Patient referred for visual loss after cataract surgery
There were no complications with the surgery, but vision in the right eye dropped to counting fingers 1 day postop.
An 85-year-old woman was referred urgently for poor vision on the first postoperative day after cataract extraction of the right eye. She reported moderate pain the night of surgery, which resolved by the following day. Her preoperative vision was 20/70, and on postoperative day 1, her vision was limited to counting fingers. The referring ophthalmologist reported an uncomplicated cataract operation.
Her ocular history was remarkable for suspicion of glaucoma and cataracts. Medical history was significant for hypertension and hypothyroidism. Medications included lisinopril, Lasix (furosemide, Sanofi-Aventis) and Synthroid (levothyroxine, Abbott Laboratories). The patient had no known allergies, and her family history, social history and review of systems were unremarkable.
Vision measured counting fingers in the right eye and 20/40 in the left eye. The pupil was mid-dilated and nonreactive in the right eye. Extraocular movements were full, and IOP measured 17 mm Hg bilaterally.
Eyelids and orbits demonstrated no ptosis or proptosis. The conjunctiva of the right eye had trace injection, and the wound was Seidel negative. The cornea showed mild diffuse stromal haze, and the pupil was irregular with engorged vessels. The anterior chamber demonstrated a 1-mm hypopyon with 4+ cell with 2+ flare. The IOL was centered in the capsular bag, and fibrin was noted on the anterior surface of the optic (Figure 1).
Images: Yoon SJ, Duker JS
A red reflex was present, but no details of the fundus were appreciated on ophthalmoscopy. B-scan ultrasonography demonstrated no lens fragments, no retinal detachment and minimal vitreous debris (Figure 2).
What is your diagnosis?
The differential diagnosis of visual loss on the first postoperative day after cataract surgery includes disparate entities such as diffuse corneal edema, lens dislocation, wrong IOL placement, toxic anterior segment syndrome, endophthalmitis, central retinal artery occlusion, ischemic optic neuropathy, retinal detachment, hypotony, aminoglycoside toxicity or a traumatic ocular injury related to regional anesthesia.
The anterior segment in this case demonstrated an acute inflammatory response with severe anterior chamber reaction, hypopyon, fibrin formation and an inflammatory membrane noted by the pupil malformation.
The operative report noted an uncomplicated procedure using a peribulbar block. The presumed diagnosis was infectious endophthalmitis vs. sterile inflammation (toxic anterior segment syndrome). The patient underwent an anterior chamber tap and injection of vancomycin (1 mg/0.1 mL), ceftazidime (2.5 mg/0.1 mL) and dexamethasone (400 mcg/0.1 mL), and the aqueous fluid was sent for Gram stain and culture. The patient was sent home on prednisolone acetate drops every hour, gatifloxacin four times a day, cyclopentolate twice a day and ciprofloxacin 500 mg orally twice a day for 3 days.
Two additional patients operated on by the same ophthalmologist in the same operating room as this patient on the previous day were also seen on postoperative day 1 because of postoperative inflammation. All were treated the same way. The Gram stain and cultures of all three patients were negative. Differentiating between toxic anterior segment syndrome and infectious endophthalmitis can be difficult, but given the circumstance and response to treatment, we believe these cases to be a cluster of toxic anterior segment syndrome.
Toxic anterior segment syndrome (TASS) is a sterile postoperative inflammation due to a noninfectious substance that enters the eye, resulting in toxic damage to intraocular tissues. Typically, the inflammation peaks within 24 hours of surgery and is limited to the anterior segment. The Gram stain and cultures are negative in TASS, and the condition improves with steroid treatment.
Clinically, TASS is characterized by a precipitous decrease in vision, mild discomfort, diffuse limbus-to-limbus corneal edema, severe anterior chamber reaction with fibrin formation, possible hypopyon, and inflammatory membranes that may induce trabecular meshwork damage and pupillary distortion. There is an absence of vitritis and posterior segment inflammation; however, there may be spillover of cells into the vitreous cavity due to the intensity of the anterior chamber reaction.
TASS has become a more widely recognized entity in recent years, and multiple multi-case outbreaks occurring in many states have been reported. The etiology of TASS may include several causes. Ophthalmic instrument contaminants, irrigating solutions, ocular medications and IOLs have been suggested. Improper sterilization of instruments and detergents may also be a cause. Detergents can accumulate as deposits on the surface of instruments and may not be adequately deactivated at the temperatures reached by most autoclaves. These deposits are only removed with sterile deionized water. Autoclave reservoirs may also harbor gram-negative bacteria, which may create heat stable endotoxins attaching to instruments. Despite proper sterilization techniques, such endotoxins may only be removed with alcohol or acetone. Oxidized residues can also form on tubing or cannulas when gas sterilization is used.
