One of the main advantages of superficial anterior lamellar keratoplasty (SALK) is the low frequency of complications. The rejection is very rare and, in case the graft fails, it will be easy to replace. However, the possible problems that may arise are very varied; knowing how to recognize and deal with them on time will in many cases be the difference between success and failure.

INTRAOPERATIVE COMPLICATIONS

From the preparation of the donor tissue:

- Disc or lenticule too fine or punctured.

- Disc or lenticule too thick.

- Irregular disk or lenticule.

From the preparation of the receiving bed:

- Incomplete lamellar cutting (due to loss of microkeratome suction).

- Very small bed.

- Irregular bed.

- Off-center bed.

While a bad carving of the donor is solved with a new tissue, a second deeper cut can be made in the receiving bed, or the disc can be replaced, and a new attempt made two months later. A certain disproportion between donor and recipient due to excess in the donor can be solved (as described in the technical chapters) by cutting the graft or scraping the epithelium in an area around the bed. In extreme cases it is possible to convert the procedure into deep anterior lamellar keratoplasty (DALK) or even into penetrating keratoplasty.

POSTOPERATIVE COMPLICATIONS

They can be classified into different groups:

- Superficial:

• Delayed epithelialization and persistent epithelial defect.

• Ulceration, whether trophic or infectious.

• Chronic epitheliopathy.

• Epithelial rejection.

• Sub-epithelial scarring.

- Related to sutures: infiltrates, infections, neovascularization.

- From the graft-recipient interface:

• Epithelial invasion.

• Neovascular or fibrovascular invasion.

• Aseptic inflammation (diffuse lamellar keratitis type).

• Infection in the interface.

• Opacities in the bed, residual or excessive scarring.

- Of the grafted tissue:

• Early dislocation (in cases without sutures).

• Presence of unnoticed opacities in the donor tissue.

• Recurrence of pathology (dystrophies, degeneration, herpes, etc.).

• Stromal rejection.

• Necrosis or fusion of the graft.

• Late ectasia.

• Late traumatic dislocation.

- Refractive and visual:

• Residual ametropia.

• Irregular astigmatism.

• Poor visual acuity without evident cause.

Superficial complications

The superficial complications are usually related to the previous state of the ocular surface. If there are conditions such as dry eyes or palpebral alterations, it is essential to have resolved them or at least treated and stabilized before attempting the SALK. If the epithelium of the donor is in good condition it is preferable not to remove it. If it has to be done, we must insist on lubricants, maintain the therapeutic contact lens and be attentive to its regeneration. If it takes more than 7 days, we can talk about a delay in it (Figure 1).

We can apply the full battery of advanced measurements available for these situations – from autologous serum, plasma rich in growth factors, carboxymethyl glycose polysulfate (Cacicol®), special contact lenses, to tarsorrhaphy, but first of all we have to try determine the causes: if there is insufficient lubrication, drug toxicity or poor compliance of the patient, palpebral malposition or nocturnal opening that produces exposure, even a poor quality of the donor tissue, before appealing to a neurotrophic commitment or limbal function. It is preferable to act quickly because, if the defect persists, it can lead to the formation of persistent opacities, favor secondary infection or even graft necrosis (Figure 2).

Sometimes the epithelium regenerates but an irregularity that limits vision persists chronically, and that it will also require an adequate diagnosis and treatment. Rarely, an epithelial immune reaction can occur, which appears as a whitish line that dyes with fluorescein and migrates through the surface and represents an exchange front between the epithelium of the donor and that of the recipient (Figure 3). It can affect vision if it involves the visual axis, and if it is accompanied by an inflammatory reaction, it will require a longer corticoid therapy to avoid the formation of opacities at the interface or the evolution towards a stromal rejection.

Complications of the interface and the graft itself

At the interface level, the main complications are epithelial and fibrovascular invasion. The first is usually due to the fact that the graft is larger than the bed and its edge has been applied over the receptor epithelium in some sector, or to a bad adherence of that edge that has allowed the entrance of the epithelium in regeneration (Figure 4). The treatment is similar to that of the cases after refractive surgery (lifting the tissue, cleaning both sides with scraping and ethanol, ensuring good adhesion, if necessary with sutures, etc.).

