The cornea is the transparent, dome-shaped outermost layer of the eye that functions as its primary lens, focusing light onto the retina. Corneal melt, also known as keratolysis, is a severe, sight-threatening ophthalmologic emergency involving the rapid, progressive dissolution of the corneal structure. This degenerative condition is characterized by an uncontrolled breakdown of the corneal tissue, leading to thinning and a potential loss of the eye’s structural integrity. It is considered an urgent medical crisis because it can swiftly progress to corneal perforation, resulting in permanent vision loss if not immediately halted.
The Mechanism of Corneal Destruction
The fundamental biological process underlying corneal melt is the excessive, uncontrolled degradation of the corneal stroma, the thick, collagen-rich middle layer. This destruction is driven by the over-activity of specific enzymes known as proteinases, which are released in response to significant inflammation. The most prominent of these degradative enzymes are the Matrix Metalloproteinases (MMPs), a family of zinc-dependent endopeptidases.
While MMPs are normally involved in tissue remodeling, during a melt event, inflammatory cells and pathogens release these enzymes in high concentrations. These activated MMPs aggressively cleave corneal collagen and other structural proteins, effectively dissolving the tissue’s framework. The distinction between infectious and sterile melt lies in the source of the inflammatory trigger, but both result in rapid, localized dissolution that compromises the eye’s integrity.
Primary Causes and Systemic Risk Factors
Local and Infectious Triggers
The destructive enzymatic cascade is initiated by local infections, systemic autoimmune disorders, or traumatic injuries. Infectious causes are a leading contributor, particularly microbial keratitis, which is an infection of the cornea. Bacteria, especially virulent strains like Pseudomonas aeruginosa, as well as fungi or amoebas, can trigger a rapid melt. Improper use or poor hygiene associated with soft contact lenses is a common scenario that predisposes the cornea to these severe infections. Additionally, chemical or thermal injuries to the eye can also initiate a severe inflammatory response, leading to a localized enzymatic breakdown of the tissue.
Autoimmune and Ocular Surface Disease
Corneal melt can indicate an underlying systemic condition, often involving an autoimmune response. Diseases like Rheumatoid Arthritis (RA) and Granulomatosis with Polyangiitis (GPA) are frequently associated with sterile corneal thinning. In these non-infectious cases, the immune system targets the peripheral cornea, a manifestation often termed peripheral ulcerative keratitis (PUK). Severe ocular surface diseases, such as advanced dry eye syndrome or Sjögren’s syndrome, also create a chronically inflamed and compromised environment. This persistent inflammation, combined with a lack of protective tear film components, increases the risk of developing a sterile melt. Certain topical medications, particularly nonsteroidal anti-inflammatory drugs (NSAIDs) used after eye surgery, have also been linked to corneal melt.
Recognizing the Urgent Signs of Trouble
The onset of corneal melt is typically rapid, and patients experience severe symptoms that signal an immediate emergency. Common complaints include sudden, intense eye pain and a foreign body sensation that is not relieved by blinking. A rapid decline in visual acuity is a hallmark, as the dissolving tissue impairs the cornea’s optical clarity. Visually, the eye often appears intensely red due to conjunctival injection, and the patient may exhibit photophobia, or extreme sensitivity to light.
A specific sign requiring urgent attention is a localized, crescent-shaped area of thinning on the cornea, appearing as a gray or white opaque patch. This thinning can progress quickly to the point of imminent perforation. If a full-thickness defect occurs, a corneal perforation results, often accompanied by a sudden gush of aqueous humor. This leakage causes the eye’s internal pressure to drop and the front chamber to flatten, necessitating immediate transfer to an emergency ophthalmology service.
Emergency Treatment Strategies
The treatment for corneal melt focuses on two simultaneous objectives: halting the enzymatic destruction and addressing the underlying cause of the inflammation. Medical management is aggressive, often beginning with high-dose, broad-spectrum topical antibiotics, which may be administered hourly, if an infectious cause is suspected. Systemic antibiotics, such as oral tetracyclines like doxycycline, are frequently used because they function as collagenase inhibitors, blocking MMP activity to slow the destructive process.
For sterile, autoimmune-related melts, the primary strategy involves aggressive systemic immunosuppression to control the underlying disease. This often requires high-dose systemic corticosteroids or other powerful immunosuppressive agents, managed in coordination with a rheumatologist. Topical steroids are approached with caution, as they can sometimes worsen the melt by interfering with corneal healing.
When thinning is severe or has resulted in a small perforation, surgical interventions are necessary to restore the eye’s integrity. Small perforations (typically less than two millimeters) can often be sealed using a tissue adhesive such as cyanoacrylate glue. This glue acts as a temporary patch, allowing the underlying tissue to heal while it protects the eye from further damage. For larger areas of tissue loss, a more complex surgical procedure is required, such as an amniotic membrane graft or an emergency therapeutic penetrating keratoplasty (a full-thickness corneal transplant). The prognosis for vision depends heavily on the speed of intervention and the ability to control the underlying inflammation.