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Endophthalmitis
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Sriram Simakurthy
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Koushik Tripathy
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Continuing Education Activity
Endophthalmitis is defined as an inflammation of inner coats of the eye, resulting from intraocular colonization of infectious agents with
exudation within intraocular fluids. It is a potentially blinding condition. The category or type of endophthalmitis such as postoperative, posttraumatic, or endogenous, etc. influences the clinical presentation, microbiology, and visual outcome. If left untreated or inadequately treated, it
progresses to panophthalmitis requiring evisceration or enucleation of the eyeball. This activity reviews the evaluation and treatment of
endophthalmitis and highlights the role of the interprofessional team in evaluating and treating patients with this condition.
Objectives:
Describe the pathogenesis of endophthalmitis.
Summarize the relevant history and physical examination of patients with endophthalmitis.
Review the evaluation process of patients with endophthalmitis.
Outline the interprofessional care of patients with endophthalmitis.
Introduction
Endophthalmitis is defined as an inflammation of inner coats of the eye, resulting from intraocular colonization of infectious agents with
exudation within intraocular fluids (vitreous and aqueous).[1] Based on the mode of entry of the organism, it is divided into 'exogenous' and
'endogenous.' Depending on the causative event, the exogenous endophthalmitis can be either post-traumatic or postoperative.[2] Some of the
definitions used in endophthalmitis are listed in figure 1 (classification of endophthalmitis). Unless diagnosed and treated promptly, acute
endophthalmitis can lead to severe vision loss. The category or type of endophthalmitis such as postoperative, post-traumatic or endogenous,
and others influence the clinical presentation, microbiology, and visual outcome. Endophthalmitis is one of the most serious ophthalmic
emergencies which require urgent medical attention and treatment to save the vision or to salvage the integrity of the eye.
Etiology
Depending on the infectious agent producing endophthalmitis, two important categories are recognized, bacterial and fungal endophthalmitis.
In a recent study on microbial causes of all types of endophthalmitis, 85.1% of all isolates were due to gram-positive bacteria, 10.3% due to gramnegative bacteria, and 4.6% of all cases were due to fungi.[3] The most common bacterial pathogens isolated are Staphylococcus epidermidis
(30.3%), other coagulase-negative Staphylococcus (9.1%), Streptococcus viridans (12.1%), Staphylococcus aureus (11.1%), Enterobacteriaceae
(3.4%), and Pseudomonas aeruginosa (2.5%).[3]
The predominant organism depends on the source (vegetable matter or retained intraocular foreign body), route of spread (post-surgery,
trauma, or delayed onset or hematogenous dissemination), geographic location, and patient characteristics.
In cases of post-traumatic endophthalmitis, Staphylococci and Bacillus cereus are the most common isolates.[4]
Acute postoperative endophthalmitis (within 6 weeks of surgery) results most commonly due to contamination of the intraocular structures with
normal bacterial flora of the adnexa such as Staphylococcal epidermidis.
Delayed or chronic post-cataract surgery endophthalmitis (after 6-week of surgery) is characterized by slow course and panuveitis like picture
with granulomatous keratic precipitates, inflammatory deposits over the IOL (intraocular lens), white capsular plaque, anterior chamber
reaction, vitritis, and cystoid macular edema (CME) which may respond to periocular or systemic steroid but usually recurs.[5] The common
causative organism is usually bacterial (most commonly Propionibacterium acnes followed by Coagulase-negative Staphylococcus), though
fungal infections (including Aspergillus, Candida, and others) can also occur.[6]
In cases of delayed onset, endophthalmitis associated with bleb (trabeculectomy)/glaucoma drainage implants Streptococci species, and
Haemophilus are the predominant culture isolates.[7][8]
The most common organisms isolated in post intravitreal injection endophthalmitis are coagulase-negative staphylococci followed by
streptococci.[9]
In certain conditions, exogenous endophthalmitis can occur without a full-thickness breach in ocular coats. For example, after scleral buckling
(due to buckle exposure or secondary infections), secondary to contact lens keratitis, and post LASIK.[10][11][12]
Most cases of endogenous endophthalmitis are secondary to fungemia (predominantly Candida species). Among bacterial causes,
staphylococcal species predominate in the western population, and among the East Asian population, Klebsiella pneumoniae predominates.
