. During surgery silicone plugs were placed in the lower punctum. Postoperatively he received Acular, prednisolone and antibiotic drops and ointment. Two weeks later he presented with a corneal melt, descemetocele a microperforation, and a shallow anterior chamber. Octyl cyanoacrylic glue and a contact lens were applied, the AC deepened and a penetrating keratoplasty was performed.
Third Case – 70 year old female with Sjogren’s Syndrome who had a refractive lens exchange for +9 D and was placed on a non-steroidal anti-inflammatory drug (NSAID). A week later the corneal perforated. It was sealed with glue and a contact lens and a penetrating keratoplasty and lateral tarsorrhaphy were performed. Current vision with contact lens is 20/25.
Fourth Case – A 65 year old male had a corneal melt 3 weeks after cataract extraction. He also had a neurotrophic keratopathy, Sjogren’s Syndrome, and patches of punctate keratopathy. He had been receiving Acular post-operatively. After a keratoplasty the vision was 20/150.
These cases have many similarities. Cases 1, 2 & 4 had a superficial punctate keratitis. All of them had dry eyes. Cases 2 & 4 had absent corneal sensation. Acular was used PO in cases 1,2, & 4 and a different NSAID in case 3. The melts did not occur at the site of the corneal incisions, but more centrally. All the patients underwent penetrating keratoplasty and were placed on Restasis post-op. A lateral tarsorrhaphy was performed in cases 2 & 3. Doxycycline was given in cases 2 & 4 and autologous serum in cases 2 & 3.These are inhibitors of Matrix Mucopolysaccharides (MMPs) that are released from polymorphonuclear cells (PMNs) and can dissolve collagen and other components of the extra-cellular matrix (ECM). Under ordinary circumstances the MMPs and ECM both increase during the healing of a corneal wound. If the amount of ECM is inadequate and the collagen produced is unstable, the collagen melts. Inadequate collagen deposition is seen in collagen diseases like rheumatoid arthritis and lupus.
NSAIDs that are used in conjunction with cataract surgery to reduce the incidence of cystoid macular edema and to decrease PO pain by reducing corneal sensation may interfere with wound healing and can be partially responsible for the corneal melts.
Poor or absent sensation has been traced to depletion of substance P and acetylcholine which induce epithelial proliferation. This neurotrophic keratitis is staged in Mackie’s classification; Stage I has punctate epithelial keratopathy, Stage II has persistent epithelial defects (PED) and Stage III has melting of the stroma and perforation.
Based upon the complications that occurred in these cases, we propose the following guidelines in high risk cases:
Use a higher thresh-hold for indications for surgery Evaluate pre-op the corneal sensation & tear production
Closely observe patients with ocular surface and systemic collagen diseases peri-operatively. Avoid NSAIDs in patients with ocular surface disease.
Aggressively lubricate the eyes in the peri-operative period. This includes using non-preserved tear supplements, cyclosporine A (Restasis), punctal plugs, therapeutic soft contact lenses and, if necessary, tarsorrhaphy.
Use of inhibitors of MMP production – oral doxycycline, autologous blood serum which contains the MMP inhibitor alph2-macroglobulin.
References
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