OVERVIEW: What every practitioner needs to know
Are you sure your patient has endophthalmitis? What should you expect to find?
The key symptoms are pain, photophobia, ocular and periocular redness, lid swelling, conjunctival discharge, and blurring or decreased vision.
The key physical findings are: erythematous and swollen eyelids; injected conjunctiva and sclera; corneal edema; reduced visual acuity; anterior chamber cells and flare (slit lamp exam), hypopyon (dependent layering of inflammatory cells and exudate); fibrin membrane formation; vitritis (vitreous clouding precluding view of retinal vessels); cotton-wool spots; reduced or absent red reflex (See Figure 1).
How did the patient develop endophthalmitis? What was the primary source from which the infection spread?
Endophthalmitis implies infection by bacteria and fungi of the intraocular cavities (i.e. vitreous or aqueous humors). There are two main types of endophthalmitis: endogenous (metastatic) and exogenous.
Endogenous endophthalmitis accounts for about 2-15% of all cases. It results from hematogenous spread from a distant, concurrent source in the host (e.g. endocarditis) or from an indwelling external source (e.g. intravenous line or catheter). Endogenous endophthalmitis ipsilateral in 14-25%, often with one eye (right eye is twice as likely) more heavily affected. Endogenous fungal endophthalmitis has been reported in the range of 3-45% of patients with disseminated fungal infection. The higher numbers were from several decades ago; this is much less frequently seen now that recommendations are to treat all patients with candidemia with antifungal agents.
Exogenous endophthalmitis results most commonly from intraocular surgery (70%), penetrating ocular trauma with or without a foreign body (20%), blunt trauma, bleb-associated, and as extension from severe microbial keratitis. In addition, there are rare reports of endophthalmitis associated with glaucoma shunts and keratoprostheses.
Which individuals are of greater risk of developing endophthalmitis?
Endogenous endophthalmitis occurs with an incidence of 5 per 10,000 in hospitalized patients. The most important host sources of infectious agents include endocarditis, gastrointestinal (GI) tract, genitourinary (GU) tract/pyelonephritis, skin and wound infection, pulmonary infections, meningitis, and septic arthritis/osteomyelitis. External sources include invasive procedures with predisposing factors such as hemodialysis, bladder catheterization, gastrointestinal endoscopy, total parental nutrition, chemotherapy, dental procedures, and intravenous drug abuse.
Endogenous bacterial endophthalmitis accounts for 2-8% of all cases, usually due to S. aureus and Gram-negative bacteria. Many patients are diagnosed with medical conditions including diabetes, hypertension, gastrointestinal disorders, cardiac disorders, malignancy, and immunosuppression or prolonged surgical complications. Systemic symptoms (fever) rather than acute ocular symptoms have been the most common reason to present and many cases are misdiagnosed with loss of vision.
Endogenous fungal endophthalmitis has been reported over a wide range of 3-45% of patients with disseminated fungal infection. Candida albicans endophthalmitis is the most frequent (75-80% of fungal cases), but with a changing epidemiology. It has become more common in patients with long-term indwelling lines and catheters. Overall, it is less common because of the now standard practice of treating all patients who have candidemia. Aspergillosis is the second most common especially in intravenous drug users.
Exogenous endophthalmitis results most commonly from intraocular surgery (60-70%), followed by penetrating trauma. The incidence of post-cataract surgery endophthalmitis is 0.05 – 0.3%; risk factors include loss of vitreous, disrupted posterior capsule, poor wound closure, and prolonged surgery. In the early, acute post-operative period (<6 weeks), the vast majority are Gram-positive bacteria including coagulase-negative staphylococci (70%), Staphylococcus aureus (10%), Streptococcus species (11%), and Gram-negatives only account for 6%. In the delayed, chronic post-operative period (>6 weeks) (also called chronic pseudophakic referring to infection of the implanted intraocular lens), Propionibacterium acnes (41-63%), coagulase-negative staphylococci (16%), and fungi (21%) (mostly Candida, then Aspergillus sp.) are the most common. Gram-negatives (6%), atypical mycobacteria (3%), and Nocardia occur rarely.
