TASS is an uncommon, non-infectious condition causing severe inflammation of the anterior segment structures without vitreous involvement [1],[2],[5]. The name TASS was coined by Monson and colleagues in 1992 [1],[3]. It is usually associated with phacoemulsification surgery but can also happen after procedures like penetrating keratoplasty, descemet stripping automated endothelial keratoplasty, deep anterior lamellar keratoplasty, vitrectomy and anterior and posterior segment phakic intraocular lenses. The alternative names of TASS include sterile post -operative endophthalmitis, toxic lens syndrome, toxic endothelial cell destruction syndrome and localized endophthalmitis [1],[3],[7].

1. What is TASS?

It is an acute sterile post-operative inflammatory condition affecting the anterior segment structures following intraocular surgery. It is usually seen within 12-48 hours of surgery and is due to the reaction of anterior segment structures to some toxic substance usually associated with cataract surgery [1],[5],[7].

2. Hallmark of TASS ^[3]

• Diffuse corneal edema which extends from limbus to limbus due to widespread damage to endothelium.
• Severe anterior segment inflammation resulting in hypopyon formation.
• Fibrin deposition on the iris or intraocular lens in severe cases.
• Absence of vitreous involvement – can be spill over from the anterior segment inflammation
• Culture negative for fungal and bacterial from taps.
• Excellent response to topical steroids.

3. When to suspect

Vision loss within 24-48 hours after surgery, pain, photophobia, conjunctival injection and chemosis, diffuse limbus to limbus corneal edema, anterior chamber reaction with or without hypopyon and fibrin deposition, irregular and non-reactive pupil, raised intraocular pressure, clear vitreous or minimal spill into the anterior vitreous and transient increase in central macular or choroidal thickness as a part of the surgery or due to TASS [1],[3],[5],[6],[8].

4. Complications

Inflammatory deposits on the iris can lead to dilated and fixed pupil, long-standing inflammation leads to iris ischemia and iris atrophy leading to pupillary distortion and poor pupillary dilatation, ocular hypertension and later glaucoma due to chronic trabeculitis secondary to toxic substance or chronic inflammation leading to peripheral anterior synechiae and reducing the trabecular outflow, severe corneal endothelial damage, epithelial ingrowth, cystoid macular edema, capsular phimosis and posterior capsular opacification [1],[5].

5. Causes are multifactorial

Inflammation from Intraocular lenses – design or composition from sodium hydroxide or contamination from aluminum or other heavy metals, Ocular viscoelastic devices (OVD) – the residual denatured OVD in improperly cleaned reusable irrigation and aspiration cannulas, intracameral solutions and intraocular medications - incorrect pH, presence of contaminants or improper mixing, dosing and handling of BSS, antibiotics, anesthetics, intraocular dyes, ointments, and intravitreal injections, inadequate instrument cleaning and sterilization - particularly inadequate flushing of handpieces, use of enzymatic detergents and ultrasonic baths and improper maintenance of autoclave, bacterial endotoxins contaminating BSS and addition of preservatives like benzalkonium chloride, edetic acid, sodium bisulpite and thiomersal and improper contact between gloved hands containing powder during IOL manipulation [1],[2],[3],[8].

6. Pathophysiology

Cellular toxicity due to the toxic substance, free radical damage due to toxic chemical substance leading to apoptosis, breakdown of blood-aqueous barrier leading to inflammatory reaction, breakdown of endothelial junctions with loss of barrier function leading to corneal edema and decompensation if severe [1],[5].

7. Differential diagnosis ^{[1],[5],[6],[7],[8]}

• Infectious endophthalmitis - onset is 2-7 days, lid edema present, associated with severe pain, localized corneal edema if there is trauma, intraocular pressure usually not elevated, moderate to severe anterior chamber reaction with fibrin and hypopyon, vitritis present, pupils are not dilated and fixed as in TASS and can be reactive, decreased visual acuity and response to steroids may be detrimental until and unless the culture is negative.
• Severe uveitis.
• Retained lens material – gonioscopy examination to confirm.

8. Investigations

Anterior chamber aspirate, vitreous tap, vitreous biopsy for bacterial – both aerobic and anaerobic and fungal cultures to rule out infectious endophthalmitis, polymerase chain reaction which may be more useful, ultrasound B Scan to rule out any posterior segment involvement in case of severe corneal edema [1],[5],[6],[7],[8].

9. Management ^{[1],[5],[6],[7]}

Medical – Topical steroids (1% prednisolone acetate) on a half-hourly basis initially after ruling out infectious endophthalmitis, frequent and careful monitoring and follow up for the reduction of inflammation, eye pressure, and clearance of corneal edema on an everyday basis to confirm that it is indeed TASS and not infectious endophthalmitis, gradual tapering of topical steroids, topical NSAIDS can be an adjunct to topical steroids, systemic steroids, subconjunctival dexamethasone or intravitreal triamcinolone based on the severity and intracameral recombinant tissue plasminogen activator to lyse the fibrin.

Surgical - Irrigation of anterior chamber, explantation of IOL if that is the cause of inflammation, DSAEK in case of the decompensated cornea and glaucoma filtering procedures for refractory glaucoma.

10. Prognosis and prevention ^{[1],[5],[7],[8]}

Mild presentation of corneal edema clears rapidly with no sequelae, the moderate presentation will take several weeks to clear and may have an impact on the visual acuity and intraocular pressure, severe presentation can lead to any of the above-mentioned complications and lead to Urrets-Zavalia syndrome.

Primary prevention is to make the staff and surgeon aware of the protocols and educate and train them, avoid preservatives in intraocular solutions, antibiotics, intracameral medications and irrigating solutions, adequate cleaning, and sterilization of ophthalmic surgical instruments, maintaining proper pH and ionic composition, and avoiding contamination of BSS, use of new and fresh OVD.

References

1. Erick Hernandez-Bogantes, Alejandro Navas, Andrea Naranjo, Guillermo Amescua, Enrique O. Graue-Hernandez, Harry W. Flynn, Ike Ahmed, Major review Toxic anterior segment syndrome: A review, survey of ophthalmology 6 4 (2 0 1 9) 4 6 3 - 4 7 6.
2. Simon P. Holland Douglas W. Morckc and Tracy L. Lee, Update on toxic anterior segment syndrome, Curr Opin Ophthalmol 18:4–8.
3. Nick Mamalis, Henry F. Edelhauser, Daniel G. Dawson, Jesse Chew, Russell M. LeBoyer, Liliana Werner, Review/update - Toxic anterior segment syndrome, J Cataract Refract Surg 2006; 32:324–333.
4. Sabyasachi Sengupta, David F. Chang, Rajiv Gandhi, Hemal Kenia, Rengaraj Venkatesh, Incidence and long-term outcomes of toxic anterior segment syndrome at Aravind Eye Hospital, J Cataract Refract Surg 2011; 37:1673–1678.
5. Sadiqa. K. Stelznar, Alpa. S. Patel, Brad. H. Feldman, Douglas. M. Wisner andMelina Morkin, Toxic Anterior Segment Syndrome, Eyewiki.
6. Choul Yong Park, Jimmy K. Lee and Roy S. Chuck, Toxic anterior segment syndrome – An updated review, BMC Ophthalmology (2018) 18:276.
7. Toxic Anterior Segment Syndrome – Medscape – Jean Deschenes.
8. N. Demet Ozcelik, Kadir Eltutar, Burak Bilgin, Toxic anterior segment syndrome after uncomplicated cataract surgery, Eur J Ophthalmol 2010; 20 (1):106-114.