CASE REPORT: The child was a male, 12 years old. He was admitted to the hospital on November 5, 2008 due to 8 years of double vision confusion. There was no discomfort associated with eye redness, eye pain, photophobia, lacrimation, or visual distortion. He was in good physical health and denied any history of ocular trauma or genetic or drug allergy. Specialized examination: visual acuity: right eye 0.15, corrected 0.15. left eye 0.15, corrected 0.15. IOP: right 14 mmHg, left 13 mmHg, both eyes without conjunctival congestion, corneal transparency, deep anterior chamber, KP (-), atrial flash (-), round pupil, 3 mm in diameter, responsive to light, lens The lens was unevenly clouded (Figure 1), and the vitreous humor and fundus were unclear. Auxiliary examinations: Ocular A/B ultrasound showed that the right eye had an axial length of 23.5 mm and the left eye had an axial length of 23.3 mm, the lens was cloudy in both eyes, and the right posterior scleral chylomicron was not abnormal. Corneal endothelial cell count: 2911.8 cells/mm2 in the right eye (Figure 2) and 2910 cells/mm2 in the left eye. corneal endothelial cell morphology was normal. Diagnosis: congenital cataract in both eyes. The cataract aspiration combined with IOL implantation was performed on the right eye under local anesthesia at 14:30 on November 10, 2008, with one +19 D IOL implanted in the capsule bag and 1% carbimicrin pupil reduction followed by eye irrigation solution replacement. On the first postoperative day at 8:00 pm (14 hours postoperative), the general condition was good, no ocular pain; right eye visual acuity was 0.12, intraocular pressure was 5 mmHg, mild ciliary congestion, light central corneal edema, KP (+), atrial flash (++), slightly shallow anterior chamber, partial posterior iris adhesion, pupil under-rounded about 4 mm, pupil A/B ultrasonography showed a mild clouding of the anterior vitreous of the right eye. The clinical diagnosis of infectious endophthalmitis was made, and systemic ceftizoxime and dexamethasone were given as sedative drops, subconjunctival injections of gentamicin and dexamethasone, and topical corneal nourishing drugs such as compound neomycin sulfate drops, compound tropicamide drops, diclofenac sodium drops and vitamin palm gel were administered. On the 2nd postoperative day, the visual acuity of the right eye was 0.1, with diffuse foggy corneal edema, increased exudation from the anterior chamber, most of the posterior iris adhesions, and a plum-shaped pupil; the above treatment was continued. Anterior chamber flushing was performed under surface anesthesia on the 3rd postoperative day, and vancomycin 1 mg and dexamethasone 400 μg were injected. The operation was successful, and postoperative systemic anti-inflammatory treatment was continued. The anterior chamber fluid extracted during surgery was sent for bacterial and fungal culture. On the 4th postoperative day, the right eye had a naked visual acuity of 0.04, an IOP of 23 mmHg, a marked increase in anterior chamber exudation, and increased diffuse corneal edema. After consultation and discussion, the possibility of “toxic anterior segment syndrome (TASS)” was considered, but the possibility of intraocular infection could not be completely excluded. We continued to give ceftizoxime and dexamethasone drops systemically, and intensified local anti-inflammatory treatment with tobramycin dexamethasone drops once/hour, diclofenac sodium drops 6/day, and compound tropicamide drops to continue to move the pupil. On the 5th postoperative day, the visual acuity of the right eye was 0.06, ciliary congestion was reduced, corneal edema was reduced, and anterior chamber exudation was significantly reduced. Negative bacterial and fungal cultures of anterior chamber fluid were obtained on postoperative day 7. In combination with the clinical impression, systemic drug therapy was discontinued. On the 10th postoperative day, the naked visual acuity of the right eye was 0.1 and the intraocular pressure was 22 mmHg. Considering the epithelial damage caused by frequent eye drops, the frequency of drops was reduced, and corneal epithelial growth factor and autologous serum were added to the eye. After that, the condition gradually improved. On the 21st postoperative day, the visual acuity of the right eye was 0.1 with a correction of 0.15. The intraocular pressure was 19 mmHg, the peripheral clear zone of the cornea was increased, the central zone was still edematous, and the epithelium was intact. He was discharged on the 22nd postoperative day. On review 2 weeks after discharge, the visual acuity of the right eye was 0.15, the intraocular pressure was 16 mmHg, the central area of the cornea was still lightly edematous (Figure 3), and the epithelium was intact.
Discussion In 1992, Monson et al [1] first proposed the concept of TASS, which is an acute noninfectious inflammation of the anterior segment of the eye and a postoperative complication of anterior segment surgery, most commonly after cataract surgery. It is generally accepted that TASS is a postoperative aseptic inflammation caused by non-infectious factors entering the anterior chamber, including damage to intraocular tissues caused by intraoperative instruments and and medications used.