[13] Pseudomonas is a virulent and aggressive organism that can also cause endogenous endophthalmitis.[14]
Endophthalmitis after infectious keratitis is usually bacterial (usually Pseudomonas aeruginosa, Staphylococcus sp, and Streptococcus sp),
though fungal endophthalmitis (including Aspergillus sp, Fusarium sp) may also occur.[15][16]
Epidemiology
The relative frequency of various subtypes of endophthalmitis varies depending upon the geography, level of specialization at the ophthalmic
center, and study duration. For example, studies before 2005 have very few cases of post intravitreal anti-VEGF (vascular endothelial growth
factor) injection endophthalmitis as anti-VEGF agents received first FDA approval in 2004.
In a recent retrospective cohort study in the U.S., acute onset endophthalmitis occurred in 0.04% of cataract surgeries and 0.016% of patients
receiving an intravitreal injection.[17][18] The incidence of post-traumatic endophthalmitis varies from 0.9% to 17%.[19][20]
Case series from Asian countries have reported an incidence of 0.023% to 0.076% of endophthalmitis in post-cataract surgery setting and 0.01%
to 0.10% post intravitreal injections.[21][22][23][24]
Among the intraocular surgeries, secondary intraocular lens implantation seems to have a very high risk (0.36%) for acute endophthalmitis, and
trabeculectomy may have a high risk (1.8%, maybe up to 5.7%) for delayed or late-onset endophthalmitis especially after the advent of
mitomycin-C or 5-fluorouracil.[2][25][26]
Endophthalmitis after pars plana vitrectomy had the lowest rates (0.046%) when compared with other ocular surgeries [secondary IOL-0.366%,
combined penetrating keratoplasty (PK) with cataract surgery- 0.194%, PK- 0.178%, glaucoma surgeries -0.124%, combined trabeculectomy and
cataract surgery- 0.114%, overall incidence after intraocular surgery-0.093%, and cataract surgery with or without IOL-0.082%] in a study.[25]
There is no significant difference in the rates of endophthalmitis after intravitreal injection of various anti-VEGF agents.[27][28] Cluster
endophthalmitis cases have occurred after intravitreal use of bevacizumab due to either lapse in the cold chain, sub-optimal compounding of
bevacizumab aliquots, or fake drug.[29][30]
Pathophysiology
The most critical factor in the causation of endophthalmitis is the breakdown of the ocular blood barrier and intraocular colonization by
The most critical factor in the causation of endophthalmitis is the breakdown of the ocular blood barrier and intraocular colonization by
pathogens (bacteria/fungi). In exogenous endophthalmitis, the inciting injury or surgery causes disruption of globe integrity, which allows
invasion of the pathogens. In rare cases of delayed postoperative endophthalmitis, the organisms (usually Propionibacterium acnes sequestered
in the capsular bag after cataract surgery) may get released after YAG capsulotomy causing endophthalmitis.[31] In endogenous
endophthalmitis, common sources of bacteremia and fungemia include endocarditis, urinary tract infections, intravenous infusions, indwelling
catheters or invasive procedures, liver abscess, and others.
The pathogen's ability to cause intraocular damage depends on its virulence and host response. Virulence of an organism depends on:
Its ability to synthesize toxic factors such as hemolysin BL, cytolysin, pneumolysin, lipopolysaccharide (bacterial outer envelope), and
others[32][33][34][35]
The rapidity of intraocular growth[36]
Motility of organism[37]
The ability of the host's innate immunity to mount an effective inflammatory response depends on the virulence of the organism. The acute
inflammatory response may clear the less virulent organism; However, more virulent organisms may evade the host's immune response by
secreting toxins or biofilm around it, in which case the inflammatory response can result in damage to intraocular tissues and loss of vision. The
peak of inflammatory mediators such as TNFα, interleukin 1-beta, interferon-gamma coincides with increased inflammatory signs such as fibrin
in the anterior chamber, iris synechiae formation, hypopyon, and loss of the red reflex.[38] The elevated levels of complement factors in aqueous
and vitreous in cases of intraocular infection contribute to the damage of the uveoretinal tissue.
