Graft rejection treatment and postoperative problems

4. Emergency Management of Endothelial Graft Rejection

New redness, photophobia or reduced vision in a graft requires urgent examination. Document epithelial integrity, infiltrates, keratic precipitates, anterior chamber activity, oedema, pressure and attachment. Endothelial rejection can lack a Khodadoust line, especially after DMEK. Infectious endotheliitis, epithelial infection, detachment and pressure-related oedema are important mimics.

For clinically suspected rejection, institute intensive topical corticosteroid treatment promptly under specialist supervision, commonly hourly prednisolone acetate 1%, with early reassessment. The preparation, overnight dosing, subsequent taper and long-term maintenance depend on severity and response. Severe, recurrent or high-risk episodes may also require periocular or systemic corticosteroids; intravenous pulses are not compulsory for every graft reaction. Assess diabetes, infection and other systemic contraindications before additional treatment.

Steroid-sparing systemic immunosuppression is an individual corneal/transplant decision rather than an automatic regimen. Discuss infection screening, renal function, blood counts, interactions and adherence. Check pressure during rescue and taper. Persistent oedema requires reassessment of the diagnosis, endothelial reserve and need for further surgery.

5. Graft Rejection versus Graft Failure

Accurate differentiation between active rejection and graft failure is critical for prognostic evaluation and therapeutic decision-making:

• Graft Rejection: An active, immune-mediated, cell-directed inflammatory process directed specifically against donor histocompatibility antigens. Reversible if caught early!
• Graft Failure: Irreversible loss of corneal clarity and endothelial function, resulting in permanent edema, bullous keratopathy, and vision loss. May stem from immune or non-immune mechanisms:

Clinical Entities of Non-Immune Graft Failure

• Primary donor failure: Persistent oedema from the early postoperative period due to inadequate endothelial function or surgical injury. Exclude pressure elevation, DMEK/DSAEK detachment or inversion, Descemet detachment after PK and inflammation. Day-one oedema alone is not sufficient to diagnose irreversible failure or mandate immediate regrafting.
• Late Endothelial Decompensation (Secondary Graft Failure): The insidious, gradual loss of endothelial function occurring months to years after successful surgery without preceding immune rejection episodes. Corneal grafts experience accelerated endothelial cell attrition ($1–3\%$ annual cell loss compared to $0.6\%$ in the normal aging cornea). When density drops below the critical functional threshold ($\sim 500\text{ cells/mm}^2$), the graft decompensates.

Diagnostic Comparison: Rejection vs Primary Failure vs Late Decompensation

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6. Post-Keratoplasty Complications & Management

Secondary Glaucoma

Secondary glaucoma affects 15% to 30% of penetrating keratoplasty eyes, representing a major cause of irreversible graft failure and visual loss.

• Pathogenesis: Trephination-induced distortion or mechanical collapse of the trabecular meshwork; postoperative corticosteroid-induced ocular hypertension (steroid responders); peripheral anterior synechiae (PAS) bridging the angle; retained viscoelastic material; pupillary block.
• Tonometry: Standard Goldmann applanation tonometry may be inaccurate due to corneal edema or astigmatism; an alternative device may help, but Tono-Pen and dynamic contour readings also depend on the altered graft. Select and interpret measurements with corneal examination and longitudinal nerve/field findings.
• Management: Topical aqueous suppressants (beta-blockers, alpha-2 agonists, carbonic anhydrase inhibitors). Consider prostaglandin analogues individually, including inflammation, macular-oedema risk and graft status; these concerns are not a universal contraindication. If medical therapy fails, surgical options include trabeculectomy with mitomycin C, or implantation of a glaucoma drainage device (Ahmed or Baerveldt tube shunt placed into the ciliary sulcus or pars plana to avoid endothelial contact).

Suture-Related Complications

• Broken, Loose, or Exposed Sutures: Loose 10-0 nylon sutures compromise wound stability, accumulate mucus, attract bacterial biofilm, trigger microbial keratitis, and induce deep vascularisation that directly precipitates allograft rejection.
• Suture management: Assess wound integrity and infiltrate urgently. Remove or replace a loose/infected suture when safe, with sampling and antimicrobial cover as indicated; slit-lamp removal is not automatically safe in an unstable wound.

Post-Keratoplasty Astigmatism

High irregular and regular astigmatism ($> 4–5\text{ D}$) frequently limits visual rehabilitation despite a perfectly clear graft.

• Selective Suture Removal: Starting at 6 to 12 months, interrupted sutures on the steep topographic axis are sequentially removed.
• Refractive Correction: Spectacles, rigid gas-permeable (RGP) or scleral contact lenses.
• Surgical Correction: Astigmatic keratotomy (AK) / relaxing incisions in the graft-host junction, compression sutures on the flat axis, topography-guided photorefractive keratectomy (PRK), or toric intraocular lens implantation.