Updated: Feb 12, 2009
Bacterial endophthalmitis is an inflammatory reaction of the intraocular fluids or tissues caused by microbial organisms.
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.
Incidence after intraocular surgery is less than 0.1%. Incidence of culture-proven endophthalmitis is similar to that of extracapsular cataract extraction and phacoemulsification.
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.
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.
Causes are related to classification of exogenous and endogenous.
| Acute Retinal Necrosis | Ocular Manifestations of Syphilis |
| Ankylosing Spondylitis | Sarcoidosis |
| Cataract, Traumatic | Uveitis, Anterior, Granulomatous |
| Endophthalmitis, Fungal | Uveitis, Anterior, Nongranulomatous |
| Foreign Body, Intraocular | Uveitis, Intermediate |
| Hemorrhage, Vitreous | Vitreous Wick Syndrome |
| HLA-B27 Syndromes | |
| Hyphema |
Retained lens material following cataract surgery
Bacterial endophthalmitis is an ocular emergency, and urgent treatment is required to reduce the potential of significant visual loss.
Surgical intervention is usually performed urgently except in the delayed onset category where elective surgery may suffice.
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.
Therapy must be comprehensive and cover all likely pathogens in the context of this clinical setting.
Potent antibiotic directed against gram-positive organisms and active against Enterococcus 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.
Topical: 50 mg/mL q1h
Intravitreal: 1 mg/0.1 mL
Periocular: 25 mg
Systemic: 1 g IV q12h
Topical: Administer as in adults
Intravitreal: Administer as in adults
Systemic: 10 mg/kg/dose IV q6h
Erythema, histaminelike flushing, and anaphylactic reactions may occur when administered with anesthetic agents; taken concurrently with aminoglycosides, risk of nephrotoxicity may increase above that with aminoglycoside monotherapy; effects in neuromuscular blockade may be enhanced when coadministered with nondepolarizing muscle relaxants
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Corneal toxicity; in systemic administration ototoxicity, nephrotoxicity reversible neutropenia may occur; adjust dose in renal insufficiency; caution in renal failure, neutropenia; red man syndrome is caused by too rapid IV infusion (dose given over a few minutes) but rarely happens when dose given IV over 2 h administration or as PO or IP administration; red man syndrome is not an allergic reaction
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.
Topical: 50 mg/mL q1h
Intravitreal: 2.25 mg/0.1 mL
Periocular: 100 mg
Systemic: 1 g IV q12h
Not established
Can cause false-positive results in glucose-urine testing with copper reduction test (Benedict or Fehling solution); false-negative results in ferricyanide test; positive Coombs test; nephrotoxicity may increase with aminoglycosides, furosemide, and ethacrynic acid; probenecid may increase ceftazidime levels
Documented hypersensitivity
B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals
Adjust dose in severe renal insufficiency (high doses may cause CNS toxicity); superinfections, and promotion of nonsusceptible organisms may occur with prolonged use or repeated therapy
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.
Topical: 13.6 mg/mL
Intravitreal: 0.4 mg/0.1 mL
Systemic: 75 mg/kg IV q12h
Administer as in adults
Coadministration with other aminoglycosides, penicillins, cephalosporins, and amphotericin B increases nephrotoxicity; enhances effects of neuromuscular blocking agents; causes respiratory depression; irreversible hearing loss may occur with coadministration of loop diuretics
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Not intended for long-term therapy; caution in patients with renal failure (not on dialysis), hypocalcemia, myasthenia gravis, and conditions that depress neuromuscular transmission
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.
Topical: 1 gtt qid to q1h
Systemic: 750 mg PO q12h
Not established
Antacids, iron salts, and zinc salts may reduce serum levels; administer antacids 2-4 h before or after taking fluoroquinolones; cimetidine may interfere with metabolism of fluoroquinolones; ciprofloxacin reduces therapeutic effects of phenytoin; probenecid may increase ciprofloxacin serum concentrations
May increase toxicity of theophylline, caffeine, cyclosporine, and digoxin (monitor digoxin levels); may increase effects of anticoagulants (monitor PT)
Documented hypersensitivity
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
In prolonged therapy, perform periodic evaluations of organ system functions (eg, renal, hepatic, hematopoietic); adjust dose in renal function impairment; superinfections may occur with prolonged or repeated antibiotic therapy
Have anti-inflammatory properties and cause profound and varied metabolic effects. Corticosteroids modify the body's immune response to diverse stimuli.