History and Physical
In typical postoperative endophthalmitis, poor visual acuity, corneal edema, hypopyon, vitreous inflammation, and poor fundus visualization are
the most common clinical signs.[39]
Reduced vision and worsening pain - In Endophthalmitis Vitrectomy Study (EVS) study, reduction in vision and pain accounted for 94% and 74%
of all symptoms while in the ESCRS study, it accounted for 92.9% and 79% of all symptoms.[40][41][40] These studies show that though pain is a
significant diagnostic sign, pain can be absent in up to 25% of cases. The other common presenting features are swollen eyelid, redness of the
eye, circumcorneal congestion, photophobia, ocular discharge, fibrinous membranes in the anterior chamber, iris synechiae formation, loss of
fundal red reflex, and floaters. Bleb related endophthalmitis initially presents as bacterial conjunctivitis with signs and symptoms such as
conjunctival hyperemia and discharge, yellowish colored filtering bleb, and variable anterior chamber inflammatory reaction, which later
progresses to involve the posterior chamber as well. Certain signs, if seen such as corneal ring abscess, is highly suggestive of Bacillus, while gas
bubbles in the anterior chamber, amaurosis, or green-brown hypopyon indicates Clostridium.[42][43]
In chronic endophthalmitis, patients present with low-grade anterior chamber inflammation and vitritis. Visual acuity can remain preserved until
late in the presentation. Organisms such as Propionibacterium tend to get localized within the capsular bag and present as posterior capsular
plaque.[44] The vital history that should raise suspicion of chronic endophthalmitis following keratitis or intraocular surgery is prolonged uveitis
in a subject with no previous history of inflammation and either inadequate response to topical steroids or inability to wean them.[45]
In patients with endogenous endophthalmitis, the presentation can be bilateral with systemic morbidities like sepsis, nausea, vomiting, and
fever. Endogenous bacterial endophthalmitis presents with pain, blurred vision, and redness with a variable degree of both anterior chamber
and vitreous involvement. A subretinal abscess may be noted.[46] Endogenous fungal endophthalmitis presents initially as focal choroiditis or
chorioretinitis, which later extends into the vitreous cavity. Retinal vascular sheathing and vascular occlusion may be present with satellite
lesions in certain conditions.[47]
Endophthalmitis after infectious keratitis presents with hypopyon and severe visual loss, sometimes with an inaccurate projection of rays.
Ultrasound evaluation of the posterior segment can help to detect vitreous involvement in the form of echoes in the vitreous and confirm the
diagnosis.
Progression of the disease may lead to panophthalmitis, corneal infiltration and perforation, and phthisis bulbi.
Due to severe damage to ocular structures, the workup of endophthalmitis is done on an emergency basis.
History
Inciting event – surgery/trauma/contiguous spread (keratitis)/endogenous endophthalmitis/other procedure
Onset – fulminant/acute/chronic: Most cases of fulminant endophthalmitis are caused by highly virulent organisms such as
Pseudomonas aeruginosa / Bacillus species (see figure on the classification of endophthalmitis)
The rapidity of progression – Rapid or gradual: Bacterial endophthalmitis progresses faster than fungal endophthalmitis.
Systemic illness – history of intravenous infusion, prolonged hospitalization, diabetes, renal or liver problems: Helps to localize any
source of endogenous endophthalmitis, calibrating drug dosage.
Ophthalmic Assessment
Clinical
1. Visual acuity including projection of rays- When visual acuity is less than counting fingers, EVS standards help in the maintenance of uniform
records. After occluding the better eye, with light directed from behind the patient:
Hand movements are tested at a distance of 60 cm
Perception of light is tested at a distance of 90 cm with the bright light of indirect ophthalmoscope
At least four out of five responses should be correct for reading to be considered.
