Caring for patients with inflammatory disease of the eye.
Red Eye Evaluation
A red eye is a cardinal sign of ocular inflammation, which can be caused by several conditions. Most cases are benign and can be managed effectively by the primary care provider. The key to management is recognizing cases with underlying disease that require ophthalmologic consultation.
A red eye is caused by dilation of blood vessels in the eye. Diagnosis may be aided by the differentiation between ciliary and conjunctival injection. Ciliary injection involves branches of the anterior ciliary arteries and indicates inflammation of the cornea, iris, or ciliary body. Conjunctival injection mainly affects the posterior conjunctival blood vessels. Because these vessels are more superficial than the ciliary arteries, they produce more redness, move with the conjunctiva, and constrict with topical vasoconstrictors.
CONJUNCTIVITIS is an inflammation of a mucous membrane and therefore in most types there is a red eye, thickening of the conjunctival tissue and some discharge of mucous or mucous and inflammatory cells. The causes of Conjunctivitis include; bacterial infection, viral infection and allergic reactions.
Acute Bacterial Conjunctivitis. The patient will present with injection of the bulbar conjunctival and episcleral vessels, and perhaps also the palpebral conjunctiva. Infection may begin in one eye and subsequently spread to the fellow eye. There may be mild photophobia and discomfort, but pain is not typical. There will be concurrent mucopurulent discharge, and the patient usually reports that the eyelids and eyelashes are matted shut upon waking. Visual function typically is normal. The discharge is
corneotoxic and frequently results in a coarse punctate epitheliopathy. Significant epitheliopathy may cause vision reduction and discomfort in some cases. Due to drainage of the infection through the nasolacrimal system, there is no preauricular node involvement.
Management: As in any bacterial infection, microbiologic studies with cultures and sensitivities is the optimum means to reach a conclusive diagnosis. However, due to the expense of microbiologic studies and relatively benigature of the condition, most clinicians advocate the use of broad-spectrum, empirical therapy and reserve culturing for hyperacute conditions or those that fail to respond to initial therapy.
Although antibiotics will eradicate the antigenic bacteria, they will do nothing to suppress the concurrent inflammation, f there is no significant corneal disruption, then you can use corticosteroids such as Pred Forte (prednisolone), Flarex (fluorometholone) or Lotemax (loteprednol) concomitantly with the antibiotics to speed resolution of the inflammation. Steroid-antibiotic combinations such as Maxitrol (neomycin-polymixin B-dexamethasonen), Pred-G (gentamicin-prednisolone), and Tobra Dex (tobramicin-dexamethasone) are also excellent initial choices for therapy when the cornea is intact.
Viral Conjunctivitis (Pharyngoconjunctival Fever & Epidemic Keratoconjunctivitis).
Most viral infections produce a mild, self-limiting conjunctivitis, but some have the potential to produce severe, disabling visual difficulties. The two most common self-limiting forms of viral conjunctivitis are epidemic keratoconjunctivitis and pharyngoconjunctival fever.
Pharyngoconjunctival fever (PCF) is characterized by fever, sore throat and follicular conjunctivitis. It may be unilateral or bilateral. It is caused regularly by adenovirus 3 and occasionally 4 or 7. Corneal infiltrates are rare. The disorder varies in severity but usually persists for four days to two weeks. While the virus is shed from the conjunctiva within 14 days, it remains in fecal matter for 30 days.
Epidemic Keratoconjunctivitis (EKC) often presents as a bilateral, inferior, palpebral, follicular conjunctivitis, with epithelial and stromal keratitis. Subepithelial corneal infiltrates are much more common in EKC than in PCF and are typically concentrated in the central cornea. EKC is regularly caused by adenovirus types 8 and 19.
The key clinical signs of both conditions include: conjunctival injection, tearing, serous discharge, edematous eyelids, pinpoint subconjunctival hemorrhages, pseudomembrane formation and palpable preauricular lymph nodes. In severe cases, conjunctival desiccation causes scarring and symblepharon formation (adherence of the bulbar and palpebral conjunctivas).