The fibrovascular invasion is more serious, since once established it tends to create deposits of lipids and it is difficult to resolve without having to change the graft. The lamellar interface is a virtual space of low resistance to vascular growth in the presence of persistent inflammation or other angiogenic stimulus. It is essential to prevent it with a good follow-up and anti-inflammatory treatment, remove the sutures early, and immediately if they become loose. Aseptic inflammations of the "diffuse lamellar keratitis" type (Figure 5) can be seen, such as those described after LASIK, or those due to herpes recurrence (Figure 6) or a new infection. An immune reaction can also appear as a series of infiltrates more or less nummular, subepithelial or at the interface level.

Secondary infection is an uncommon possibility in the context of lamellar keratoplasty¹. It has occurred more often as a result of an epithelial defect or a weak suture, but before one or more nodular infiltrates under the graft in the first days of the postoperative period, we must suspect it and take the appropriate measures – lift the disc, take samples, apply treatment with fortified antibiotics, etc.

In the absence of vascularization, the opacities under the graft may be residual, by an incomplete resection of the original pathology (Figure 7) or be formed by an excess of postoperative scarring. This would be the result of excessive inflammation or the different quality of the surfaces obtained as a function of the technology², although we have also observed this problem with the femtosecond lasers of last generation (Figure 8).

In some cases, it will be possible to treat them by ablation with excimer laser (PTK) after lifting the disc. The poor adherence of this to the bed can persist in the long term – as happens after a LASIK, although here there is usually more scarring, and it would explain the cases of late dislocation after trauma or even spontaneous ectasia (Figure 9).

The original pathology as a dystrophy, as well as certain degenerations, will tend to relapse in the graft. If this were exclusively superficial it can be treated by laser ablation. If it affects the entire parenchyma of the graft and the interface, it will be more practical to replace this.

Refractive and visual complications

Finally, one of the most frequent complications, in common with all types of anterior keratoplasty, is astigmatism. Minimizing it requires taking measures that range from the selection of the donor, through the surgical technique, to the various measures that can be applied in the postoperative period^3,4. In the case of a SALK with sutures, its intraoperative adjustment is important, which requires a keratoscope preferably fixed under a microscope. Selective withdrawal is also useful in the postoperative period, although having very few sutures this is a limited option. Once all the sutures are removed, in case of high regular astigmatism the different treatments can be applied, although here it is easier to perform laser ablation by lifting the graft like a LASIK flap, it is special if we also want to correct a residual spherical ametropia.

But the biggest problem in the visual section, with regard to SALK, is irregular astigmatism and poor vision without apparent cause. The first may be due to an error in the indication, especially in cases in which in the original cornea the irregularity already predominated over opacities as a cause of poor vision, which are bad candidates for SALK. Said irregularity will be reproduced in the bed carved with microkeratome or femtosecond laser and the graft will acquire it. This also explains that very thin discs are associated with more astigmatism. Perhaps a thicker one could "disguise" the irregularity of the bed better, but we know that a greater thickness also degrades the visual quality. Irregular astigmatism can be treated in some cases with laser ablation based on topography, although a rigid permeable contact lens may be the simplest solution and, in any case, it is recommended as a diagnostic test.

In the absence of irregular astigmatism, no irregularity detectable by topography or visible opacities or irregularities at the interface, the poor vision associated with lamellar keratoplasties, especially those of medium thickness, remains a mystery. Theories such as destructive polarization due to the orientation of the collagen fibers between the donor and the receiver have been invoked, or it is possible that it is due to the sum of multiple factors, each of which separately is not very apparent. In many cases the vision slowly improves over time, so a certain patience is recommended. The strength of SALK lies in its simplicity and the ease of replacing the graft, but if a situation that leads to poor vision is identified in spite of an impeccable technique, it will be better to opt for a DALK or even a penetrating one.