2. Examination of the ocular adnexa- especially to look for severe blepharitis, meibomitis, stye, chronic dacryocystitis, and other sources of
infection3. Ocular movements- Reduced or absent ocular movements in a case of endophthalmitis with proptosis and pain, clinically point to
the diagnosis of panophthalmitis4. Anterior segment examination [close focus at the sites of entry – SICS(small incision cataract surgery)
tunnel/ Corneal entry wound / Bleb/ perforating trauma] look for corneal clarity; corneal infiltrate, Posterior capsular plaque, vitreous in the
wound, open wound, unsutured wound, hypopyon, fibrin, posterior synechia5. Intraocular pressure6. Fundus examination (dilated) if media
permits to look for any specific pattern as well as mimics such as dropped lens matter/ intraocular foreign body (IOFB)
Grading of vitreous haze (EVS standard) [clinical examination with an indirect ophthalmoscope][40]
Grade 1: More than 20/40 (6/12) view of the retina
Grade 2: Second order retinal vessels are visible
Grade 3: Some vessels visible but not the second-order vessels
Grade 4: No retinal vessels are visible, only red reflex present
Grade 5: No red reflex is seen
Evaluation
Imaging
Slit-lamp photography to document
Fundus photographs- especially ultra-widefield imaging (Optos) using scanning laser ophthalmoscope principle which can image
through the small pupil and vitreous haze[48][49]
Fundus fluorescein angiogram (FFA) if the fundus is visible- May help to rule out other diseases
Optical coherence tomography (OCT)- When fundus is visible, OCT can help to characterize the location and other characteristics of
retinochoroidal or vascular involvement
Anterior segment OCT in case of endophthalmitis after infective keratitis and others
Ultrasound B scan – Endophthalmitis gives rise to vitreous inflammation, which is seen as point echoes in the vitreous cavity with mild
to moderate amplitude. Ultrasound examination is also used to look for other features, including retinochoroidal thickening,
posteriorly dislocated lens/IOL, concomitant retinal detachment, choroidal detachment, or IOFB, to follow up vitreous inflammatory
reaction serially post intravitreal injection. A subretinal abscess at macula may be present, especially in endogenous endophthalmitis.
CT scan orbits to look for IOFB in post-trauma cases
Ocular Sampling
1. Anterior chamber tap
With the patient looking straight, a 30G/27G needle is introduced via a selected site on the peripheral cornea tangentially keeping
direction parallel to the iris, with the needle directed towards exudate/hypopyon. With active suction, 0.1 to 0.2 cc of aqueous/exudate is
aspirated. Cotton tip applicator is applied, and the needle is removed.
2. Vitreous tap/biopsy
Vitreous cultures usually produce more accurate results than do aqueous cultures.[50]
Vitreous Tap
A 26 G needle is connected to 2 cc syringe and is entered through pars plans (3 mm behind limbus in aphakic, 3.5 mm behind limbus in
pseudophakic, and 4 mm behind the limbus in phakic). A sample of 0.2 to 0.3 cc is aspirated. It is controversial in non-vitrectomized eyes due to
the possibility of vitreous traction and subsequent retinal detachment. In such cases, vitreous biopsy via vitrectomy cutter is preferred.
Vitreous biopsy
This can be obtained via one port vitrector or by combining with three-port diagnostic/ therapeutic pars plana vitrectomy. A 5 ml syringe is
connected to the suction port of the vitrectomy cutter, and once the cutter port is visualized through the pupil, surgical assistant aspirates,
without starting the infusion. At the same time, the surgeon activates the cutter until the eye softens visibly. When combined with three-port
vitrectomy, the fluid infusion is turned on once the sample has been collected as described.
Samples are sent for microbiological and molecular diagnostic (PCR) testing. Though PCR allows improved pathogen detection even with low
pathogen counts, cost, increased risk of contamination, lack of antibiotic sensitivity testing, lack of quality control standards limit its widespread
usage.[51]
The standard microbiological procedure includes smear preparation for specific stains and inoculation of selective culture media for recovery of
intraocular pathogens and antibiotic sensitivity testing. Commonly used stains and culture media are elaborated in figure 2 (commonly used
stains and culture media for the detection of microbial agents).
Systemic Assessment
Look for signs of septicemia – fever, elevated ESR (erythrocyte sedimentation rate)
Blood culture in cases of endogenous endophthalmitis
Blood tests – hemogram, renal and liver function tests (to look for drug toxicity)
Search for the focus of infection in endogenous endophthalmitis
Treatment / Management
Endophthalmitis is a true ophthalmic emergency and requires appropriate and prompt therapy. The main objectives in endophthalmitis
treatment are:
To eradicate or control infection
Management of inflammation
Supportive therapy
1. To Eradicate or Control Infection
A. Systemic antibiotics
The use of systemic antibiotics in the setting of exogenous endophthalmitis is controversial as most of the drugs given have poor intraocular
penetration. The best-documented drugs achieving therapeutic levels in vitreous are fourth-generation fluoroquinolones[52], meropenem, and
linezolid.[53]
EVS study used ceftazidime 2 g every 8 hourly, amikacin 7.5 mg/kg initial dose followed by 6 mg/kg every 12 hourly. EVS study has concluded
that the use of systemic antibiotics does not affect the final visual outcome in postoperative endophthalmitis.[40]
In endogenous endophthalmitis, systemic antimicrobials, in conjunction with intravitreal antimicrobials, reduce the rates of evisceration or
enucleation.[54]
B. Local antibiotics (topical/subconjunctival)
A combination of two drugs is preferred during the initial presentation, one having a potent effect on Gram-positive organisms and another on
Gram-negative organisms. Once antibiotic sensitivity is determined, targeted intervention is done. In the presence of corneal ulcer or wound
abscess, fortified drops (including cefazolin 5% and tobramycin 1.4%) are used. Sub conjunctival antibiotic injections are not routinely used due
to issues with patient comfort, subconjunctival hemorrhage, and watering from the eye.
