Endophthalmitis is an inflammatory condition of the intraocular cavities (ie, the aqueous and/or vitreous humor) usually caused by infection. Noninfectious (sterile) endophthalmitis may result from various causes such as retained native lens material after an operation or from toxic agents. Panophthalmitis is inflammation of all coats of the eye including intraocular structures.
The 2 types of endophthalmitis are endogenous (ie, metastatic) and exogenous. Endogenous endophthalmitis results from the hematogenous spread of organisms from a distant source of infection (eg, endocarditis). Exogenous endophthalmitis results from direct inoculation of an organism from the outside as a complication of ocular surgery, foreign bodies, and/or blunt or penetrating ocular trauma.
Under normal circumstances, the blood-ocular barrier provides a natural resistance against invading organisms.
In endogenous endophthalmitis, blood-borne organisms (seen in patients who are bacteremic in situations such as endocarditis) permeate the blood-ocular barrier either by direct invasion (eg, septic emboli) or by changes in vascular endothelium caused by substrates released during infection. Destruction of intraocular tissues may be due to direct invasion by the organism and/or from inflammatory mediators of the immune response.
Endophthalmitis may be as subtle as white nodules on the lens capsule, iris, retina, or choroid. It can also be as ubiquitous as inflammation of all the ocular tissues, leading to a globe full of purulent exudate. In addition, inflammation can spread to involve the orbital soft tissue.
Any surgical procedure that disrupts the integrity of the globe can lead to exogenous endophthalmitis (eg, cataract, glaucoma, retinal, radial keratotomy, intravitreal injections).
Endogenous endophthalmitis is rare, occurring in only 2-15% of all cases of endophthalmitis. Average annual incidence is about 5 per 10,000 hospitalized patients. In unilateral cases, the right eye is twice as likely to become infected as the left eye, probably because of its more proximal location to direct arterial blood flow from the right innominate artery to the right carotid artery. Since 1980, candidal infections reported in IV drug users have increased. The number of people at risk may be increasing because of the spread of AIDS, more frequent use of immunosuppressive agents, and more invasive procedures (eg, bone marrow transplantation).
Most cases of exogenous endophthalmitis (about 60%) occur after intraocular surgery. When surgery is implicated in the cause, endophthalmitis usually begins within 1 week after surgery. In the United States, postcataract endophthalmitis is the most common form, with approximately 0.1-0.3% of operations having this complication, which has increased over the last 3 years.  Although this is a small percentage, large numbers of cataract operations are performed each year making the chances that physicians may encounter this infection higher. Endophthalmitis may also occur after intravitreal injections, although this risk in an analysis of over 10,000 injections is estimated at 0.029% per injection. 
Posttraumatic endophthalmitis occurs in 4-13% of all penetrating ocular injuries. Incidence of endophthalmitis with perforating injuries in rural settings is higher when compared with nonrural settings.  Delay in the repair of a penetrating globe injury is correlated with increased risk of developing endophthalmitis.  Incidence of endophthalmitis with retained intraocular foreign bodies is 7-31%.
Decreased vision and permanent loss of vision are common complications of endophthalmitis. Patients may require enucleation to eradicate a blind and painful eye.
Mortality is related to the patient's comorbidities and the underlying medical problem, especially when considering the etiology of hematogenous spread in endogenous infections.
An association appears to exist between the development of endophthalmitis in cataract surgery and age greater than or equal to 85 years. 
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