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.
1 gtt qid to q1h
Administer as in adults
None reported
Documented hypersensitivity; viral, fungal, or tubercular infections
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in hypertension; known to cause cataract formation with long-term use; suspect fungal invasion in any persistent corneal ulceration where a corticosteroid has been used or is in use (obtain fungal cultures when appropriate)
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.
Intravitreal: 0.4 mg/0.1 mL
Not established
None reported
Documented hypersensitivity; active bacterial, viral, or fungal infection
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Prolonged use may increase hazard of secondary ocular infection; suspect fungal invasion in any persistent corneal ulceration where a corticosteroid has been used or is in use (obtain fungal cultures when appropriate)
Treats inflammatory dermatosis responsive to steroids. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability.
Periocular: 40 mg
Not established
None reported
Documented hypersensitivity; fungal, viral, and bacterial skin infections
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Do not use in decreased skin circulation; prolonged use, applications over large areas, and use of potent steroids and occlusive dressings may result in systemic absorption; systemic absorption may cause Cushing syndrome, reversible HPA axis suppression, hyperglycemia, and glycosuria
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.
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.
Topical: 1 gtt bid
Not established
Coadministration with other anticholinergics have additive effects; pharmacologic effects of atenolol and digoxin may increase with atropine; antipsychotic effects of phenothiazines may decrease with this medication; tricyclic antidepressants with anticholinergic activity may increase effects of atropine
Documented hypersensitivity, thyrotoxicosis, narrow-angle glaucoma, and tachycardia
C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus
Caution in patients with Down syndrome and/or children with brain damage to prevent hyperreactive response; caution also in coronary heart disease, tachycardia, congestive heart failure, cardiac arrhythmias, hypertension, peritonitis, ulcerative colitis, hepatic disease, and hiatal hernia with reflux esophagitis; in prostatic hypertrophy, prostatism can have dysuria and may require catheterization
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bacterial endophthalmitis, bacterial infection in the eye, bacteria in the eye, bacterial eye infection, eye infection, ocular infection
Robert H Graham, MD, Senior Associate Consultant, Department of Ophthalmology, Mayo Clinic, Scottsdale, Arizona
Robert H Graham, MD is a member of the following medical societies: American Academy of Ophthalmology, American Medical Association, and Arizona Ophthalmological Society
Disclosure: WebMD/eMedicine Salary Employment
Andrew W Lawton, MD, Medical Director of Neuro-Ophthalmology Service, Section of Ophthalmology, Baptist Eye Center, Baptist Health Medical Center
Andrew W Lawton, MD is a member of the following medical societies: American Academy of Ophthalmology, Arkansas Medical Society, and Southern Medical Association
Disclosure: Nothing to disclose.
Simon K Law, MD, PharmD, Assistant Professor of Ophthalmology, Jules Stein Eye Institute; Chief of Section of Ophthalmology Surgical Services, Department of Veterans Affairs Healthcare Center, West Los Angeles
Simon K Law, MD, PharmD is a member of the following medical societies: American Academy of Ophthalmology, American Glaucoma Society, and Association for Research in Vision and Ophthalmology
Disclosure: Nothing to disclose.
R Christopher Walton, MD, Professor, Director of Uveitis and Ocular Inflammatory Disease Service, Department of Ophthalmology, Assistant Dean for Graduate Medical Education, University of Tennessee College of Medicine; Consulting Staff, Regional Medical Center, Memphis Veterans Affairs Medical Center, St Jude Children's Research Hospital
R Christopher Walton, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Healthcare Executives, American Uveitis Society, Association for Research in Vision and Ophthalmology, and Retina Society
Disclosure: Nothing to disclose.
Lance L Brown, OD, MD, Ophthalmologist, Affiliated With Freeman Hospital and St John's Hospital, Regional Eye Center, Joplin, Missouri
Disclosure: Nothing to disclose.
Hampton Roy Sr, MD, Associate Clinical Professor, Department of Ophthalmology, University of Arkansas for Medical Sciences
Hampton Roy Sr, MD is a member of the following medical societies: American Academy of Ophthalmology, American College of Surgeons, and Pan-American Association of Ophthalmology
Disclosure: Nothing to disclose.
The authors and editors of eMedicine gratefully acknowledge the contributions of previous coauthors, David T Wong, MD, FRCS(C), and Hesham Lakosha, MBChB, MS, FRCS, to the development and writing of this article.
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