EVS study used vancomycin (25 mg/0.5 ml), ceftazidime (100 mg/0.5 ml) for subconjunctival injection, and topical vancomycin (50 mg/ml) and
amikacin (20 mg/ml) every 4 hourly for routine cases or every hour if wound leak was present.[40]
C. Intravitreal injections
The intravitreal route of drug administration helps in achieving high concentrations of the drug in the vitreous cavity without associated
systemic side effects. It is essential to ensure the proper dosage of the drug. While inadequate doses cause treatment failure, the excess dose
can cause toxic effects on the retina. Two broad-spectrum antibiotics are chosen initially, EVS study utilized intravitreal vancomycin (1 mg/0.1 ml)
and amikacin (0.4 mg/0.1 ml).[40] However, due to the higher retinotoxic potential of amikacin, it has been superseded by ceftazidime (2.25
mg/0.1 ml). Commonly used drugs in the treatment of endophthalmitis and their concentrations are enumerated in figure 3 (Commonly used
antibiotics in the treatment of endophthalmitis). Intravitreal gentamicin can cause macular infarction.[55]
Recently, there is a trend towards the use of other intravitreal antibiotics such as:
Ampicillin 5000 mcg/0.1 ml[56]
Piperacillin/tazobactam 225 mcg (piperacillin 200 mcg and tazobactam 25 mcg/0.1 ml)[57]
Imipenem/cilastatin (rabbit 50 to 100 mcg and 50 to 100 mcg/0.1ml)[58]
Carbenicillin (rhesus monkey, 1000 mcg/0.1 ml)[59]
Ticarcillin 3000 mcg/0.1 ml in albino rabbits[60]
Cefazolin 2250 mcg/0.1 ml,[56]
Cefotaxime 400 mcg/0.1 ml[56]
Ceftriaxone 2000 mcg/0.1 ml[61]
Cefuroxime 1000 mcg/0.1 ml[61]
Clindamycin 1000 mcg/0.1 ml[61]
Levofloxacin 625 mcg/0.1 ml[56]
Moxifloxacin 500 mcg/0.1 ml[62] ( from the sterile moxifloxacin drop 0.5%, the reported patient had vitrectomized eye)
Ciprofloxacin 100 mcg/0.1 ml[56]
Aztreonam 100 mcg/0.1 ml[56]
Colistin 100 mcg/0.1 ml[63][56][61]
Viruses usually do not cause suppurative inflammation of the eye or endophthalmitis, and rather they cause retinitis, which may be associated
with retinitis. Many of such cases are treated by specific antivirals
D Vit
t
D. Vitrectomy
Vitrectomy has several advantages over conservative therapy. Vitrectomy improves retinal oxygenation, reduces the inflammatory load within
the eye, provides specimens for diagnostic evaluation, allows direct inspection of the retina, allows definitive treatment, reduces the load of
infection, and reduces the severity of the disease and accelerates visual rehabilitation.[64] There are two schools of thought: one based on EVS
study and another based on complete and early vitrectomy for endophthalmitis (CEVE) study.[40][64]
According to EVS study, vitrectomy was better than vitreous tap and intravitreal antibiotics for the most severe cases, i.e., for patients with initial
presenting vision being the perception of light alone, and vitrectomy, if performed, is limited to core vitrectomy without inducing posterior
vitreous detachment. Contrary to EVS study, CEVE (complete and early vitrectomy for endophthalmitis) advocates complete vitrectomy, which
includes induction and removal of posterior vitreous to prevent exudates from settling over the macula. However, in the periphery, the surgeon
must be conservative to avoid iatrogenic break formation.