In conjunctival filtering bleb-associated endophthalmitis, the onset may be after several years, and the etiologic agents include Streptococcus sp. (47%), coagulase-negative staphylococci (22%), and Haemophilus influenzae (16%).
The incidence of post-traumatic endophthalmitis after a perforating injury is 2-17%, but the presence of a foreign body at least doubles the risk of endophthalmitis (7-31%) with the higher incidence in rural compared to non-rural settings. Risk factors include retained intraocular foreign body, delayed surgery (>24 hours), rural setting with soil contamination, and disrupted crystalline lens. The signs of infection occur early, but are often masked by the injured inflamed tissue. The rapidly destructive Bacillus sp. (B. cereus) accounts for 24%, while Staphylococcus sp. (39%) and Gram-negative organisms (7%) account for less. Fungi (particularly filamentous fungi) may play an important role in soil, wood, or organic matter contaminated wounds.
Beware: there are other diseases that can mimic endophthalmitis:
Uveitis (inflammation of any of three components of uveal tract: iris, ciliary body, or choroid)
Sterile inflammation (prolonged intraoperative surgical manipulations, especially involving the vitreous)
Retained lens material
Rebound inflammation after sudden decrease in postoperative steroids
Toxic anterior segment syndrome (TASS; acute postoperative anterior chamber reaction and corneal edema due to contaminants from surgical instruments, intraocular [IOL] solutions, or IOL implant) – usually within 1-2 days post-surgery
Intraocular foreign body
Anterior segment ischemia (from carotid artery disease) (ocular ischemia syndrome)
Rectus muscle surgery (usually on multiple rectus muscles on the same eye at the same surgery)
What laboratory studies should you order and what should you expect to find?
Results consistent with the diagnosis
If endogenous endophthalmitis is suspected, peripheral WBC and differential, C-reactive protein, sedimentation rate, and several blood cultures. In exogenous endophthalmitis, less than one-third of patients have elevated WBC.
Results that confirm the diagnosis
Vitreous (0.2-0.3mL) and Aqueous (0.1-0.2mL) fluid aspirates: One drop each on blood, chocolate, Sabouraud media, anaerobic media, and meat broth and one drop for Gram-stain. If vitrectomy is performed, 3mL of the vitreous wash should be centrifuged, the pellet smeared on a slide for a Gram stain, and calcofluor white stain if fungus is suspected. The remainder of the washing is filtered through 0.45-micron membrane and the filter paper should then be plated on the above media. Vitreous WBC is performed if sample is adequate.
Aqueous aspirate cultures are positive in only 40%, vitreous aspirate cultures are positive in 75%, while vitrectomy obtained vitreous cultures are 90% yield. Gram stains are positive in only 45% of cases.
Consider PCR of vitreous sampling or washing with the universal eubacterial (and fungal) primers, particularly in chronic endophthalmitis (CPE). In CPE, if tap not diagnostic, mechanical biopsy of the vitreous through pars plana vitrectomy. The highest diagnostic yield is by sampling the white plaque in the posterior lens capsule if present, utilizing specialized culture media, as well as prolonging the culture time to several weeks to cover slow-growing organisms. Contamination limits its usefulness and refers to (ocular) specialty molecular biology centers that handle smaller volumes.
What imaging studies will be helpful in making or excluding the diagnosis of endophthalmitis?
B-scan (ultrasound of the eye) to look for vitreous debris (increased echogenicity of the vitreous) and retinal detachment. $
Optional computed tomography (CT) scan of the orbits to assess for foreign bodies, displaced glaucoma shunts, concurrent orbital cellulitis or sinusitis. $$
What consult service or services would be helpful for making the diagnosis and assisting with treatment?
If you decide the patient has endophthalmitis, what therapies should you initiate immediately?
Intravitreal injection of antibiotics is the cornerstone of treatment.
