Penetrating Keratoplasty: Indications, Techniques, and Recovery

A full-thickness corneal transplant, known as penetrating keratoplasty (PK), replaces a damaged or diseased cornea with a donor graft. Despite advancements in partial-thickness transplants, PK remains essential for conditions affecting the entire corneal thickness.

Corneal Layers Relevant To P.K.

The cornea is a transparent, multi-layered tissue, each layer contributing to structural integrity and optical function. PK involves replacing the full corneal thickness, making precise alignment critical for graft survival and visual outcomes.

The outer epithelium acts as a protective barrier and plays a role in tear film stability. It regenerates rapidly, aiding early graft adherence. Beneath it, Bowman’s layer, a collagen-rich structure, adds mechanical strength but does not regenerate. Its absence in the donor graft does not significantly affect visual recovery, as the epithelium compensates functionally.

The stroma, comprising about 90% of corneal thickness, is crucial for transparency and biomechanical stability. Its uniform collagen arrangement maintains optical clarity. In PK, proper alignment of the donor and recipient stroma minimizes post-operative astigmatism. Scarring or edema in the stroma can severely impair vision, necessitating full-thickness replacement.

Descemet’s membrane, a resilient basement membrane, supports the endothelium, which regulates corneal hydration. Endothelial cells have minimal regenerative capacity, making a healthy donor endothelium vital for graft clarity. Endothelial failure remains a leading cause of graft rejection and long-term failure.

Indications For Full-Thickness Transplant

PK is performed when corneal pathology affects the entire thickness, making partial-thickness procedures inadequate. Conditions requiring PK include progressive ectatic disorders, endothelial dysfunction, and full-thickness corneal scarring.

Ectatic Disorders

Ectatic diseases like keratoconus and pellucid marginal degeneration cause progressive thinning and irregular curvature, distorting vision. Early-stage cases may be managed with contact lenses or cross-linking, but advanced cases with severe thinning, scarring, or acute hydrops require PK.

A study in Cornea (2021) found PK remains a viable option for keratoconus patients with central scarring or extreme steepening beyond the range of specialty lenses. Unlike deep anterior lamellar keratoplasty (DALK), which preserves the recipient’s endothelium, PK replaces the entire cornea, ensuring optical regularity. Postoperative outcomes depend on graft clarity and suture management to control astigmatism.

Endothelial Dystrophies

Endothelial dysfunction, particularly Fuchs’ endothelial corneal dystrophy (FECD), can necessitate PK when endothelial keratoplasty (EK) is not feasible. FECD leads to progressive endothelial cell loss, corneal edema, and visual deterioration. While Descemet membrane endothelial keratoplasty (DMEK) is preferred for isolated endothelial failure, PK is required when stromal scarring or previous graft failure is present.

A study in American Journal of Ophthalmology (2022) reported PK as an effective option for advanced FECD cases with irreversible stromal opacification. The procedure restores corneal clarity by replacing both the dysfunctional endothelium and affected stroma, though recovery is longer than EK due to full-thickness wound healing.

Traumatic Scarring

Corneal trauma from mechanical injury, chemical burns, or infectious keratitis can cause dense stromal scarring that impairs vision. When scarring extends through the full corneal thickness, PK is often the only option to restore clarity.

A multicenter study in Ophthalmology (2023) found trauma-related PK outcomes vary based on anterior segment damage and vascularization. Unlike elective PK for dystrophies or ectasias, trauma cases often involve irregular wound edges and anterior chamber abnormalities, complicating graft placement and healing. Surgical planning must address potential synechiae, lens involvement, or secondary glaucoma. Despite these challenges, PK remains a viable treatment for visually significant scarring.

Steps In Surgical Performance

PK begins with precise preoperative planning, including corneal measurements to ensure an optimal graft-host match. The donor cornea, screened for infections and endothelial viability, is selected slightly larger than the recipient bed to reduce wound tension and enhance stability.

Under anesthesia, a trephine creates a full-thickness incision, excising the diseased cornea and exposing the anterior chamber. The donor button, prepared with a matching trephine, is positioned on the recipient bed to preserve natural curvature. Suturing is performed using interrupted or continuous techniques with monofilament nylon sutures, chosen based on wound tension and anatomical considerations.

Intraoperative challenges, such as anterior chamber instability or pressure fluctuations, require real-time adjustments. Viscoelastic substances help maintain chamber depth and protect intraocular structures. Proper suture placement prevents wound dehiscence and minimizes astigmatism. Intraoperative keratoscopy assists in optimizing suturing for better visual outcomes.

Graft Biology After Surgery

Following PK, a complex biological process determines graft integration and function. Initially, host epithelial cells migrate over the donor tissue, re-establishing the protective barrier within days. Rapid epithelial healing reduces infection risk and stabilizes the tear film.

Beneath the epithelium, stromal remodeling strengthens the graft-host interface. Keratocytes respond to surgical trauma by producing extracellular matrix components that reinforce structural cohesion. Excessive fibrosis can lead to interface scarring, affecting optical quality. Younger patients typically exhibit more pronounced wound healing responses.

Suture placement influences stromal remodeling, as prolonged retention can induce localized fibrosis, requiring careful postoperative adjustments. Maintaining graft clarity depends on endothelial function, as endothelial failure remains a primary cause of long-term graft complications.