In delayed-onset endophthalmitis secondary to propionibacterium acnes, pars plana vitrectomy is combined with total capsulectomy and IOL
exchange/removal or wash of the capsular bag with antibiotics.[44]
2. Management of Inflammation
Corticosteroids are the most potent anti-inflammatory agents used in the management of endophthalmitis. To be useful, they must be given
early and in appropriate doses. They should, however, not be used in fungal endophthalmitis as it enhances fungal growth by weakening
defense mechanisms within the body. They can be used either as an intravitreal injection, topical drops, or systemically.
The most commonly used corticosteroid intravitreally is dexamethasone (0.4 mg/ 0.1 ml). However, there is no clear consensus regarding the
role of intravitreal corticosteroid.[65] Topical steroids can penetrate an intact cornea, and its efficacy is proportional to the frequency of
installation. Systemic steroids are preferred at a dose of 1 to 1.5 mg/kg body weight administered in three divided doses to achieve uniform
concentration during the day, unlike in chronic uveitis where once a day regimen is preferred.[66]
EVS study utilized only topical (prednisolone acetate 1% eye drops), subconjunctival (dexamethasone 6 mg/0.25 ml), and systemic steroids
(prednisolone 30 mg twice a day for 5 to 10 days).[40]
3. Supportive Therapy
Cycloplegic agent (homatropine 2%, atropine 1%) is an essential part of treatment which relieve ciliary spasm and prevent synechiae formation.
In patients with elevated intraocular pressure, oral and topical medications need to be added. Vitreous tap before intravitreal injection also
reduces intraocular pressure.
Hypertonic saline (5% drop or 6% ointment) may be needed in cases of severe corneal edema.
Prophylaxis
Endophthalmitis cannot be prevented entirely, but due to various measures taken in recent times, its incidence has come down. Most of the
cases of endophthalmitis are exogenous, which prompts for taking prophylactic action.
Proposed measures as prophylaxis of postoperative endophthalmitis include preoperative 5% povidone-iodine antisepsis of conjunctival cul de
sac, check for lid infections preoperatively, checking the patency of nasolacrimal duct, use of intracameral cefuroxime 1000 mcg/0.1 ml[67]
[41] (according to the guideline by European society for cataract and refractive surgery)[68]/moxifloxacin (0.5% weight by volume from the
sterile moxifloxacin drop 0.5%)[69][70]at the end of the surgical procedure, prompt repair of conjunctival erosions, leaking blebs.[71]
A large study on 2 million eyes undergoing cataract surgery in the Aravind Eye Care System showed that intracameral moxifloxacin reduced the
incidence of postcataract surgery endophthalmitis, especially in cases with complicated cataract surgery with posterior capsular rent.[70]
However, caution needs to be exercised regarding the use of intracameral antibiotics, as there are reports of retinal toxicity with certain
antibiotics. For example, hemorrhagic occlusive retinal vasculitis (HORV) has been reported after the use of intracameral vancomycin.[72]
Most common contaminants in cases of post intravitreal injections are streptococci, which are common members of oral flora, and oral flora
bacteria may be aerosolized during the speech. The use of masks and adhering to a strict no-talking policy has been noted to be effective in
reducing the overall incidence of post-injection endophthalmitis and particularly the incidence of streptococcal endophthalmitis.[73][74][73]
Prompt surgical repair of open globe injuries and prophylactic intravitreal injection of antibiotics (particularly in the setting of retained
intraocular foreign body) with or without systemic antibiotics have been associated with reduced rates of post-traumatic endophthalmitis.[75]
[76]
Di erential Diagnosis
Post-surgical Endophthalmitis
Toxic anterior segment syndrome (TASS) is an acute inflammatory condition presenting within 24 hours of surgery with a severe
anterior chamber reaction, limbus to limbus corneal edema. However, there is no adnexal involvement, and the patient responds
dramatically to the addition of steroids.[77] Various features differentiating TASS from acute postoperative endophthalmitis are listed
in figure 4 (common differentiating features of TASS with endophthalmitis).
Posteriorly dislocated lens matter
Fibrinous reaction post vitrectomy
Phacoanaphylaxis etc.
Non-surgical Endophthalmitis
Chronic uveitis – certain cases of chronic indolent endophthalmitis may be confused for chronic panuveitis.
