Endophthalmitis Clinical Presentation
- Author: Daniel J Egan, MD; Chief Editor: Robert E O'Connor, MD, MPH more...
History should be focused toward practices or procedures that would increase risk of endogenous or exogenous endophthalmitis (eg, intravenous drug use, other risks for sepsis or endocarditis, recent invasive ophthalmologic procedure). See discussion below in Causes.
Bacterial endophthalmitis usually presents acutely with pain, redness, lid swelling, and decreased visual acuity. Also, some bacteria (eg, Propionibacterium acnes) may cause chronic inflammation with mild symptoms. This organism is typical skin flora and usually is inoculated at the time of intraocular surgery.
Fungal endophthalmitis may present with an indolent course over days to weeks. Symptoms are often blurred vision, pain, and decreased visual acuity. A history of penetrating injury with a plant substance or soil-contaminated foreign body may often be elicited.
Individuals with candidal infection may present with high fever, followed several days later by ocular symptoms. Persistent fever of unknown origin (FUO) may be associated with an occult retinochoroidal fungal infiltrate.
History of ocular surgery, ocular trauma, hammering steel with steel, working with baling wire, or working in an industrial setting may be elicited.
In cases of postsurgical endophthalmitis, infection most often occurs approximately 1 week after surgery but may occur months or years later as in the case of P acnes.
Symptoms may include the following:
Visual symptoms in any hospitalized patient or patient taking immunosuppressive therapy
Eye pain and irritation
Intense ocular and periocular inflammation
Physical findings correlate with structures involved and degree of infection or inflammation. A thorough eye examination should be performed to include acuity, external examination, funduscopic examination, and slit lamp examination. Seek signs of uveitis and other findings as described below. Emergent referral to an ophthalmologist for further evaluation, including more exhaustive physical examination, is indicated if endophthalmitis is seriously considered.
Eyelid swelling and erythema
Injected conjunctiva and sclera
Hypopyon (layering of inflammatory cells and exudate [pus] in the anterior chamber)
Reduced or absent red reflex
Proptosis (a late finding in panophthalmitis)
Corneal edema and infection
White lesions in the choroid and retina
Vitreal mass and debris
Cells and flare in the anterior chamber on slit lamp examination
Note: Absence of pain and hypopyon do not rule out endophthalmitis, particularly in the chronic indolent form of P acnes infection.
In cases of endogenous endophthalmitis, the emergency physician needs to further evaluate the patient for the underlying source of infection.
In most clinical series, gram-positive organisms are the most common causative organisms of endophthalmitis. The most common organisms are coagulase-negative Staphylococcus epidermidis, Staphylococcus aureus, and Streptococcus species. Gram-negative organisms like Pseudomonas, Escherichia coli, and Enterococcus are observed in penetrating injuries. However, when endogenous endophthalmitis is considered alone, the percentage of bacterial organisms drops markedly because of a greater proportion of fungal infections. It is very rare for endophthalmitis to be caused by viral infections. Classically, viruses are responsible for uveitis.
Individuals at risk for developing endogenous endophthalmitis usually have comorbidities that predispose them to infection. These include conditions such as diabetes mellitus, chronic renal failure, cardiac valvular disorders, systemic lupus erythematosus, AIDS, leukemia, gastrointestinal malignancies, neutropenia, lymphoma, alcoholic hepatitis, and bone marrow transplantation.
Invasive procedures, which may result in bacteremia, such as hemodialysis, bladder catheterization, gastrointestinal endoscopy, total parenteral nutrition, chemotherapy, and dental procedures, also can lead to endophthalmitis.
Recent nonocular trauma or surgery, prosthetic heart valves, immunosuppression, and intravenous drug abuse may predispose to endogenous endophthalmitis.
Sources for endophthalmitis include meningitis, endocarditis, urinary tract infection, and wound infection. Additionally, pharyngitis, pulmonary infection, septic arthritis, pyelonephritis, and intra-abdominal abscess also have been implicated as sources of infection.
Fungal organisms can occur in up to 50% of all cases of endogenous endophthalmitis. Candida albicans is by far the most frequent cause (75-80% of fungal cases). Aspergillosis is the second most common cause of fungal endophthalmitis, especially in IV drug users. Less frequent are other candidal species and Torulopsis, Sporotrichum, Cryptococcus, Coccidioides, and Mucor species.
