Clinicians know to keep a close eye on post-op and post-trauma patient for any signs of glaucoma, as it is a well-known—and often severe—complication. Until recently, the pathogenesis of this damage remained murky, at best. Now, researchers in Boston used an animal model to uncover an inflammatory pathway that might be implicated.

The review included studies on post-injury and post-surgery glaucoma in mice and rabbits. The researchers looked at the test subjects’ clinical outcomes focusing mostly on the retinal ganglion cells. In animals with alkali burn to the cornea, damage to the retina can occur within 24 to 72 hours, the researchers found. They noted acute anterior segment trauma or surgery rapidly initiated an inflammatory, IOP-independent pathway to glaucoma mediated by tumor necrosis factor alpha (TNF-α). This and other inflammatory cytokines, generated anteriorly, rapidly diffuse posteriorly to cause apoptosis of the ganglion cells. During this time, the IOP remains much lower than the values often thought necessary to cause ganglion cell damage.

The researchers believe that immediate administration of infliximab, a TNF-α antibody, or corticosteroids could noticeably protect the ganglion cells. A modified treatment paradigm for patients with chemical burn might start promptly in the emergency department (in addition to standard treatment such as lavage) with the local administration of Kenalog (triamcinolone, Bristol-Myers Squibb), injected sub-Tenon or subconjunctivally. The researchers suggest starting with a corticosteroid allows the practitioner to perform a tuberculosis test and observe its results—which takes 24 hours—before considering biologics.