After repair of penetrating anterior segment trauma, therapy is directed at preventing infection, suppressing inflammation, controlling IOP, and relieving pain. Intravenous antibiotics (eg, a cephalosporin and an aminoglycoside) for 48 hours, followed by an oral antibiotic such as moxifloxacin (400 mg PO daily) for 3–5 days, should be considered. Topical antibiotics are generally instilled 4 times a day for 7 days or until epithelial closure of the ocular surface is complete. Topical corticosteroids and cycloplegics are slowly tapered, depending on the degree of inflammation. A fibrinous response in the anterior chamber may respond well to a short course of systemic prednisone.

Corneal sutures that do not loosen spontaneously are generally left in place for at least 3 months and then removed incrementally over the next few months. Fibrosis and vascularization are indicators that enough healing has occurred to render suture removal safe. Applying fluorescein at each postoperative visit is mandatory to ensure that suture erosion through the epithelium has not occurred, as these eroded sutures can induce infection.

Traumatized eyes are also at increased risk of retinal detachment, so frequent examination of the posterior segment is mandatory. If media opacity precludes an adequate fundus examination, evaluation for an afferent pupillary defect and B-scan ultrasonography are helpful in monitoring retinal status.

Refraction and correction with contact lenses or spectacles can proceed when the ocular surface and media permit. Because of the risk of amblyopia in a child or loss of fusion in an adult, visual correction should not be unnecessarily delayed.

For more information on wound repair, see BCSC Section 4, Ophthalmic Pathology and Intraocular Tumors.

Macsai M. Surgical management and rehabilitation of anterior segment trauma. In: Krachmer JH, Mannis MJ, Holland EJ, eds. Cornea. 3rd ed. Vol 2. Philadelphia: Elsevier/Mosby; 2011:1655–1669.

Surgical Trauma

Corneal Epithelial Changes From Intraocular Surgery

The corneal epithelium functions as a barrier to corneal absorption of fluid from tears, including medication instilled topically and pathogens residing on the ocular surface. Breakdown of the epithelial barrier function, resulting in epithelial edema and stromal swelling, can follow

inadvertent intraoperative trauma to the epithelium by surgical instruments desiccation of the epithelium through inadequate intraoperative hydration

toxic keratopathy resulting from excessive preoperative instillation of topical ophthalmic preparations (and their preservatives)

accidental instillation of preoperative periocular facial scrub detergents

Although epithelial damage allows fluid to reach the stroma, the fluid is resisted by the IOP and pumped out by the endothelium. Thus, endothelial damage has a far greater effect on corneal edema than does epithelial damage. Intraoperative damage to the corneal endothelium and/or Descemet membrane can result in a positive stromal fluid pressure and subsequent epithelial edema. Epithelial edema begins in the basal cell layers of the epithelium and spreads through the epithelium, occasionally resulting in subepithelial bullae.

With epithelial edema, this layer loses its homogeneity, and the corneal surface becomes irregular, leading to symptoms of glare, photophobia, and halos around lights from light scattering. In bright light, edematous epithelium causes enhanced light scattering and can have a marked effect on vision. Surface irregularities caused by epithelial edema are more damaging to vision than stromal edema or scarring. The influence of epithelial surface irregularities on vision is often underestimated, whereas the role of stromal scarring and edema is overestimated.

Descemet Membrane Changes During Intraocular Surgery

The distensibility of Descemet membrane allows stretching or distortion, followed by return to its original shape. When the stroma imbibes fluid and thickens, the increased volume is distributed posteriorly, producing bowing and folding of Descemet membrane (striate keratopathy). Detachment of Descemet membrane can occur when an instrument or IOL is introduced through the surgical incision or when fluid is inadvertently injected between the membrane and the corneal stroma, resulting in stromal swelling and epithelial bullae localized in the area of detachment (Figs 13-20, 1321). Particular care should be taken when clear corneal incisions are enlarged prior to lens implantation during cataract surgery, because Descemet membrane can be easily stripped off the stroma during reintroduction of the keratome through the incision during this step. The membrane can be reattached with air tamponade. Recurrence may require suturing after Descemet membrane is repositioned in its native position.

Figure 13-20 Traumatic detachment of Descemet membrane following cataract extraction accompanied by secondary

corneal edema. (Courtesy of James J. Reidy, MD.)

Figure 13-21 A detachment of Descemet membrane after deep anterior lamellar keratoplasty, as imaged by anterior segment OCT. Note membrane within the anterior chamber (arrow). (Courtesy of David Rootman, MD.)

Corneal Endothelial Changes From Intraocular Surgery

Normal functioning of the corneal endothelium is highly pertinent to retaining normal stromal and epithelial hydration. Corneal hydration involves the following factors:

stromal swelling pressure

barrier function of the epithelium and endothelium the endothelial pump

evaporation from the corneal surface IOP

Corneal edema following surgical procedures often has many causes; these are related to the health of the patient’s endothelium, as well as to iatrogenic factors such as surgical technique, duration of surgery, and intraocular irrigating solutions. Patients with underlying corneal endothelial dysfunction such as Fuchs corneal dystrophy are at risk of developing postoperative corneal edema, even after uncomplicated surgery.

Cataract surgery and IOL implantation

See BCSC Section 11, Lens and Cataract.

Laser burns

Endothelial damage occurs following argon laser procedures as a result of the thermal effects of iris

photocoagulation. Endothelial burns are usually dense white with sharp margins; they may result in focal endothelial cell loss. Increases in mean endothelial cell size and endothelial cell loss associated with the use of greater laser power have also been reported. In follow-up periods of up to 1 year, endothelial cell loss following laser iridectomy has not been found to be statistically significant, however.

Conjunctival and Corneal Changes From Extraocular Surgery

Conjunctival chemosis with prolapse may result from orbital surgery or trauma. Exposed conjunctiva should generally not be excised but rather be reposited and kept in place with patching or, if recurrent, mattress sutures.

Orbital surgery and trauma can cause proptosis of the globe, leading to exposure keratopathy. Therapy includes lubricants, eyelid patching or taping, moist-chamber dressings, and temporary tarsorrhaphy.