Key principles of therapy
Check B-scan ultrasonography for vitritis and retinal detachment.
Perform prior to therapy: intravitreal tap, mini-vitrectomy (vitreous ’biopsy’), or core vitrectomy within one hour
Obtain anterior chamber and vitreous fluid (Gram-stain and cultures)
When to perform vitreous aspiration (’tap and inject’) versus vitrectomy
Vitreous tap may be used for initial diagnosis in vision loss less than light perception or if obtaining vitrectomy (best by retinal specialist) would lead to delay in diagnosis and delivery of intravitreal antibiotics.
Anterior or pars plana (core) vitrectomy for severe vision loss (light perception); loss of red reflex; rapidly, fulminant infection; Gram-negative or fungal infection; or failure of initial therapy over 24-48 hours.
Intravitreal antibiotic injection may be repeated in 24-48 hours, and even a third time 48-72 hours with more targeted therapy.
Intravitreal dexamethasone is used in fulminant bacterial infections (if diagnosis known); contraindicated in fungal infections.
The intraocular lens implant does not need to be removed, except in chronic pseudophakic (P. acnes), fungal, or atypical mycobacteria endophthalmitis.
*Benefit of systemic antibiotics benefit is controversial. We recommend initial systemic vancomycin until cultures are final. The EVS study did not evaluate vancomycin, and suggested no benefit to intravenous therapy (studied amikacin and ceftazidime). EVS study examined post-cataract surgery endophthalmitis; they did not examine post-traumatic, bleb-associated or endogenous endophthalmitis.
1. Anti-infective agents
If I am not sure what pathogen is causing the infection what anti-infective should I order?
Table I. Etiology of Endophthalmitis, Usual Pathogens and Suggested Initial Therapy
|Classification||Etiologies||Initial Empiric Therapy||Adjunct Diagnostics/Comments|
|Acute Post-OperativeEndophthalmitisOften Severe(<6 weeks)||Coagulase-negative staphylococciStaphylococcus aureusStreptococciGram-negatives:H. influenzaeP. aeruginosaProteus mirabilisSerratia marcesansE. coli, KlebsiellaBacillus sp.||I. Intravitreal:Vancomycin: 1.0mg/0.1mL andAmikacin: 400microgm/0.1mLORVancomycin: 1.0mg/0.1mL andCeftazidime 2.25mg/0.1mLANDConsider dexamethasone 400microgm/0.1 mLII. Systemic*:Vancomycin 1gm IV q12h and Ceftazidime 2gm IV q12hORVancomycin 1gm IV q12h andTobramycin 2.0mg loading dose, then 1.5 mg/kg IV q 12hConsider fluoroquinolone (Ciprofloxacin 500mg po BID or Moxifloxacin 400mg po q D x 7days)III. Topical (fortified):Vancomycin: 14 or 25mg/ml and Tobramycin 14mg/mL and +/- corticosteroids||Ophthalmic EMERGENCY!Severe:Pain,photophobia and floaters +/- hypopyonMarked vitritisFundus not visibleVision <20/400If vision is light perception, core vitrectomy.Mild:coagulase-negative staphylococcusor culture-negativephotophobia and floatersmild vitritis +/- painVision >20/400Vitreous tap is adequate|