Retained intraocular foreign body
Old vitreous hemorrhage
Toxoplasma retinochoroiditis
Necrotic retinoblastoma
Acute retinal necrosis
Severe panuveitis
Seasonal hyperacute panuveitis (SHAPU)
Intravitreal cysticercus with intraocular inflammation
Prognosis
Visual outcome in a patient with endophthalmitis depends on various variables.
Nature of endophthalmitis: Better visual acuity has been reported in cases with culture-negative post-surgical endophthalmitis.[78] Bleb
associated endophthalmitis carries a poor visual prognosis.[79] Endogenous bacterial and fungal endophthalmitis also carries poor visual
prognosis.[54][80]
Organism: Endophthalmitis due to Streptococcus,[78] Bacillus,[81] Pseudomonas,[82] and Candida[83] carry poor visual prognosis.
Presenting visual acuity: In EVS study, it has been noted that presenting visual acuity remains more powerful than microbiological
factors in predicting visual outcome and response to vitrectomy.[40]
Time to initiation of appropriate therapy: It is of utmost importance in cases of post-traumatic endophthalmitis, especially with Bacillus
species.[84] In EVS study, in the group with a vision of light perception only, early vitrectomy resulted in a three-fold increased chance to
achieve ≥ 20/40 (33%), a two-fold increased chance to achieve ≥ 20/100 (56%) and was less likely to worsen <5/200 (20%).[40]
Systemic stability of the patient: Immunocompromised patients, patients with endogenous endophthalmitis, have concurrent
polymicrobial infections which influence the final outcome.[54]
In EVS study in post-cataract surgery endophthalmitis, it was noted that only 53% of treated eyes had final visual acuity of 20/40 or better, and
15% had a final visual acuity of 20/200 or worse.[40]
If left untreated or inadequately treated, endophthalmitis progresses to panophthalmitis, requiring evisceration or enucleation of the eyeball. It
is noted that patients suffering from a corneal ulcer, endogenous endophthalmitis, and low visual acuity are at higher risk of requiring
evisceration or enucleation.[85]
Complications
Panophthalmitis
Glaucoma
Orbital cellulitis
Intracranial spread
Septicemia
Loss of vision
Phthisis
Hypotony
Painful blind eye
Deterrence and Patient Education
Patients should be explained about the warning signs of endophthalmitis such as pain, redness of eye and blurring of vision, etc. at discharge
after any intraocular procedure. Early detection and prompt treatment is the key. Patients should be explained the seriousness of the condition
and the need for intensive pharmacotherapy.
Enhancing Healthcare Team Outcomes
Most cases of endophthalmitis are exogenous and are seen in the postoperative period. Patients with uncontrolled blood sugar levels, high
temperature (can be secondary to underlying septicemia) are prone to postoperative endophthalmitis. Hence the nursing staff and physician
must check for systemic stability before any surgical procedure to reduce the chances of postoperative endophthalmitis. Nursing staff posted at
the daycare or inpatient ward should look for preoperative risk factors such as blepharitis, dacryocystitis, open wound, etc. before shifting the
case to the operating room. Nursing staff plays a vital role in monitoring the patient, charting the vital parameters, and reporting the issues to
the treating physician. Certain cases with fulminant endophthalmitis might require evisceration/ enucleation; hence pre-surgical counseling of
patients by a psychiatrist helps to reduce the morbidity. Cases with endogenous endophthalmitis have systemic comorbidities such as invasive
aspergillosis or chronic renal failure with prolonged catheterization, etc. and hence may not primarily present to the ophthalmologist with ocular
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complaints. Therefore specialists other than an ophthalmologist must be aware of such an entity and promptly refer such cases to improve
outcomes.
(Click Image to Enlarge)
Figure 1: Classi cation of Endophthalmitis
Contributed by Simakurthy Sriram, MD
(Click Image to Enlarge)
Figure 2: commonly used stains and culture media for the detection of microbial agents
Contributed by Simakurthy Sriram, MD
(Click Image to Enlarge)
Figure 3: Commonly used antibiotics in the treatment of Endophthalmitis
Contributed by Simakurthy Sriram, MD
(Click Image to Enlarge)
Figure 4: Common di erentiating features of TASS with Endophthalmitis
C
t ib t d b Si
k th S i
Contributed by Simakurthy Sriram
References
[1]
Durand ML, Endophthalmitis. Clinical microbiology and infection : the official publication of the European Society of Clinical
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