Background

Bacterial endophthalmitis is an inflammatory reaction of the intraocular fluids or tissues

caused by microbial organisms. See the images below.

Bacterial endophthalmitis. Retinopathy induced by Enterococcus

faecalis endotoxin. Bacterial endophthalmitis. Hypopyon, 3 days after

phacoemulsification.
Pathophysiology
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.

Epidemiology
Frequency
United States
Incidence after intraocular surgery is less than 0.1%. Incidence of culture-proven
endophthalmitis is similar to that of extracapsular cataract extraction and
phacoemulsification.
 Mortality/Morbidity
If not properly treated, a risk of complete vision loss and the possibility of persistent
ocular pain exist. Infection very rarely spreads beyond the confines of the sclera and
tracks into surrounding tissue structures.

History
The clinical presentation is dependent on the route of entry, the infecting organism, and
the duration of the disease. In general, patients complain of a decrease in vision, often
with a red eye. Most patients also may complain of a deep ocular pain. Classification is
based on routes of entry.[1]

 Exogenous source
Acute postoperative (< 6 wk postoperative)[2, 3]
o
 Infection usually occurs 2-10 days after surgery.
 Patients present with visual loss greater than expected in the usual postoperative
course.
 Ocular pain is seen in 75% of patients.
 The use of postoperative antibiotic and anti-inflammatory drugs may blunt the
severity of the disease and possibly delay medical attention.
o Delayed onset or chronic pseudophakic postoperative (>6 wk postoperative) [2]
 Patients typically present with mild-to-moderate inflammatory red eye, reduced
vision, and photophobia.
 Chronic indolent course is present.
 Patients may be diagnosed with idiopathic uveitis and treated with topical steroids
with temporary improvement.
 Fungal species must be ruled out.
o Filtering bleb associated: Clinical features are similar to acute postoperative infection
with purulent bleb involvement.[4]
o Posttraumatic: History of trauma is present, and infection usually progresses
rapidly.[5]
 Endogenous source
o No recent history of ocular surgery is present.
o Confusion with delayed onset or chronic postoperative is possible if suspicion for
endogenous route is not ruled out.
o The symptoms are rarely bilateral.
Physical
 General findings
 Visual acuity decreased below the level expected
 Lid edema
 Conjunctival hyperemia
 Corneal edema
 Anterior chamber cells and flare
 Keratic precipitates
 Hypopyon[6]
 Fibrin membrane formation
  Vitritis
 Loss of red reflex
 Retinal periphlebitis if view of fundus possible[7]
 Specific findings
 Delayed onset or chronic: Occasionally, findings display a white plaque within the
equator of the remaining lens capsule.
 Filtering bleb associated: A purulent bleb is seen occasionally with areas of necrosis
in the sclera from the use of antimetabolites.
 Posttraumatic: Evidence of penetrating trauma is seen with the possibility of
an intraocular foreign body.[8, 9]
 Endogenous: Patient may appear systemically ill.
Causes
Causes are related to classification of exogenous and endogenous.[10]

 Exogenous
Ocular surgical procedure - Increased risk when complications arise
o
Trauma
o
Ocular surface infection (eg, corneal ulcer)
o
Filtering bleb associated - Use of antimetabolites or contaminated contact lenses
o
 Endogenous
o Septicemia
o Patients who are debilitated
o Indwelling catheters
o Intravenous drug use
 Bacteria involved include the following[11] :
o Acute pseudophakic postoperative - Coagulase-negative
staphylococci, Staphylococcus aureus, and Streptococcus, Enterococcus, and gram-
negative species[12, 9, 13, 14, 5]
o Delayed onset or chronic pseudophakic postoperative -Propionibacterium
acnes, and coagulase-negative andCorynebacterium species[12, 9, 13, 14, 5, 15]
o Filtering bleb associated[16] -Streptococcus and Staphylococcusspecies
and Haemophilus influenzae
o Posttraumatic -Bacillus[17] and Staphylococcus species[18]
o Endogenous -S aureus, Escherichia coli, and Streptococcusspecies

Differentials
 Acute Retinal Necrosis
 Ankylosing Spondylitis
 Cataract, Traumatic
 Endophthalmitis, Fungal
 Foreign Body, Intraocular
 Hemorrhage, Vitreous
 HLA-B27 Syndromes
 Hyphema
 Ocular Manifestations of Syphilis
  Sarcoidosis
 Uveitis, Anterior, Granulomatous
 Uveitis, Anterior, Nongranulomatous
 Uveitis, Intermediate
 Vitreous Wick Syndrome

Laboratory Studies
 Perform culture and sensitivity studies on aqueous and vitreous samples to determine
the type of organism and antibiotic sensitivity. [19, 20]
 If endogenous bacterial endophthalmitis is suspected, a systemic workup for the source
is required. This workup includes the following[21] :
 Blood culture
 Sputum culture
 Urine culture
Imaging Studies
 B-scan ultrasound[22]
 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.[22]
 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.
 If an endogenous route is considered, perform other imaging modalities to rule out
potential sources.
 Two-dimensional echocardiogram
 Chest x-ray
Procedures
 Anterior chamber tap: A 30-gauge needle on a tuberculin syringe is used to obtain a 0.1
cc sample under topical anesthesia through the limbus.
 Vitreous tap
 A retrobulbar block or a sub-Tenon block with lidocaine with epinephrine is given.
 A sub-Tenon block has the advantage over a retrobulbar block because it does not
create increased intraocular pressure that may cause recent surgical wounds to open.
 A 21-gauge needle on a tuberculin syringe is used to obtain an adequate vitreous
sample of 0.1-0.2 cc. Smaller gauge needles may be used but with increasing
difficulty to create the aspiration vacuum necessary to obtain a sample.
 Vitreous biopsy: A 23-gauge vitrectomy cutter may be used if available.

