Time is vision: Act fast after ocular chemical burns

Chemical injuries to the ocular surface can be challenging to manage because they lie at the intersection of urgency and long-term consequences. The severity of these injuries depends on the type of offending agent, its pH and the duration of exposure. Such injuries often have significant negative effects on patients’ visual and health-related quality of life, as well as their psychological well-being.¹

Because many ocular chemical injuries are not seen in hospitals, their true prevalence is difficult to capture. A conservative estimate suggests approximately 10 cases per 100,000 population per year worldwide.¹ In the US, we fortunately fall on the lower end of that spectrum, but the burden of these injuries remains far from insignificant.² Although the highest rates of ocular surface chemical injury occur in young working adult men, young children are also particularly vulnerable, with some studies reporting higher rates of serious injury in this population.^1,2

The frequency of my personal interactions with patients who have chemical burns has varied throughout my career. When I worked at a large tertiary referral centre, I averaged about five new acute cases per month. Now, when I see patients with chemical injuries, they are usually further along in their disease course and facing a variety of sequelae.

Understanding severity and the ideal therapeutic window

The severity of chemical burns is primarily graded based on the degree of limbal involvement, using classification systems such as those proposed by Roper-Hall or Dua et al. Both systems assess limbal damage, in addition to corneal epithelial loss and stromal haze (Roper-Hall) or the proportion of conjunctival involvement (Dua et al).¹ Mild injuries, with minimal limbal ischemia, generally have a favourable prognosis when managed with appropriate treatment and follow-up. Moderate burns require careful attention to areas of partial stem cell loss. In severe burns, characterized by extensive limbal destruction and ischemia, permanent vision loss becomes a very real threat.³

When considering the treatment of ocular chemical burns, the acute phase of the injury presents the greatest window of opportunity.² Thoughtful and aggressive intervention during this period provides a meaningful chance of preventing or minimizing long-term sequelae.³ However, once these long-term manifestations have developed, the ability to reverse them becomes extremely limited.

Acute management: The foundation of outcomes

The critical first step in treating an ocular chemical burn is irrigation to remove the alkaline or acidic residue. Alkaline burns, in particular, continue to cause damage as long as the chemical remains on the ocular surface.³

After irrigation, the focus shifts to restoring the epithelium and protecting the cornea from melt by controlling inflammation with topical corticosteroids. Topical antibiotics should also be used to reduce the risk of infection. Next, aggressive lubrication is essential, ideally with preservative-free artificial tears to avoid further irritation of the already fragile ocular surface.¹ Autologous serum tears or umbilical cord serum tears can provide an additional layer of growth factors that meaningfully enhance healing.⁴ Oral doxycycline may be used for its anti-inflammatory and antimelting properties, while systemic administration of vitamin C supports collagen synthesis and stromal integrity.⁵

IOP often rises in patients who have experienced an alkaline burn, so oral pressure-lowering medications are essential to prevent optic nerve damage.⁵ Cycloplegics can also help reduce photophobia and prevent scarring of the iris to the lens capsule or cornea in cases where inflammation extends into the interior of the eye.⁶

Surgically, amniotic membrane (AM)transplantation has become a cornerstone of care for these injuries.⁷ I use it liberally, even for burns classified as mild, because the downsides are minimal while the potential benefits for epithelialization, pain control, inflammation reduction and scarring prevention are substantial.⁷ Debridement of necrotic tissue is also important, as necrotic epithelium can impede healing of the ocular surface.⁵

Navigating long-term sequelae in the chronic phase

Once patients reach the chronic phase, therapeutic goals shift toward addressing the structural and functional consequences of the injury. Fornix reconstruction may be necessary in cases of cicatrization or symblepharon, and AM can serve as a scaffold to support reconstruction and promote healing during this process. Although I usually avoid punctal plugs and cautery in the acute phase due to their potential to trap inflammatory mediators on the ocular surface, they can be useful in the chronic phase to manage dryness or an unstable tear film.⁸

In eyes with limbal stem cell deficiency and significant corneal pathology, limbal stem cell transplantation is essential to restore both corneal integrity and vision.⁸ This approach is particularly effective in unilateral disease, where autologous transplantation is an option. In bilateral cases, donor-derived transplantation may be used, but it requires systemic immunosuppression, and there should be extensive discussion of the risks with patients and their families.⁹

Keratoplasty, when indicated, is typically delayed until the ocular surface is stabilized.³ Without functional stem cells, a graft has little chance of success.

In cases where limbal stem cell transplantation cannot be performed or is unsuccessful, keratoprosthesis may be considered; however, it carries significant long-term management challenges.⁸

Individualizing treatment with patient- and disease-specific considerations

Several factors influence how I tailor management: patient age, preexisting ocular disease, mechanism of injury and access to timely care. Most importantly, children require special attention and aggressive treatment. Because they often cannot cooperate during examinations, I maintain a low threshold for performing an exam under anesthesia to ensure accurate assessment.³

Regardless of age, preexisting ocular surface disease is associated with worse outcomes, warranting closer surveillance. The mechanism of injury is also critical: alkaline burns cause more extensive damage than acidic burns, as they penetrate deeper into the corneal stroma and can affect the cornea and anterior chamber structures. Consequently, these patients require particularly intensive care.^1,2

Recent advances and evolving tools

The past decade has brought significant innovation in ocular surface therapeutics, and the number of growth-factor–rich products for restoring epithelial health is expanding rapidly.⁸

AM technology, in particular, has advanced considerably. Cryopreserved AM, including ultra-thick membrane derived from the umbilical cord, remains the gold standard because it retains key biological components.¹⁰ However, dehydrated and extract-based formulations are also generating interest.^11,12

Umbilical cord serum is another promising development, although it remains primarily in research settings.⁴ The field is evolving quickly, and I anticipate that future comparative studies will help better define the optimal role of each product.

Another meaningful development has been the use of anti-VEGF therapies, particularly bevacizumab, to target corneal neovascularization.¹³ I have increasingly employed intravascular injection techniques to directly target these new vessels. This approach shows particular promise in the subacute phase, when neovascularization first emerges.

Conclusion

If there were one message I would want to impart to clinicians encountering ocular chemical burns, it is this: early, aggressive intervention is paramount. Immediate irrigation, prompt initiation of corticosteroids, infection control, doxycycline, vitamin C, lubrication, AM and IOP management form the backbone of therapy for ocular chemical injuries and are key to preventing long-term vision loss.

Although the therapies we employ in the chronic setting continue to evolve, no product in the chronic stage can replace the opportunity we have in the acute phase to change the trajectory of disease before irreversible damage occurs.

Hajirah N. Saeed, MD, MPH
E: [email protected]
Saeed is a visiting associate professor and associate director, Ocular Regenerative Medicine Fellowship, in the Department of Ophthalmology and Visual Sciences at the University of Illinois College of Medicine in Chicago, Illinois, USA. Saeed reports affiliations with Loyola University Medical Center and Massachusetts Eye and Ear/Harvard Medical School. She receives grant funding from the National Institutes of Health and the Department of Defense, some of which are relevant to treatments described in this article. Saeed also holds a patent for ocular drug delivery, including amniotic membrane delivery.

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