|Chronic (Pseudophakic) Post-Operative EndophthalmitisMild(>6 weeks)||Coagulase-negative staphylococci(3 months – 2 years):P. acnes (41-63%)P. granulosumAchromobacterCorynebacteriumRare mycobacteriaRare NocardiaFungiC. albicansAspergillus spOther rare fungi||BacteriaI. Intravitreal:Vancomycin: 1.0mg/0.1mLII. Systemic*:Consider fluoroquinolone (Levofloxacin 500-750mg qD or Moxifloxacin 400mg po qD x 7days)III. Topical (fortified):Vancomycin: 14 or 25mg/mlFungiIntravitreal:Amphotericin B 5-10microgm/0.1mLSystemic:Fluconazole 400-800mg po qD x 1-3month (Candida sp, not C. krusei or C. glabrata)Voriconazole 200mg po BID x 3mth (Candida sp and Aspergillus sp)Topical:amphotericin B 0.15% q1h||Bacteria:Gradual onsetMinimal painMild vitritis +/- small hypopyonMay present as steroid responsivePerform anaerobic culture and incubate x 14 daysCoag-neg Staph: nongranulomatous keratitic precipitatesP. acnes: granulomatous keratic precipitates;white plaque within capsular bag; consider excision of plaque; suggest vitrectomy, posterior capsulectomy, and IOL removalAnaerobic cultures and incubate x 14 daysFungi:granulomatous keratitic precipitates;yellow-white lesions with fluffy borders in posterior pole; retinitis progressing to vitreous exudates; may appear “headlight in fog”; peripheral pars planitisVitrectomy and examine vitreous smears with calcofluor white to identify fungal elements.|
|Post-Traumatic Endophthalmitis||Coagulase-negative staphylococciBacillus cereus (soil)StreptococciStaphylococcus aureusGram-negatives:Consider Yeast andFilamentous Fungi (Fusarium, Aspergillus)(soil, organic matter, wood contaminated wounds)||I. Intravitreal:Vancomycin: 1.0mg/0.1mL andAmikacin: 400microgm/0.1mLand +/- Amphotericin B 5-10microgm/0.1mLORVancomycin: 1.0mg/0.1mL andCeftazidime 2.25mg/0.1mLand +/- Amphotericin B 5-10microgm/0.1mLANDConsider dexamethasone 400microgm/0.1 mL (not fungi)II. Systemic*:Vancomycin 1gm IV q12h and Ceftazidime 2gm IV q12hORVancomycin 1gm IV q12h andTobramycin 2.0mg loading dose, then 1.5 mg/kg IV q 12hConsider fluoroquinolone (Ciprofloxacin 500mg po BID or Moxifloxacin 400mg po q D x 7days) and +/-Voriconazole 200 mg po BID x 3mth (Aspergillus sp)III. Topical (fortified):Vancomycin: 14 or 25mg/ml and Tobramycin 14mg/mL and +/- amphotericin B 0.15% q1h +/- corticosteroids (not fungi)||Ophthalmic EMERGENCY!Severe:Painphotophobia and floaters +/- hypopyonMarked vitritisFundus not visibleVision <20/400If vision is light perception, core vitrectomy.MIld:coagulase-negative staphylococcusor culture-negativephotophobia and floatersmild vitritis +/- painVision >20/400Vitreous tap is adequate|
|Conjunctival Filtering-Bleb orGlaucoma Shunt -associated Endophthalmitis(or other ophthalmic devices that cross ocular surface into the eye)May be early or very late(0-3 years)||Coagulase-negative staphylococciStreptococciS. pneumoniaeGram-negativesH. influenzae||I. Intravitreal:Vancomycin: 1.0mg/0.1mL andCeftazidime 2.25mg/0.1mLORVancomycin: 1.0mg/0.1mL andAmikacin: 400microgm/0.1mLII. Systemic*:Vancomycin 1gm IV q12h and Ceftazidime 2gm IV q12hORVancomycin 1gm IV q12h andTobramycin 2.0mg loading dose, then 1.5mg/kg IV q 12hConsider fluoroquinolone (Ciprofloxacin 500mg po BID or Moxifloxacin 400mg po q D x 7days) or Ampicillin-sulbactam 3gms IVq DIII. Topical:Vancomycin: 14 or 25mg/ml and Tobramycin 14mg/mL and +/- corticosteroids||Red eyeDischargeDecreasing visionPainHypopyonVitritis-poor view of fundusVitrectomy indicatedAlso culture conjunctiva and bleb or shuntNote: Blebitis without vitreal involvement:Red eye with extensive anterior chamber reaction only. Needs treatment to prevent extension into vitreous.|
