Toxic anterior segment syndrome (TASS) is an acute, sterile postoperative anterior segment inflammation following any anterior segment surgery. By definition, TASS is sterile or noninfectious. This entity was initially described as sterile postoperative endophthalmitis, but in 1992, Monson et al.¹ accurately termed this condition “toxic anterior segment syndrome.” In addition, cases of TASS, which are characterized by localized corneal endothelial damage, have been termed “toxic endothelial cell destruction syndrome (TECDS).”^2,3,4,5,6 TASS has been thoroughly discussed in a review/update paper and its accompanying editorial, as well as a clinical module for ophthalmologists.^7,8,9

TASS most commonly occurs acutely following anterior segment surgery, but in rare instances, can have a delayed onset. The postoperative inflammation is sterile or noninfectious and is felt to be secondary to a toxic substance of some kind that enters the anterior segment either during or immediately after anterior segment surgery, causing inflammation. A recent retrospective case series from the Aravind Eye Hospital in India reported an incidence of 0.22% (60 eyes out of 26,408 cataract surgeries).¹⁰

The most common symptom of TASS is blurry vision. Pain is usually absent from patients with TASS in distinction to those with postoperative infectious endophthalmitis, most of whom will experience pain. The hallmark of TASS is that the inflammation usually has a relatively immediate onset, certainly within 12 to 48 hours of surgery. The most common clinical finding is a diffuse corneal edema that has been described as “limbus-to-limbus” corneal edema (Fig. 4.1). This diffuse edema results from the widespread damage of corneal endothelial cells. This pattern differs significantly from the focal corneal edema that is often seen following cataract surgery.

Another signature feature of TASS is marked anterior segment inflammation (Fig. 4.2). This is characterized by a diffuse breakdown of the blood-aqueous barrier with increased inflammatory cells in the anterior chamber. Many cases will develop a hypopyon. In addition, fibrin may form across the pupil, iris, and surface of the intraocular lens (IOL), and inflammatory keratitic precipitates may be present. This syndrome can result in damage to the iris, which can cause a permanently dilated, irregular, and/or atrophic pupil. If the inflammation is severe, damage to the trabecular meshwork and formation of peripheral anterior synechia may occur, leading to a difficult-to-control glaucoma (Fig. 4.3).

It is important to differentiate the sterile inflammation seen in TASS from an infectious postoperative endophthalmitis. One of the features that is most helpful in differentiating these two entities is that TASS almost always presents within the first 24 to 48 hours, whereas the typical signs of bacterial endophthalmitis generally appear between 4 and 7 days, postoperatively, although a recent study by Moshirfar et al.¹¹ suggests that the time to presentation may often be longer, with an average of 9.3 days between the day of cataract surgery and the diagnosis of endophthalmitis. There are also differences in symptomatology. Greater than 75% of patients who have an infectious endophthalmitis will have pain, but most cases of TASS are pain free. The anterior segment inflammatory changes in both of these entities are often very similar, with significant inflammation and hypopyon formation, but vitreous involvement is much more typical of endophthalmitis. When the vitreous is involved in TASS, it is usually in the form of a moderate spillover from the anterior chamber. Also, the diffuse corneal edema, which is typically seen in TASS, is not often present in an infectious endophthalmitis. These clinical differences are not absolute, however, and when there is any suspicion of an infectious etiology, anterior chamber and vitreous samples should be taken for staining, culture, and PCR.