Endophthalmitis

This is the inflammation of the intraocular space occupied by the vitreous.¹ When the inflammation spreads throughout the globe and involves all the layers ± the peri-ocular tissues, it is known as panophthalmitis, a devastating fulminant condition with a very bleak outlook. Endophthalmitis may be endogenous (or metastatic, e.g. spread of organisms from endocarditis) or exogenous (e.g. following penetrating ocular trauma). Furthermore, it may be acute or follow a chronic course, depending on the infecting pathogen.

Pathophysiology

Normally, the blood-ocular barrier prevents invasion from infective organisms but if this is breached (directly through trauma or indirectly due to a change in its permeability secondary to inflammation), infection can occur. Endophthalmitis can be:²

• Associated with surgery: acute or delayed post-operative, bleb-associated
• Traumatic: bacterial or fungal endophthalmitis
• Endogenous: bacterial or fungal endophthalmitis
• Associated with corneal infection (microbial keratitis)

This is a rare condition. Post-operative endophthalmitis occurs following about 0.1% of cataract procedures and post-traumatic endophthalmitis has been estimated, by one study, to occur in 6.8% of cases.³

Risk factors⁴

• In non-accidental injury (surgery): prior presence of infection (e.g. bacterial conjunctivitis), poor surgical technique and contaminated intraocular lens.
• In accidental injury: retained infected foreign material, particularly if this is organic.
• Ophthalmic risk factors: contact lens wear (where there is poor hygiene) or chronic corneal ulceration.
• Non-ophthalmic risk factors: debility, distant infection (e.g. in-dwelling catheter) and immunosuppression.

Associated with surgery

• Acute post-operative endophthalmitis
  • History - this arises one to several days after surgery. There is sudden decrease of vision and increasing eye pain.
  • Signs - without the slit-lamp, you may see lid oedema, intense conjunctival injection and chemosis and you may spot a hypopyon (pus in the anterior chamber which looks like a white fluid level sitting at the base of the iris). The red reflex is decreased. Slit-lamp examination will reveal severe inflammation in the anterior chamber and the vitreous.
• Delayed post-operative endophthalmitis
  • History - develops a week to a month (or more) after surgery. It may even take years to develop but the average is 9 months. There is insidious decrease of vision and gradually increasing redness and minimal or no pain.⁵
  • Signs - without the slit-lamp, look for conjunctival injection, a hypopyon and you may just see clumps of exudate (little white blobs) in the anterior chamber, on the iris or around the pupillary margin. The cornea may look cloudy (due to oedema). These signs are clearly seen with the slit-lamp, as is the anterior chamber and vitreous inflammatory reaction.
• Bleb-associated endophthalmitis
  When drug therapy fails in the treatment of glaucoma, patients may go on to have surgery. A trabeculectomy is a procedure that creates a fistula which allows the aqueous to drain from the anterior chamber. A so-called bleb is formed over this area, seen as a smooth, raised patch just over the cornea, under the upper lid. Occasionally, this gets infected ('blebitis') but when the vitreous is also involved, it becomes a bleb-associated endophthalmitis. There is a short history of rapidly worsening pain and vision with marked redness and the bleb itself will appear milky white. There may be a hypopyon too.

Not associated with surgery

There are a number of causes of red eye post-operatively, including:

• Raised intraocular pressure as a direct result of the procedure.
• Retained lens material - if the crystalline lens is not fully removed at the time of cataract surgery, the small remaining piece can cause an intraocular inflammatory reaction. This is an autoimmune reaction to the exposed lens protein. The lens material can often be seen with a slit lamp if the patient is asked to move their eyes (it is seen floating up in the aqueous or vitreous before settling down again when the eye is still).
• Aseptic endophthalmitis is more likely to occur after a prolonged procedure and results from excessive tissue manipulation. Symptoms and signs are usually mild.
• Inflammatory reactions can occasionally occur in response to the substances used in cataract surgery (e.g. those used to sterilise the intra-ocular lens).
• In immunocompromised host where there might be candida endophthalmitis, other differentials include cytomegalovirus retinitis, toxoplasmosis and a number of other conditions that have similar lesions and that will be assessed by the ophthalmologist (e.g. infections with herpes simplex, nocardia, aspergillus and cryptococci)

Remember that post-operative and trauma patients can also develop a red eye due to a new problem that is unrelated to the procedure or trauma.

General causes of Red Eye are more fully discussed in our dedicated record.

Initial diagnosis is made on slit-lamp examination. An ultrasound scan (easily and painlessly performed in the out patient clinic) may also be of help. However, diagnosis is ultimately confirmed by taking a sample of vitreous for microbiological culture (diagnostic surgical vitrectomy). This is done in theatre and may also be a therapeutic procedure if the vitreous is entirely removed (to reduce the infectious load); intraocular antibiotics can be administered at the same time.

In the case of endogenous bacterial endophthalmitis and candida endophthalmitis, a full infection screen is warranted (full blood count, blood cultures and culture of all indwelling lines and catheters). The latter may also prompt a search for possible immunocompromise.

These are different depending on the type of endophthalmitis as discussed above in risk factors and presentation.

• If you suspect acute endophthalmitis, immediate same day /night referral is mandatory. If you suspect a delayed post-operative endophthalmitis, refer within 24 hours.
• The subsequent management depends on the type of endophthalmitis. All but a very few patients will be admitted for a diagnostic work-up (see investigations above) and antimicrobial treatment.
• Some patients will additionally be prescribed steroids once fungal infection has been ruled out. These are to limit the amount of inflammatory-induced damage.
• Topical cycloplegics also play a role in controlling the symptoms.
• Some patients will need surgery: a vitrectomy (removal of the vitreous) may be indicated. In addition to providing material for microbiology, it reduces infective load.
• Trauma cases also need tetanus immunization if this is not up to date.

These are mainly decrease or loss of vision. Chronic pain may become an issue in some patients.

The visual acuity at the time of the diagnosis and the causative agent are most predictive of outcome. As a rule of thumb, endogenous endophthalmitis has a worse prognosis than exogenous endophthalmitis and some patient groups such as diabetics do less well. Acute post-operative endophthalmitis has a poor prognosis with 55% of eyes managing 6/60 or less. Chronic post-operative endophthalmitis usually responds well to steroids initially but then tends to become refractory to treatment. Successfully treated bleb-associated endophthalmitis is at risk of recurring infections. In the event that vision is lost and the eye becomes chronically painful, enucleation (removal of the globe) may have to be considered.

Optimum prophylaxis in acute-post-operative endophthalmitis has yet to be determined. However, good management of pre-existing infections and meticulous pre-operative preparations do reduce the risks.

This is an inflammatory condition affecting both eyes that occurs after a penetrating injury (accidental or surgical) to one of the eyes. It is thought to possibly be an autoimmune reaction to the exposed tissue proteins within the damaged eye. It is a very rare condition, occurring in about 3 out of every 10,000,000 cases of penetrating injury. About two-thirds occur within a fortnight of the injury and 90% within the first year (range: 5 days to 66 years!). Presentation is with bilateral deterioration of vision and red eyes which are painful. Examination reveals diffuse intra-ocular inflammation. It is managed aggressively with steroids ± immunosuppressive agents. The prognosis is poor without rapid intervention; there is a reasonable chance that useful vision will be retained in those where diagnosis and appropriate treatment was prompt.