Both conditions are highly contagious. Patients will usually report recent contact with someone who had either red eyes or an upper respiratory infection. Both forms tend to start in one eye, then spread to the other eye within a few days. In rare cases, the focal subconjunctival hemorrhages can evolve into acute hemorrhagic conjunctivitis.
Viral conjunctival infections are thought to be caused by airborne respiratory droplets or direct transfer from one’s fingers to the conjunctival surface of the eyelids. After an incubation period of five to 12 days, the
disease enters the acute phase, causing watery discharge, conjunctival avascular lesions ranging from 0.2 to 2mm insize. They have lymphoid germinal centers that have responded to an infectious agent.
Adenovirus type 8 can proliferate in the coraeal epithelial tissues, procuring the characteristic keratitis and subepithelial infiltrates. This, along the shallow anterior stroma, just beneath the epithelium. Sometimes, a conjunctival membrane will form. These are made up of fibrin and leukocytes, and in prolonged cases, of fibroblast and collagen deposits.
‘T^udoincriibrancs” are much easier to remove than “true” membranes.
Management. Because EKC and PCF are contagious and self-limiting, the primary treatment once again is patient education. Instruct patients to stay home from work or school until there is absolutely no discharge. Also instruct them not to share utensils, glasses, linens or wash
Medical management can range from cold compresses and artificial tears to topical vasoconstrictors (e.g., naphazoline) and steroids (Vexol, Flarex, Pred Forte) two to four times daily. If a membrane is present, peel it ott with a wet, cotton-tipped applicator or forceps. After removal, prescribe a topical antibiotic-steroid combination such as Tobradex or Maxitrol q.i.d. Anti-viral drugs such as Viroptic are ineffective against adenovirus.
Recently, there has been a breakthrough in the management of sdenovirai keratoconjunctivitis. Cidofovir (Vistide), an anti-viral drug used
adenoviral keratoconjunctivitis. The topical form creates a faulty viral DNA structure. Twice daily instillation is recommended. This topical anti-viral is also possibly effective against herpes simplex and zoster, and Epstein-Barr virus.
Allergic Conjunctivitis. The human allergic response has various objective signs and physical symptoms. Ocular allergic conditions vary from the subtle signs of itchy, watery eyes with mild hyperemia to extensive inflammatory interactions between the ocular coats and adenexa. Symptoms typically include itching, burning and tearing of the eyes with watery discharge. In most cases the patient will report a history of allergies. The important observable clinical signs include tissue swelling (chemosis); red, edematous eyelids; conjunctival papillae; and a lack of a palpable preauricular node.
Management: Because there are many levels of ocular allergic reactions, management is primarily aimed at reducing symptoms. The most effective treatment for allergic conjunctivitis is to eliminate the potentially offending allergen, although this is not usually possible. Cold compresses, artificial tears and ointments soothe, lubricate and wash away or dilute the antigens on an as-needed basis.
Topical decongestants produce vasoconstriction, reducing hyperemia, chemosis and other symptoms by retarding the release of the chemical mediators into the tissues from the blood stream. The topical nonsteroidal anti-inflammatory drugs—such as Acular (ketorolac) and Voltaren (diclofenac)–may offer relief in moderate cases; topical steroids-such as
Pred Forte (prednisolone) and Lotemax (loteprednol 0.5%)~are typically reserved tor more severe presentations.
Vernal Keratoconjunctivitis (VKC) is a chronic, bilateral inflammation of the superior and limbal palpebral conjunctiva. The warmer the climate, the greater its prevalence. Onset typically occurs between ages 3 and 25 years. Males typically are affected more than females.
Symptoms often include severe itching with thick, ropy discharge. In most cases, patients have a history of allergies or infantile eczema. The important clinical signs include large conjunctival papillae on the back of the superior tarsus; raised Horner-Trantas dots (gelatinous, white clumps of degenerated eosinophils usually located at the superior limbus); areas of superficial punctate keratitis (SPK) and, in severe cases, well-demarcated, sterile corneal shield ulcers, located superiorly. You can differentiate VKC from atopic keratoconjunctivitis (AKC) based on age, location, dermatitis and lack of seasonal variability.