|Endogenous Endophthalmitis:BacterialFungal||Gram-positives (72%):Streptococci (38%) (endocarditis)S. aureus (20%) (cutaneous infections)Clostridium septicum (7%)B. cereus (3-4%)(IV drug users)Gram-negatives (28%):E. coli (17%)Klebsiella, Serratia, PseudomonasN. meningitidisH. influenzae (less now)Candida sp (majority)||I. Intravitreal:Vancomycin: 1.0mg/0.1mL andCeftazidime 2.25mg/0.1mL and +/- Amphotericin B 5-10microgm/0.1mLORVancomycin: 1.0mg/0.1mL andAmikacin: 400microgm/0.1mLand +/- Amphotericin B 5-10microgm/0.1mLANDConsider dexamethasone 400microgm/0.1 mLII. Systemic*:Vancomycin 1gm IV q12h and Ceftazidime 2gm IV q12hORVancomycin 1gm IV q12h andTobramycin 2.0mg loading dose, then 1.5 mg/kg IV q 12h and +/- antifungal:Liposomal Amphotericin B, 3-5 mg/kg/dORFluconazole 800mg po q D (Candida sp, not C. krusei or C. glabrata)ORVoriconazole 200mg po BID (Candida sp and Aspergillus sp) x 1-6 monthsIII. Topical (fortified) little to no role:Vancomycin: 14 or 25mg/ml and Tobramycin 14mg/mL and +/- corticosteroids; no role for topical antifungals||Systemic and ophthalmic EMERGENCY!Bacteria:Blood-borne spread of bacteria or fungi in chronically ill, immunosuppressed, diabetic, post-operative.Common sites of infection: septicemia, infected IV line, endocarditis, kidney or liver abscess;colon cancer: Clostridial, S. bovisAcute onset of headache and eye painSudden decreased visionHypopyon, vitritisMay be bilateral, but often right eyeCulture anterior chamber, vitreous, blood, and other suspected sitesTherapeutic vitrectomyFungi:Hyperalimentation, indwelling IV catheters, immunosuppressed, renal dialysisFungemia may be absentChorioretinitis focal or multifocal +/-abscessGranulomatous or nongranulomatousVitritis +/-cellular aggregatesCulture anterior chamber, vitreous, blood on blood agar and Sabouraud plates); Gram stain and calcofluor white.Vitrectomy if vitritis presentExamine vitreous biopsy specimens by Giemsa, PAS, methenamine silver staining|
Table II. Treatment of Specific Ocular Pathogens Causing Endophthalmitis
|Organism||Intravitreal Antibiotic||Systemic Antibiotics||Alternative|
|Coagulase-negative Staphylococci, S. aureus(methicillin-sensitive)||Cefazolin 1.0mg or Oxacillin 0.5mg||Oxacillin 2gm IV Q4H or Cefazolin 1.5g Q8H||Clindamycin 1.0mg intravitreal and Clindamycin 600mg IV Q6H|
|Methicillin-resistant coagulase-negative Staphylococci (MRSE) or Methicillin-resistant S. aureus(MRSA)||Vancomycin 1.0mg||2g/d (divided Q12H) and consider Rifampin1200mg daily(divided Q12H)||Clindamycin 1.0mg intravitreal and Clindamycin 600mg IV q 6h if susceptible|
|Streptococci sp. (MIC < 0.1)||Ceftriaxone 1.0mg||Ceftriaxone IV 2g/day or Pcn 2 mU IV q 4h||Clindamycin 1.0mg intravitreal and Clindamycin 600mg IV q 6h – may consider in addition|
|Streptococci sp (MIC >0.1), Penicillin-resistant S. pneumoniae||Vancomycin 1.0mg and Gentamicin 0.1mg||Vancomycin 1gm IV q 12 h and Gentamicin 2mg/kg load, then 1.5 mg/kg IV q 8h||Clindamycin 1.0mg and Gentamicin 0.1mg intravitreal plus Clindamycin 600mg IV q 6h and Gentamicin 2mg/kg load, then 1.5mg/kg IV q 8h|
|Enterococci sp. (dependent on susceptibilities)||Ampicillin 0.5mg and Gentamicin 0.1mg or Vancomycin 1.0mg and Gentamicin 0.1mg||Ampicillin 2gm IV q4h OR Vancomycin 1g IV q 12h and Gentamicin 2mg/kg load, then 1.5mg/kg IV q 8h||Chloramphenicol 2.0mg intravitreal and Linezolid 600mg po/IV BID for resistant organisms|
|Bacillus sp.||Vancomycin 1.0mg and Gentamicin 0.1mg||Vancomycin 1gm IV q 12 h and Gentamicin 2mg/kg load, then 1.5mg/kg IV q 8h||Clindamycin 1.0mg and Gentamicin 0.1mg intravitreal plus Clindamycin 600mg IV q 6h and Gentamicin 2mg/kg load, then 1.5mg/kg IV q 8h|