The single most commonly involved gram positive organism is S. aureus, which often is implicated with skin infections or chronic systemic disease, such as diabetes mellitus or renal failure. Streptococcal species including Streptococcus pneumoniae, Streptococcus viridans, and group A streptococci also are common. Other streptococcal species, eg, group B in newborns with meningitis or group G in elderly patients with wound infections or malignancies, also have been isolated. Bacillus cereus has been implicated in intravenous drug abuse and intravenous injections. Clostridium species have been implicated in association with bowel carcinomas.
Gram-negative bacteria are other bacterial etiologies. E coli is the most common among the gram-negative bacteria. Haemophilus influenzae, Neisseria meningitidis, Klebsiella pneumoniae, Serratia species, and Pseudomonas aeruginosa also can cause endogenous endophthalmitis.
Nocardia asteroides, Actinomyces species, and Mycobacterium tuberculosis are acid-fast bacteria that may cause endogenous endophthalmitis.
Organisms that reside at the conjunctiva, eyelid, or eyelashes and are introduced at the time of surgery usually cause postoperative endophthalmitis.
Most cases of exogenous endophthalmitis develop postoperatively or after trauma to the eye. In fact, postoperative endophthalmitis is the most common cause of the disease. Of these cases, gram-positive organisms account for almost 90% of cases, of which the majority are coagulase-negative Staphylococcus from the natural conjunctival flora.
The single most common cause of exogenous endophthalmitis is S epidermidis, which is a normal flora of the skin and conjunctiva. Other common gram-positive bacteria are S aureus and streptococcal species.
The most common gram-negative organisms associated with postoperative endophthalmitis are P aeruginosa and Proteus and Haemophilus species.
Although very rare, many different fungi have caused postoperative endophthalmitis, including Candida, Aspergillus, and Penicillium species.
The rates of endophthalmitis postoperatively after cataract surgery appear to be declining in the last decade.[9, 10]
The use of intracameral antibiotics is associated with a decreased occurrence of postoperative endophthalmitis.
Bacteria or fungi are introduced at the time of injury. Endophthalmitis can occur in up to 13% of cases of penetrating injury to the globe. Since penetrating trauma usually occurs in a nonsterile environment, most objects that strike the eye are contaminated with multiple infectious agents.
The risk of developing traumatic endophthalmitis by foreign objects carrying soil or vegetable matter is highest in rural settings. Staphylococcal, streptococcal, and Bacillus species usually cause traumatic endophthalmitis. B cereus causes much more infections in the traumatic population than in either of the other two groups, and can cause serious infection. A history of penetrating trauma with intraocular foreign body contaminated with organic matter implicates Bacillus species.
Patients with open globe injuries are at risk of developing endophthalmitis. Specifically, those with pure corneal injuries, intraocular foreign bodies, lens rupture, or needle-related injuries have a higher incidence.
Patients with larger lacerations, delay in time to repair of open globe, and those with more virulent organisms tend to do worse than patients with traumatic etiology.
Taban M, Behrens A, Newcomb RL. Acute endophthalmitis following cataract surgery: a systematic review of the literature. Arch Ophthalmol. 2005 May. 123(5):613-20. [Medline].
Englander M, Chen TC, Paschalis EI, Miller JW, Kim IK. Intravitreal injections at the Massachusetts Eye and Ear Infirmary: analysis of treatment indications and postinjection endophthalmitis rates. Br J Ophthalmol. 2013 Apr. 97(4):460-5. [Medline].
Boldt HC, Pulido JS, Blodi CF, Folk JC, Weingeist TA. Rural endophthalmitis. Ophthalmology. 1989 Dec. 96(12):1722-6. [Medline].
Thompson JT, Parver LM, Enger CL, Mieler WF, Liggett PE. Infectious endophthalmitis after penetrating injuries with retained intraocular foreign bodies. National Eye Trauma System. Ophthalmology. 1993 Oct. 100(10):1468-74. [Medline].
Lundstrom M, Wejde G, Stenevi U, Thorburn W, Montan P. Endophthalmitis after cataract surgery: a nationwide prospective study evaluating incidence in relation to incision type and location. Ophthalmology. 2007 May. 114(5):866-70. [Medline].
Ness T, Pelz K, Hansen LL. Endogenous endophthalmitis: microorganisms, disposition and prognosis. Acta Ophthalmol Scand. 2007 Dec. 85(8):852-6. [Medline].