Medical Care
 Bacterial endophthalmitis is an ocular emergency, and urgent treatment is required to
reduce the potential of significant visual loss.[23, 24]

 All patients should have therapy consisting of intravitreal and topical antibiotics, topical
steroids, and cycloplegics.[25, 26, 27, 28]
 The Endophthalmitis Vitrectomy Study (EVS) identified that the use of periocular and
intravenous antibiotics are not required in endophthalmitis following cataract surgery.
Medical therapy was found to be statistically as effective as surgical intervention when
the presenting vision was hand motion or better. Use caution in interpreting the data
from the EVS; apply it cautiously to non–cataract-related endophthalmitis.[29, 30, 31, 32, 33, 34]
 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.[9]
Surgical Care
Surgical intervention is usually performed urgently except in the delayed onset category
where elective surgery may suffice.

 Indications for surgical therapy

o Acute pseudophakic postoperative - When the presenting vision is light perception or
worse[35]
o Delayed onset or chronic postoperative - If marked inflammation or a subcapsular
plaque is identified, surgical removal is required.
o Filtering bleb associated - If marked inflammation is present. Take care not to disturb
the bleb if some function still exists. To allow the possibility of a shunt valve to be
placed at a later time, make an attempt to minimize the disturbance to the superior
conjunctiva. If the patient is aphakic, performing the pars plana vitrectomy from the
temporal side using a limbal approach may be required.
o Posttraumatic - If marked inflammation or rapid onset occurs
 Technique
o A 3-port core pars plana vitrectomy with intravitreal antibiotic injections is
performed.[36] 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.[37]
o An increased risk for retinal tears and detachments occur when the vitreous close to
the retina is removed aggressively due to the higher probability of retinal necrosis.
o 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.
 Medication Summary
 The goals of pharmacotherapy are to eradicate the infection, to reduce morbidity,
and to prevent complications. Various routes for drug administration are
available. Intravitreous is the most effective.
 Antibiotics
 Class Summary
 Therapy must be comprehensive and cover all likely pathogens in the context of
this clinical setting.
 View full drug information
 Vancomycin (Vancocin, Vancoled, Lyphocin)

 Potent antibiotic directed against gram-positive organisms and active
againstEnterococcus species. Indicated for patients who cannot receive or have
failed to respond to penicillins and cephalosporins or have infections with
resistant staphylococci.
 To avoid toxicity, current recommendation is to assay vancomycin trough levels
after third dose drawn 0.5 h prior to next dosing. Use creatinine clearance to
adjust dose in patients diagnosed with renal impairment. DOC for gram-positive
organisms.
 View full drug information
 Ceftazidime (Ceptaz, Fortaz, Tazicef, Tazidime)

 First-line choice for intravitreal gram-negative coverage. Third-generation
cephalosporin with broad-spectrum, gram-negative activity; lower efficacy against
gram-positive organisms; higher efficacy against resistant organisms. Arrests
bacterial growth by binding to one or more penicillin-binding proteins.
 View full drug information
 Amikacin (Amikin)

 Second-line choice for intravitreal injection for gram-negative coverage. For
gram-negative bacterial coverage of infections resistant to gentamicin and
tobramycin. Effective against Pseudomonas aeruginosa.
 Irreversibly binds to 30S subunit of bacterial ribosomes; blocks recognition step
in protein synthesis; causes growth inhibition. Use the patient's IBW for dosage
calculation.
 View full drug information
 Ciprofloxacin ophthalmic (Cipro, Ciloxan)

 Fluoroquinolone with activity against pseudomonas, streptococci, MRSA, S
epidermidis, and most gram-negative organisms, but no activity against
anaerobes. Inhibits bacterial DNA synthesis, and consequently growth. Provides
gram-positive coverage. Uncertain benefit in noncataract causes.
 Corticosteroids
 Class Summary
 Have anti-inflammatory properties and cause profound and varied metabolic
effects. Corticosteroids modify the body's immune response to diverse stimuli.
 View full drug information
 Prednisolone acetate (Pred Forte)

 Treats acute inflammations following eye surgery or other types of insults to eye.
 Decreases inflammation and corneal neovascularization. Suppresses migration
of polymorphonuclear leukocytes and reverses increased capillary permeability.
 In cases of bacterial infections, concomitant use of anti-infective agents is
mandatory; if signs and symptoms do not improve after 2 days, reevaluate
patient. Dosing may be reduced, but advise patients not to discontinue therapy
prematurely. Dosage dependent on severity of inflammation.
 View full drug information
 Dexamethasone (Ocu-Dex)

 For various allergic and inflammatory diseases. Decreases inflammation by
suppressing migration of polymorphonuclear leukocytes and reducing capillary
permeability. Optional; clinical data are controversial on benefit.
 View full drug information
 Triamcinolone (Aristocort)

 Treats inflammatory dermatosis responsive to steroids. Decreases inflammation
by suppressing migration of polymorphonuclear leukocytes and reversing
capillary permeability.
 Cycloplegics
 Class Summary
 Reduces ciliary spasm that may cause pain. Cycloplegic agents are also
mydriatics, and the practitioner should make sure that the patient does not have
glaucoma. This medication could provoke an acute angle-closure attack.
 View full drug information
 Atropine ophthalmic (Isopto, Atropair, Atropisol)

 DOC; acts at parasympathetic sites in smooth muscle to block response of
sphincter muscle of iris and muscle of ciliary body to acetylcholine, causing
mydriasis and cycloplegia.
 Proceed to Follow-up
