Description, Causes and Risk Factors:
Bacterial endophthalmitis is an infection of the interior of the eye that, despite appropriate therapeutic intervention, frequently results in visual loss. Recently, research has begun to elucidate the molecular and cellular events that contribute to the damage that occurs in intraocular infection. This review discusses the epidemiology and therapuetic challenges of endophthalmitis, as well as current findings from the analysis of bacterial and host interactions in the pathogenesis of eye infections. Based on these and related studies, a model for the molecular pathogenesis of endopthalmitis is advanced. A more comprehensive understanding of the contributions of the molecular and cellular interactions in endophthalmitis will likely unveil possible therapeutic targets designed to ameliorate the infection and preserve vision.
Bacteria involved include the following:
Delayed onset or chronic pseudophakic postoperative Propionibacterium acnes, and coagulase-negative and Corynebacterium species.
Filtering bleb associated - Streptococcus and Staphylococcus species and Haemophilus influenzae.
Posttraumatic - Bacillus and Staphylococcus species.
Endogenous - S aureus, Escherichia coli, and Streptococcus species.
Acute pseudophakic postoperative - Coagulase-negative staphylococci, Staphylococcus aureus, and Streptococcus, Enterococcus, and gram-negative species.
The entry of bacteria into the eye occurs from a breakdown of the ocular barriers. Penetration through the cornea or sclera results in an exogenous insult to the eye. If the entry is through the vascular system, then an endogenous route occurs. After the bacteria gain entry into the eye, rapid proliferation occurs.
The vitreous acts as a superb medium for bacteria growth, and, in the past, animal vitreous was used as a culture medium. Bacteria, as foreign objects, incite an inflammatory response. The cascade of inflammatory products occurs resulting in an increase in the blood-ocular barrier breakdown and an increase in inflammatory cell recruitment. The damage to the eye occurs from the breakdown of the inflammatory cells releasing the digestive enzymes as well as the possible toxins produced by the bacteria. Destruction occurs at all tissue levels that are in contact with the inflammatory cells and toxins.
Anterior chamber cells and flare.
Fibrin membrane formation.
Loss of red reflex.
Retinal periphlebitis if view of fundus possible.
Visual acuity decreased below the level expected.
Perform culture and sensitivity studies on aqueous and vitreous samples to determine the type of organism and antibiotic sensitivity.If endogenous bacterial endophthalmitis is suspected, a systemic workup for the source is required. This workup includes the following:
B-scan ultrasound: Perform B-scan ultrasound of the posterior pole if view of fundus is poor. Typically, choroidal thickening and ultrasound echoes in the anterior and posterior vitreous support the diagnosis. Occasionally, another source of inflammation other than or in addition to bacteria, such as retained lens material may be seen. The ultrasound is also important to provide a baseline prior to intraocular intervention and to assess the posterior vitreous face and areas of possible traction. Rarely, a retinal detachment is seen concurrently with endophthalmitis. A CT scan rarely is performed unless trauma is involved. Thickening of the sclera and uveal tissues associated with various degree of increased density in the vitreous and periocular soft tissue structures may be seen.
Bacterial endophthalmitis is an ocular emergency, and urgent treatment is required to reduce the potential of significant visual loss. All patients should have therapy consisting of intravitreal and topical antibiotics, topical steroids, and cycloplegics.
When the inflammation is severe, systemic and periocular therapy may be used in non-cataract-induced, delayed onset, filtering bleb associated, and posttraumatic endophthalmitis. In endogenous endophthalmitis, systemic, topical, and possibly periocular therapy is usually required.
Surgical intervention is usually performed urgently except in the delayed onset category where elective surgery may suffice. A 3-port core pars plana vitrectomy with intravitreal antibiotic injections is performed. If visualization is poor from anterior segment pathology, then a 2-port limited pars plana vitrectomy or endoscopic guided 3-port pars plana vitrectomy may be performed. Intravitreal antibiotics usually are given after the completion of the vitrectomy; however, if an air-fluid exchange is to be performed, the antibiotics may be mixed into the vitrectomy solution. Dilute the antibiotics in the vitrectomy solution carefully to prevent possible toxic retinopathy from incorrect dosages.
NOTE: The above information is for processing purpose. The information provided herein should not be used during any medical emergency or for the diagnosis or treatment of any medical condition.
DISCLAIMER: This information should not substitute for seeking responsible, professional medical care.
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