|Gram-negatives Proteus, Serratia, Pseudomonas||Ceftazidime 2.0mg and Tobramycin 0.1mg||Ceftazidime 2gm IV q 12h or Ciprofloxacin 500mg po BID||Tobramycin 2mg/kg load, then 1.5mg/kg IV q 8h; tobramycin may have less retinal toxicity than gentamicin|
2. Next list other key therapeutic modalities.
Other therapies helpful for reducing complications: Mydriatric-cycloplegics (e.g.atropine) are often also given.
Controversial or evolving therapies:
The use of periocular antibiotic injection (subconjunctival [anterior subtenons]) or retrobulbar (posterior tenons) remains controversial but is gaining favor. Its benefit in addition to intravitreal has not been demonstrated, but may be used if unable to deliver intravitreally in penetrating trauma.
Given the risk for loss of sight, the use of intravitreal dexamethasone in toxin-mediated destructive infections (streptococcal and S. aureus) is not uncommon. It is not used in fungal infections.
What complications could arise as a consequence of endophthalmitis?
The most deviating complications are retinal detachment, loss of vision, and even enucleation.
What should you tell the family about the patient’s prognosis?
In general, endophthalmitis has a significant loss of vision.
Purulent endophthalmitis with toxin-mediated streptococci and Bacillus cereus often result incomplete loss of vision and even enucleation.
Gram-negative infections with Pseudomonas also has poor prognosis.
Coagulase-negative staphylococci has a very good prognosis.
Interventions that delayed more than 24 hours after onset will have worse visual outcomes.
Add what-if scenarios here:
If the vitreous fluid demonstrates mycobacteria or fungi instead of bacteria, visual outcome is worse due to the failure of instituting treatment. Prolonged treatment is needed in these infections and associated late loss of vision is common.
How do these pathogens cause endophthalmitis?
Exogenous endophthalmitis (most common) results from direct inoculation of organisms from the outside (trauma, surgery, bleb-associated) or extension from keratitis (corneal infection). The spread is anterior to posterior with the anterior chamber seeded prior to vitreous chamber.
Endogenous endophthalmitis results from bacteremia or fungemia with seeding of the highly vascular choroid prior to extension anteriorly into the vitreous. Visual outcome is poor in endogenous endophthalmitis and this has not significantly improved over the past decades. It is bilateral in 14-25% of cases. The right eye is involved twice as often as the left probably due to the right eye’s proximity and direct flow from the right carotid artery.
Clinical outcome is dependent on the inoculum (dose), virulence of the organism, and rapidity of therapeutic intervention.
Fulminant infections are due to toxin-release as seen in streptococci (S. pneumoniae, S. pyogenes (Group A strep), and Staphylococcus aureus. Bacillus cereus has unique exotoxins (tripartite hemolysin BL, phospholipase C, collagenase) that are especially detrimental to ocular tissue. Gram-negatives have endotoxins associated with the lipopolysaccharide (LPS) layer.
What other additional laboratory findings may be ordered?
Universal eubacterial primers are the most promising especially for chronic, uncommon infections.
For fungal endogenous endophthalmitis, consider beta-D-glucan levels
How can endophthalmitis be prevented?