Preservatives such as benzalkonium chloride (BAK) have been linked to TASS outbreaks. Irrigating solution or medication injected intracamerally should be preservative-free because of the potential damage to the corneal endothelium. Liu and colleagues described 19 patients who developed TASS from the intraocular use of an irrigating solution with BAK. Most of these patients required corneal transplants due to persistent corneal edema and endothelial cell loss. A case series was also reported of persistent corneal edema secondary to a viscoelastic containing BAK.
TASS has also been linked to residual polishing compounds on IOLs and postoperative ointment entering the eye after tight patching with clear corneal wounds. These cases were reported to have delayed-onset TASS relative to most other presentations. One hundred twelve cases of TASS were reported from seven centers in six states, where 89% of the patients were exposed to a balanced salt solution of a single brand (AMO Endosol) that was found to have endotoxin levels exceeding the allowable limit.
The American Academy of Ophthalmology and the American Society of Cataract and Refractive Surgery announced the formation of a task force to determine the causes and share recommendations for TASS outbreaks. Two questionnaires are available on the ASCRS Web site to assist investigations. Recommendations for prevention include a team approach to ordering, cleaning and sterilizing instruments; ensuring proper pH, osmolality and non-toxicity of irrigating solutions, viscoelastics and medications; avoiding reusable instruments and cannulas; proper rinsing of irrigating and aspiration tips and phaco handpieces; the replacement of ultrasound baths daily; and changing steam autoclaves weekly.
Once the toxic agent enters the eye, management of TASS should be aimed at suppressing the inflammatory immune response. The primary goal is to rule out an infectious etiology, followed by intense topical corticosteroid treatment (prednisolone acetate every 30 minutes to every 1 hour). Close monitoring is essential to ensure improvement of the inflammatory response and IOP management. Differentiating between TASS and infectious endophthalmitis is difficult, and none of the signs are specific enough to definitively distinguish between one vs. the other. TASS typically has no pain, no vitritis, occurs within 24 hours of surgery and is culture negative. Infectious endophthalmitis is characterized by pain (75%), later onset (4 to 7 days), vitritis, culture positive (69%) and has more prevalent lid swelling, chemosis, injection and discharge.
The clinical course is highly variable depending on the type of substance that entered the anterior segment, duration of exposure and how soon treatment was initiated. Mild cases may have rapid clearing of inflammation and resolution of corneal edema after treatment. Severe cases may have permanent damage related to non-clearing corneal edema, uncontrolled IOP due to trabecular meshwork damage and cystoid macular edema from chronic inflammation.
- Eleftheriadis H, Cheong M, Saneman S, et al. Corneal toxicity secondary to inadvertent use of benzalkonium chloride preserved viscoelastic material in cataract surgery. Br J Ophthalmol. 2002;86(3):299-305.
- Endophthalmitis Vitrectomy Study Group. Results of the Endophthalmitis Vitrectomy Study: A randomized trial of immediate vitrectomy and of intravenous antibiotics for the treatment of postoperative bacterial endophthalmitis. Arch Ophthalmol. 1995;113(12):1479-1496.
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- Kutty PK, Forster TS, Wood-Koob C, et al. Multistate outbreak of toxic anterior segment syndrome, 2005. J Cataract Refract Surg. 2008;34(4):585-590.
- Liu H, Routley I, Teichmann KD. Toxic endothelial cell destruction from intraocular benzalkonium chloride. J Cataract Refract Surg. 2001;27(11):1746-1750.
- Mamalis N, Edelhauser HF, Dawson DG, Chew J, LeBoyer RM, Werner L. Toxic anterior segment syndrome. J Cataract Refract Surg. 2006;32(2):324-333.
- Werner L, Sher JH, Taylor JR, et al. Toxic anterior segment syndrome and possible association with ointment in the anterior chamber following cataract surgery. J Cataract Refract Surg. 2006;32(2):227-235.
- Steven J. Yoon, MD, and Jay S. Duker, MD, can be reached at Tufts Medical Center, 750 Washington St., Box 450, Boston, MA 02111; 617-636-4219; fax: 617-636-4866; Web site: www.neec.com.
- Edited by Jeffrey Chang, MD, and Vivek Chaturvedi, MD. Drs. Chang and Chaturvedi can be reached at New England Eye Center, Tufts University School of Medicine, 750 Washington St., Box 450, Boston, MA 02111; 617-636-4219; fax: 617-636-4866; Web site: www.neec.com.