Han DP, Wisniewski SR, Wilson LA, et al. Spectrum and susceptibilities of microbiologic isolates in the Endophthalmitis Vitrectomy Study. Am J Ophthalmol. 1996 Jul. 122(1):1-17. [Medline].
Melo GB, Bispo PJ, Regatieri CV, Yu MC, Pignatari AC, Hofling-Lima AL. Incidence of endophthalmitis after cataract surgery (2002-2008) at a Brazilian university-hospital. Arq Bras Oftalmol. 2010 Dec. 73(6):505-7. [Medline].
Kessel L, Flesner P, Andresen J, Erngaard D, Tendal B, Hjortdal J. Antibiotic prevention of postcataract endophthalmitis: a systematic review and meta-analysis. Acta Ophthalmol. 2015 Mar 16. [Medline].
Alfaro DV, Roth D, Liggett PE. Posttraumatic endophthalmitis. Causative organisms, treatment, and prevention. Retina. 1994. 14(3):206-11. [Medline].
Miller JJ, Scott IU, Flynn HW Jr, et al. Endophthalmitis caused by Bacillus species. Am J Ophthalmol. 2008 May. 145(5):883-8. [Medline].
Verbraeken H, Rysselaere M. Post-traumatic endophthalmitis. Eur J Ophthalmol. 1994 Jan-Mar. 4(1):1-5. [Medline].
Faghihi H, Hajizadeh F, Esfahani MR, et al. Posttraumatic endophthalmitis: report No. 2. Retina. 2012 Jan. 32(1):146-51. [Medline].
Gupta A, Srinivasan R, Gulnar D, Sankar K, Mahalakshmi T. Risk factors for post-traumatic endophthalmitis in patients with positive intraocular cultures. Eur J Ophthalmol. 2007 Jul-Aug. 17(4):642-7. [Medline].
Kohanim S, Daniels AB, Huynh N, Eliott D, Chodosh J. Utility of ocular ultrasonography in diagnosing infectious endophthalmitis in patients with media opacities. Semin Ophthalmol. 2012 Sep-Nov. 27(5-6):242-5. [Medline].
Ng JQ, Morlet N, Pearman JW, et al. Management and outcomes of postoperative endophthalmitis since the endophthalmitis vitrectomy study: the Endophthalmitis Population Study of Western Australia (EPSWA)'s fifth report. Ophthalmology. 2005 Jul. 112(7):1199-206. [Medline].
Endophthalmitis Vitrectomy Study Group. 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. 1995 Dec. 113(12):1479-96. [Medline].
Albert DM, ed; Jakobiec FA. Endogenous endophthalmitis. Principles and Practice of Ophthalmology. W B Saunders Co; 1994. Vol 5: 3120-3125.
Albert DM, Jakobiec FA. Postoperative endophthalmitis. Principles and Practice of Ophthalmology. W B Saunders Co; 2000. 2441-2462.
Mandelbaum S, Forster RK. Postoperative endophthalmitis. Int Ophthalmol Clin. 1987 Summer. 27(2):95-106. [Medline].
Michelson JB, Friedlaender MH. Endophthalmitis of drug abuse. Int Ophthalmol Clin. 1987 Summer. 27(2):120-6. [Medline].
Okada AA, Johnson RP, Liles WC. Endogenous bacterial endophthalmitis. Report of a ten-year retrospective study. Ophthalmology. 1994 May. 101(5):832-8. [Medline].
Parrish CM, O'Day DM. Traumatic endophthalmitis. Int Ophthalmol Clin. 1987. 27(2):112-9. [Medline].
Rowsey JJ, Jensen H, Sexton DJ. Clinical diagnosis of endophthalmitis. Int Ophthalmol Clin. 1987 Summer. 27(2):82-8. [Medline].
Uka J, Minamoto A, Shimizu R. A five-year review of patients admitted with the diagnosis of bacterial endophthalmitis. Hiroshima J Med Sci. 2005 Jun. 54(2):47-51. [Medline].
Wilhelmus KR. The pathogenesis of endophthalmitis. Int Ophthalmol Clin. 1987 Summer. 27(2):74-81. [Medline].
Wilson FM 2d. Causes and prevention of endophthalmitis. Int Ophthalmol Clin. 1987 Summer. 27(2):67-73. [Medline].
Wong JS, Chan TK, Lee HM, Chee SP. Endogenous bacterial endophthalmitis: an east Asian experience and a reappraisal of a severe ocular affliction. Ophthalmology. 2000 Aug. 107(8):1483-91. [Medline].