Pathophysiology: Allergic responses are the immune system’s overreaction to foreign substances known as immunogens or allergens. The key component of the vernal ocular allergic response is the eosinophil.
Management: Management of VKC is primarily aimed at reducing symptoms and preventing serious vision-threatening sequelae. The most effective treatment is to eliminate or avoid the allergen; however, this is often impractical. Cold compresses and artificial tears and ointments soothe, lubricate and may dilute the antigen. Topical decongestants such as naphazaline and phenylephrine produce vasoconstriction, reducing hyperemia, chemosis and other symptoms by retarding the release of
chemical mediators. Topical antihistamines—Livostin, Patanol, Zaditor, Optivar~and oral antihistamines—Benadryl, 25mg tid~are also excellent therapies. Mast-cell stabilizers such as Alomide, Alocril, Alamast and cromolyn sodium can be useful before the disease flares or to keep it under control following acute treatment; however, mast-cell stabilizers often do little to abate the symptoms. NSAIDS such as Acular and Voltaren bid-qid may offer relief in moderate cases, with topical steroidal preparations—Pred Forte, Lotemax, Alrex or Pred Mild (prednisolone 0.12%, Allergan) bid-qid–reserved for more severe presentations.
Gonococcal Conjunctivitis Gonococcal conjunctivitis, sometimes referred to as hyperacute conjunctivitis, is also a sexually transmitted ocular disease. While sexual contact is the customary route of transmission, even
casual interaction with infected individuals has been reported as a cause. Newborn infants may acquire the infection by passing through an infected birth canal. Systemically, gonococcal infections are associated with infection of the urethra, cervix and rectum. Symptoms vary from nothing to discharge and irritation.
This unusually contagious ocular disease typically presents as a hyperacute red eye of less than four weeks duration with foreign body sensation; the eye may be “glued” shut with severe purulent discharge. The conjunctivitis has an incubation period of two to seven days. Conjunctival papillae, superficial punctate keratitis and marked chemosis are almost always present. Subconjunctival hemorrhage (hemorrhagic conjunctivitis), pseudomembrane or true membrane formation and preauricular lymph nodes are usually present. In chronic, recalcitrant or severe cases, peripheral
subepithelial corneal infiltrates may occur, leading to marginal ulceration with anterior uveitis.
Management. Patients with gonococcal conjunctivitis require immediate conjunctival scrapings for culture and sensitivity testing. Medical management of gonococcal infection begins with an intramuscular loading dose of ceftriaxone lg. Ideally, the patient should be hospitalized and given one gram of ceftriaxone intravenously within 12 to 24 hours. Following discharge, resume treatment with either erythromicin 250 to 500mg p.o. q.i.d., tetracycline 250 to 500mg p.o. q.i.d. or doxycycline lOOmg p.o. b.i.d. Begin ocular management with saline lavage to clear the mucopurulent debris from the lids and conjunctiva. A topical fluoroquinolone (ofloxacin or ciprofloxacin) is appropriate if corneal infection occurs. However, because gonococcal conjunctivitis does not respond to topical antibiotics, topical therapy is usually not indicated.
KERATITIS is an inflammation of a cornea and also a disease of a red eye. Type of injection in most of keratitis is ciliary (or deep) — the red ring around the limbus occurs. In severe cases injection is mixed – the eye surface is equally red in the central and peripheral part. Bacterial Keratitis
The patient will present with a unilateral, acutely painful, photophobic, intensely injected eye. Visual acuity is usually reduced, and profuse tearing is common. There will be a focal stromal infiltrate with an overlying area of epithelial excavation. There is likely to be thick, ropy, mucopurulent discharge.
The cornea will be very edematous. The conjunctival and episcleral vessels will be deeply engorged and inflamed, often greatly out of proportion to the size of the corneal defect. In severe cases, there will be a pronounced anterior chamber reaction, often with hypopyon. Intraocular pressure may be low due to secretory hypotony of the ciliary body, but most often will be elevated due to blockage of the trabecular meshwork by inflammatory cells. Often, the eyelids will also be edematous.