TASS is most commonly seen in the early stages of anterior segment surgery with a rapid onset (12 to 24 hours). Typical cases present with an acute onset and a sterile inflammatory reaction confined to the anterior segment early after cataract or other ocular segment surgery. The characteristic features are diffuse corneal edema (caused by extensive endothelial cell damage), fibrinoid exudate in the anterior chamber, irregularly dilated pupils, and IOP that may be normal or low in the early stages, with damage such as trabecular meshwork leading to secondary hypertension and glaucoma formation in the later stages. In severe cases of TASS with fibrin formation on the surface of the anterior chamber, iris and/or IOL, TASS can lead to permanent iris damage, pupillary constriction and diastolic weakness, and damage to the trabecular meshwork. It is believed that corneal edema most often stems from the breakage of endothelial cell junctions, and acute loss of barrier function. If the remaining viable endothelial cells are unable to efficiently migrate and cover the injured area, permanent corneal edema can result. histopathological hallmarks of TASS are anterior segment damage – cell necrosis and/or apoptosis and extracellular tissue destruction. The corneal endothelium is the most sensitive anterior segment tissue to toxic factors, and therefore the cornea is the most affected tissue in TASS [2].
The current diagnosis of TASS is based on (1) mostly seen 12 to 24 hours after anterior segment surgery with a smooth surgical procedure; (2) blurred vision without significant pain or mild pain; (3) diffuse corneal edema, which may be accompanied by mild ciliary congestion, fibrinoid exudate or pus accumulation in the anterior chamber, iris atrophy and/or irregularly dilated pupils, and in severe cases, secondary glaucoma; (4) no significant posterior segment tissue involvement; (5) negative atrial or vitreous bacterial cultures; and (6) effective glucocorticoid therapy [3]. The main differential diagnosis is infectious endophthalmitis. Infectious endophthalmitis most often occurs 2 to 7 days postoperatively with manifestations of vitreous inflammation. Vitreous involvement is evident in patients with endophthalmitis, and 75% of patients with endophthalmitis have ocular pain and other signs of infection, such as eyelid swelling, conjunctival edema, increased discharge, and diffuse conjunctival congestion. TASS with severe inflammation of the anterior ocular segment with pus accumulation in the anterior chamber or fibrinoid exudate is difficult to differentiate from endophthalmitis, and early reliance on atrial fluid bacterial culture only confirms TASS if gram stain or bacterial culture is negative. no significant ocular pain; subsequent elevation of IOP above normal; ocular A/B ultrasound suggesting no posterior segment tissue involvement; atrial fluid bacterial culture (-); improvement after systemic and ocular topical application of glucocorticoids, antimicrobials, and nonsteroidal anti-inflammatory drugs. In retrospective analysis, the patient was clinically consistent with the features of TASS.
TASS is a postoperative aseptic inflammation caused by noninfectious factors that enter the anterior chamber. The causes of occurrence include chemical composition, pH, concentration or osmolarity in the intraocular perfusion solution, denatured ocular consumables, viscoelastic substances, ocular anesthetics, antibiotic factors, metal ions, preservatives, additives, detergents, disinfectants, water and water vapor in autoclaves, bacterial endotoxins, accumulation and residues of oxides, and polishing and disinfection of the IOL, repeated use of intraocular instruments , drug carriers, etc. Outbreaks of TASS have also been reported [6] TASS outbreaks are a matter of environmental factors and the degree of drug toxicity control, and require a comprehensive analysis of all drugs used during surgery and the concentration and pH of solutions entering the eye, as well as a comprehensive review and analysis of the sterilization process in the operating room. The perfusion solution, viscoelastic and pupil reduction medication used in this case were all qualified disposable consumables produced by regular manufacturers and were within their expiration dates, so it is less likely that they caused TASS. It is difficult to clarify the specific cause of this case.
Once TASS occurs, glucocorticoids and non-steroidal anti-inflammatory drugs should be applied to the eyes as soon as possible. In severe cases, systemic glucocorticoids can be applied. Although most TASS can be controlled with topical steroids or/and NSAIDs, they can also cause damage to the ocular tissue and lead to corneal epithelial damage. Anterior chamber irrigation is not currently advocated for the treatment of TASS. The IOP should also be closely monitored. The IOP may initially be low, and as the ciliary body function is restored, i.e., late in the TASS episode, the atrial fluid secreted by the ciliary process produces a steep peak, causing acute inflammation of the trabecular meshwork due to damage to the trabecular meshwork by toxic components, and long-term chronic trabecular meshwork damage in later stages, leading to increased IOP or glaucoma formation. Corneal endothelial confocal microscopy provides insight into corneal endothelial damage.The prognosis of TASS depends on many factors, such as the type and level of inducer, duration of exposure, and when to start treatment [4].
TASS prevention is extremely important for the entire ophthalmic surgical team, including the surgeon, operating room nurses, and those who clean or sterilize surgical instruments. In particular, it is important to ensure that reused surgical instruments are absolutely sterile and clean; disposable instruments or tubing should be used whenever possible, and reusable instruments should preferably be sterilized by radiation or gas instead; and ultrasound sinks should be changed once daily, as contaminated sinks are prone to the growth of gram-negative bacteria such as Klebsiella or Pseudomonas spp. that may lead to heat-resistant bacterial endotoxin accumulation. When autoclaving is applied, the water used must be changed at least once a week to prevent contamination with Gram-negative bacteria as well as latent virulent bacterial endotoxins. A high degree of vigilance should be exercised over any substances applied during anterior segment surgery such as irrigation solutions, viscoelastic agents, and any other drugs applied intraocularly, as well as the proper use of concentration, pH, and osmolarity of ocular medications is also very important [5].
In recent years, TASS has been gradually increasing in anterior segment surgery, especially since TASS can occur in an epidemiological outbreak in a particular ophthalmic center. Therefore, this serious complication should be given high priority by all personnel associated with the surgery.