What Causes a Stromal Scar and How Is It Treated?

A stromal scar is an area of opacity that develops within the connective tissue layer of an organ. It is most commonly discussed in the context of the cornea, the clear, dome-shaped outer layer of the eye. The corneal stroma makes up the majority of the tissue’s thickness and is the primary structural layer maintaining transparency. A scar in this region directly compromises the ability of light to pass through to the retina, significantly impacting vision.

The Anatomy and Biology of Scar Formation

The corneal stroma accounts for approximately 90% of the cornea’s thickness and consists primarily of highly organized collagen fibers. These fibers are arranged in hundreds of uniform, parallel layers called lamellae, a precise structure that allows light to transmit clearly. Specialized cells known as keratocytes reside between these lamellae, maintaining the stroma’s unique composition and clarity.

When the stroma sustains an injury, whether from trauma or infection, resident keratocytes are activated as part of the healing response. These cells undergo a transformation process, converting into fibroblasts and, subsequently, highly contractile myofibroblasts. Myofibroblasts generate strong mechanical forces and secrete new extracellular matrix components, including collagen.

The newly deposited collagen, however, is laid down in a haphazard and disorganized manner, differing greatly from the precise latticework of the original stroma. This irregular structure disrupts the uniform arrangement of the collagen lamellae, causing light to scatter rather than pass directly through. The resulting area of dense, opaque tissue is the stromal scar, a permanent fixture that replaces the previously transparent corneal tissue. The extent of this cellular transformation and new matrix deposition directly correlates with the density and size of the resulting opacity.

Primary Triggers of Stromal Scarring

Keratocyte transformation and subsequent scarring are initiated by external factors that damage the corneal tissue. Infectious causes represent a significant category, where pathogens directly invade and destroy the stromal structure. Common examples include bacterial keratitis, often linked to contact lens misuse, and viral keratitis, such as that caused by the Herpes Simplex Virus.

Fungal infections, though less common, can lead to particularly dense and deep scars due to the organisms’ ability to penetrate the stroma extensively. Physical trauma is another direct route to scarring, including injuries from foreign bodies that penetrate the corneal surface or chemical burns that destroy multiple cell layers. The severity of the initial injury often dictates the extent of the subsequent fibrotic response.

A third category is iatrogenic scarring, which arises as a complication following eye surgery. Procedures such as refractive surgery, while generally safe, can sometimes lead to an exaggerated or atypical wound healing response in the stroma. Any disruption to the corneal architecture carries the risk of stimulating keratocyte activity, highlighting the delicate balance required to maintain corneal clarity following intervention.

Visual Consequences and Patient Impact

The presence of a stromal scar fundamentally impairs vision because the opaque tissue blocks or heavily scatters incoming light. This prevents a clear image from being focused onto the retina, leading to a range of visual symptoms. The most immediate consequence is blurred vision and a reduction in measurable visual acuity.

Patients frequently report increased glare and halos around lights, particularly in low-light conditions, due to the scattering effect of the disorganized collagen. Light sensitivity, or photophobia, can also become a persistent issue. When a scar is located directly over the pupil, in the central visual axis, even a small opacity can cause maximum visual impairment.

The location and density of the scar determine the functional impact, ranging from minor visual disturbances to severe vision loss. Scar tissue can also lead to irregularities in the corneal surface, causing chronic irritation or discomfort. The resulting loss of visual function can severely limit daily activities, including driving and reading.

Strategies for Mitigation and Treatment

Managing a stromal scar begins with addressing the underlying cause, such as aggressive treatment of an active bacterial or viral infection, to minimize initial tissue destruction. For mild or very shallow scars, clinicians may attempt non-surgical management using topical medications. These often include corticosteroids to suppress the inflammatory response that drives keratocyte transformation, or anti-fibrotic agents, though their effectiveness in established scars is highly variable.

When a scar is well-established and significantly affecting vision, surgical intervention is typically required to restore transparency. For superficial opacities that affect only the anterior layers of the stroma, Phototherapeutic Keratectomy (PTK) is an option. This procedure uses an excimer laser to precisely vaporize and remove the scarred tissue, effectively polishing the corneal surface.

Deeper scars require partial-thickness corneal transplantation, known as lamellar keratoplasty. Procedures like Deep Anterior Lamellar Keratoplasty (DALK) allow the surgeon to selectively remove the scarred anterior stroma while leaving the patient’s healthy innermost layer, the endothelium, intact. Preserving the patient’s own endothelium reduces the risk of long-term rejection compared to a full-thickness transplant.

For severe, widespread, or very deep opacities that involve the entire thickness of the stroma, Penetrating Keratoplasty (PKP) is the final recourse. This involves replacing the entire central portion of the scarred cornea with a donor graft. While a highly effective treatment for restoring sight, PKP requires significant post-operative care and carries the highest risk of immunological rejection, making it a treatment reserved for the most visually compromised cases.