Management. As with bacterial conjunctivitis, culturing the infection is the ideal way to determine the infecting organism but is often difficult or impractical. First and foremost, you must halt bacterial proliferation; do not delay treatment while waiting for the culture results. If you have the materials available, scrape the ulcer using a platinum spatula and plate the specimen onto blood and chocolate agar culture media. A simpler but less effective method is to use a culturette.
Regardless, immediately begin therapy with a broad spectrum antibiotic. A popular initial therapy is the fluoroquinolone ciprofloxacin 0.3% (Ciloxan) two drops every 15 minutes for six hours, followed by two drops every 30 minutes for 18 hours, and then tapered depending on patient response. Another fluoroquinolone, ofloxacin 0.3% (Ocuflox) is also an effective treatment for bacterial keratitis. Both fluoroquinolones are as effective at managing bacterial keratitis as fortified antibiotics, but with significantly fewer side effects.
To increase patient comfort and minimize inflammation, strong cycloplegia is mandatory. Begin with a cycloplegic such as scopolamine 0.25% TID. If this is insufficient, switch to atropine 1% BID. Adjunctive use
oi coid compresses will also help to reduce inflammation. If there is evidence of secondary inflammatory glaucoma, Rx a topical beta-blocker BID.
Herpes Simplex Keratitis The keratitis caused by the herpes simplex virus (HSV) typically presents as a unilateral “red eye” with a variable degree of pain or ocular irritation. Photophobia and epiphora are common; however, vision may or may not be affected, depending upon the location and extent of the corneal lesion. You may see a vesicular skin rash and follicular conjunctivitis with the initial infection, but these are less common with recurrent HSV. A more common sign is secondary uveitis.
A dendritic corneal ulcer is the hallmark sign of HSV infection, accompanied by stromal keratitis in more severe presentations. These ulcers may begin as nondescript punctate keratopathies, but quickly coalesce to form the familiar branching patterns which stain brightly with sodium iluorescein dye. Because the virus invades and compromises the epithelial cells surrounding the ulcer, the leading edges (the so-called “terminal end-bulbs”) will stain with rose bengal or lissamine green.
Management. Corneal epithelial disease secondary to HSV infection must be managed aggressively and quickly to prevent deeper penetration. The treatment of choice is topical trifluridine 1% given at two hour intervals, nine times daily. As the dendrites begin to regress, taper the dosage to q3-4h until the lesion resolves completely (usually in seven to 10 days). At this point, however, have the patient continue the medication t.i.d. for another >v?ek to ensure suppression of the virus.
Avoid topical steroids in cases of active epithelial HSV keratitis. Studies show that the virus replicates more rapidly in the presence of steroids, prolonging the course of the disease. The use of oral acyclovir (400mg 5x/day) or another oral antiviral for recalcitrant ulcers has yet to be proven clinically significant. However, it has been shown recently that the use of oral acyclovir 400mg q.d. significantly reduces the recurrence of herpes simplex keratitis in imunocompetent patients. At this point, consider using oral prophylaxis therapy only in patients with confirmed recurrent HSV keratitis or patients on initial presentation who request it after being thoroughly educated.
A new development in the management of herpes simplex keratitis has come in the form of topical acyclovir ointment (Zovirax). Place the ointment in the lower cul-de-sac five times per day at four hour intervals. At this point, toxicity seems to be low.
EPISCLERITIS. Episcleritis presents as a relatively asymptomatic acute onset redness in one or both eyes. Typically, you’ll observe a sectoral injection of the episcleral and overlying conjunctival vessels, although the redness may be diffuse throughout these tissues. Occasionally, there may be a translucent white nodule centrally within the inflamed area (nodular episcleritis). While some patients complain of mild pain or tenderness to the affected region, particularly upon manipulation, often there is no associated discomfort. The cornea remains clear in this condition, although longstanding or recurrent episcleritis may lead to dellen formation. There is no associated anterior chamber reaction.
Management. Most cases of episcleritis are self-limiting, meaning that they will resolve spontaneously within two to three weeks even if the
patient does not undergo treatment. However, patients who are experiencing discomfort may benefit from a regimen of topical anti-inflammatory agents and lubricants.
