الفهرس 
EtiologyOnly 14 pages are availabe for public view
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Abstract
Toxic anterior segment syndrome (TASS) is a sterile postoperative inflammatory reaction caused by a noninfectious substance that enters the anterior segment, resulting in toxic damage to intraocular tissues. The process typically starts 12 to 48 hours after cataract surgery, is limited to the anterior segment of the eye, is always Gram stain and culture negative, and usually improves with steroid treatment. Since 1980, there have been several reports of a severe form of anterior segment inflammation after cataract surgery that resulted in hypopyon formation and varying degrees of anterior segment damage from toxic substances.
The histopathologic hallmark of TASS is toxic anterior segment damage. Cellular necrosis and/or apoptosis and extracellular damage occur, resulting in the severe acute inflammatory response. The corneal endothelium is often the most damaged structure because of its inability to regenerate and replace dead cells.
Toxic anterior segment syndrome (TASS) is an acute inflammation of the anterior chamber, or segment, of the eye following cataract surgery. A variety of substances have been implicated as causes of TASS. These substances can be divided into extraocular substances that inadvertently enter the anterior chamber during or after surgery (topical anti-septic agents, talc from surgical gloves, topical ophthalmic ointment), products that are introduced into the anterior chamber as a part of the surgical procedure (anesthetic agents, preservatives , inappropriately reconstituted intraocular preparations, mitomycin-C, intraocular lens and irritants on the surfaces of intraocular surgical instruments that have accumulated as a consequence of inadequate or inappropriate instrument cleaning (denatured ophthalmic viscosurgical devices [OVDs] , heat stable endotoxin from overgrowth of gram-negative bacilli in water baths of ultrasonic cleaners,degradation of brass containing surgical instruments from plasma gas sterilization, and impurities of auto-clave steam).
CULTURES:
Cultures can determine whether the inflammation is infectious. Vitreous involvement more likely occurs in infectious endophthalmitis. With TASS, cultures of the anterior chamber and vitreous aspirates are negative. Usually, cultures are positive with infectious endophthalmitis, although they can be negative in some cases.
CORNEAL EDEMA:
Although corneal edema exists in both conditions, the edema in TASS is more profound and characteristically is diffuse, from limbus to limbus (i.e., the marginal region of the cornea of the eye by which it is continuous with the sclera). The corneal edema present with infectious endophthalmitis tends to be specific to the area of trauma (e.g., near the wound or opposite the wound).
PAIN:
Surprisingly, most patients suffering from TASS complain of only mild to moderate pain. Patients experiencing infectious endophthalmitis generally report pain that is more severe, which usually is regarded as diagnostic. Approximately 25% of patients diagnosed with infectious endophthalmitis, however, do not report experiencing pain.
INTRAOCULAR PRESSURE (IOP):
With TASS, marked inflammation initially may be associated with lower IOP. As the days progress, however, the pressure is likely to increase suddenly as aqueous humor production increases postoperatively. Toxic anterior segment syndrome affects the trabecular meshwork. Pressures as high as 40 mm Hg to 70 mm Hg may be measured. Permanent damage to the trabecular network can result, thus creating a risk for glaucoma.
INFLAMMATION:
Toxic anterior segment syndrome is characterized by immediate and marked anterior segment inflammation, with increased presence of white blood cells as a result of the marked breakdown of the blood-aqueous barrier, flare, and especially fibrin formation. Sometimes there is hypopyon, the size of which may be out of proportion with the quantity of cells and amount of flare observed. A profound, acute breakdown of the blood-aqueous barrier produces hypopyon in TASS. With infectious endophthalmitis, there is an increased cellular reaction in the anterior chamber, which occurs over a longer period of time than the inflammation in TASS.
PUPIL:
Iris atrophy may be significant in TASS. Toxic anterior segment syndrome can impair the iris sphincter tractional causing the pupil not to react well to light.
The main focus of TASS is on prevention, because once the toxic agent enters the eye and causes damage, the clinician can only suppress the secondary inflammatory response.
Once an infectious etiology has been ruled out, treatment for TASS consists of intense topical corticosteroids DROPs, such as prednisolone 1%, every hour with close follow-up. Patients should be followed closely to make sure the inflammation is not worsening and the pressure remains stable.
With careful slit-lamp examination, surgeons can document the resolution of anterior segment inflammation and corneal edema. When treating these cases, ophthalmologists also want to make sure that they remain comfortable that this is indeed TASS and not endophthalmitis.
After treatment, if the insult is mild, patients will tend to improve fairly quickly. There will be rapid clearing of the inflammation, the cornea will clear, and there will be no resulting permanent damage. If it is a moderate toxic insult, there may be prolonged clearing (three to six weeks) with possible corneal edema or corneal damage.
However, if it is severe insult, the damage tends to be permanent. Most likely, there will also be corneal edema, (sometimes requiring a corneal transplant), sequelae of chronic inflammation, cystoid macular edema, and permanent dilated pupil. Patients with severe trabecular meshwork damage sometimes develop glaucoma that is resistant to medical treatment alone. These cases may require surgical treatment such as trabeculectomy or placement of a tube shunt.