Penetrating intraocular foreign body (IOFP) Prophylaxis: medical emergency with metal splinters from farmyard, dirty, soil-contamination. 8% IOFPs develop endophthalmitis; IOFB 50% virulent Bacillus spp.; many polymicrobial B. cereus, S. aureus, coliforms, streptococci, and Clostridium perfringens.
Remove IOFB; Intravitreal amikacin 400 microgm (or gentamicin 200 microgm) plus vancomycin 1mg and/or clindamycin 1mg. If intravitreal route not possible, subconjunctival gentamicin 40mg plus clindamycin 20mg/mL. Topical gentamicin 15mg/mL plus clindamycin 20mg/mL.
If severe injuries, give 3 days intravenous with same drugs. Consider filamentous fungi with mold contamination: amphotericin intravitreal 5-10microgm/0.1mL, topical 0.15%, and voriconazole 200mg po BID.
WHAT’S THE EVIDENCE for specific management and treatment recommendations?
“Results of the Endophthalmitis Vitrectomy Study. A randomized trial of immediate vitrectomy and of intravenous antibiotics for the treatment of postoperative bacterial endophthalmitis”. Arch Ophthalmol. vol. 113. pp. 1479-1995. (EVS study examined acute post-operative endophthalmitis. It did not study post-traumatic, bleb-associated or endogenous endophthalmitis. Vitrectomy only benefit if vision reduced to light perception or with 80% of EVS study had low grade P. acnes and coagulase-negative staphylococci. Advice does not apply for highly virulent streptococci where vitrectomy would be recommended.)
“Prophylaxis of post-operative endophthalmitis following cataract surgery: results of the EXCRS multi-centre study and identification of risk factors”. J Cat Refract Surg. vol. 33. 2007. pp. 978-88.
Taban, M, Behrens, A, Newcomb, RL. “Acute endophthalmitis following cataract surgery: a systematic review of the literature”. Arch Ophthalmol. vol. 123. 2005. pp. 613(Showed increased risk of endophthalmitis with clear corneal incision compared to suturing.)
Jackson, TL, Eykyn, S, Graham, EM. “Endogenous bacterial endophthalmitis: a 17-year prospective series and review of 267 reported cases”. Surv Ophthalmol. vol. 48. 2003. pp. 403-23.
Barry, P, Behrens-Baumann, Pleyer, U, Seal, D. “ESCRS guidelines on prevention, investigation and management of post-operative endophthalmitis”.
Lingappan, A, Wyckoff, CC, Albin, TA. “Endogenous Fungal Endophthalmitis: Causative Organisms, Management Strategy, and Visual Acuity Outcomes”. Am J Ophthalmol. vol. 153. 2012. pp. 162-166.
Garg, P. “Fungal, mycobacteria, Nocardia infections and the eye: an update”. Eye. vol. 26. 2012. pp. 245-251. (Good photographic descriptives.)
DRG CODES and expected length of stay
H44.0 – Purulent endophthalmitis
H44.009 – Unspecified purulent endophthalmitis, unspecified eye
Expected length of stay: three to seven days.
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- OVERVIEW: What every practitioner needs to know
- Are you sure your patient has endophthalmitis? What should you expect to find?
- How did the patient develop endophthalmitis? What was the primary source from which the infection spread?
- Which individuals are of greater risk of developing endophthalmitis?
- What laboratory studies should you order and what should you expect to find?
- What imaging studies will be helpful in making or excluding the diagnosis of endophthalmitis?
- What consult service or services would be helpful for making the diagnosis and assisting with treatment?
- 1. Anti-infective agents
- 2. Next list other key therapeutic modalities.
- What complications could arise as a consequence of endophthalmitis?
- What should you tell the family about the patient’s prognosis?
- How do these pathogens cause endophthalmitis?
- What other additional laboratory findings may be ordered?
- How can endophthalmitis be prevented?
- WHAT’S THE EVIDENCE for specific management and treatment recommendations?