Typically, prednisolone acetate 1% or fluorometholone acetate applied Q3-4H will speed resolution and decrease the tenderness. The patient may use cold compresses and artificial tears liberally if discomfort persists. More severe cases, particularly nodular episcleritis, may require oral NSAIDs to quell the inflammation.
SCLERITIS, Unlike the mild sensitivity of episcleritis, true scleritis
presents with severe, boring ocular pain which may also involve the adjacent head and facial regions. The scleral vessels are significantly dilated, as are the overlying vessels of the episclera and bulbar conjunctiva. The affected eye may be so injected in some cases that the eye actually takes on a deep red, almost purple, hue. This presentation may be sectoral or diffuse.
Patients typically report a gradual onset of the pain and redness, with associated photophobia, tearing and decreased vision. Slip lamp evaluation may reveal scleral nodules (nodular scleritis), peripheral keratitis and secondary uveitis in some instances. In severe cases of necrotizing scleritis, the sclera may become transparent due to chronic inflammation, revealing the underlying dark blue of the choroid.
Scleritis is a primary inflammation of the sclera, which is often (over 50 percent of cases) associated with systemic disease. Among the most common related disorders are rheumatoid arthritis, ankylosing spondylitis, systemic iupus erythematosus, polyarteritis nodosa, Wegener’s granulomatosis, herpes zoster virus, gout and syphilis.
Management. Topical medications alone are generally insufficient in managing scleritis. In addition to cycloplegia (scopolamine 0.25% BID/QID or atropine 1% BID) and a topical steroid, scleritis indicates a systemic anti-inflammatory agents as well. Treat moderate sectoral or diffuse anterior scleritis with oral NSAIDs (e.g., ibuprofen 600mg QID or indomethacin 25mg TID).
If the inflammation is severe or necrotizing, or if non-steroidals alone fail to suppress the inflammation, use a systemic steroid such as oral prednisone 80mg QD for two to three days, then slowly taper to 10 to 20mg daily. It may also be necessary for patients to receive a small maintenance dose for up to one month to control the condition. In rare cases, the patient may require immunosuppressive agents and should be managed by a rheumatologist.
UVEITIS is an inflammation of the uveal tissues, the iris, the ciliary body and/or choroid.
CLASSIFICATION depends of several features:
Anatomic location
Anterior – Iritis, iridocyclitis
Middle – Cyclitis, intermediate uveitis, pars planitis, peripheral uveitis, chronic cyclitis
Posterior – Retinitis, retinochoroiditis, chorioretinitis, choroiditis, papillitis Diffuse – Diffuse uveitis, panuveitis, endophthalmitis
Pathology – Granulomatous, nongranulomatous Lesions – Focal, multifocal, disseminated, diffuse ANTERIOR UVEITIS
The typical presentation of anterior uveitis involves pain, photophobia and excessive tearing. Patients report a deep, dull aching of the involved eye and surrounding orbit. Associated sensitivity to lights may be severe; often, these patients will present wearing dark sunglasses. The excessive tearing occurs secondary to increased neural stimulation of the lacrimal gland, and is not associated with a foreign body sensation.
Visual acuity is not usually impaired to any great extent (20/40 or better is common), although patients may report some haziness. Accommodative tasks, however, may prove more difficult and uncomfortable. Inspection may reveal mild to moderate congestion of the lids, resulting in pseudoptosis. You’ll typically see a deep perilimbal injection of the conjunctiva and episclera, although the palpebral conjunctiva is characteristically normal. The cornea may display mild edema upon biomicroscopy. In more severe reactions, you may observe grayish brown endothelial deposits, known as keratic precipitates.
The hallmark signs of anterior uveitis are “cells and flare.” Cells are leukocytes (white blood cells) floating in the convection currents of the aqueous; flare refers to liberated protein from the inflamed iris or ciliary body which gives the aqueous a particulate, or smoky, appearance. The iris may adhere to the lens capsule (posterior synechia) or, less commonly, to the peripheral cornea (anterior synechia). Additionally, you may see granulomatous nodules within the iris stroma.
Intraocular pressure in the affected eye is initially reduced due to secretory hypotony of the ciliary body. However, as the reaction persists,
inflammatory by-products may accumulate in the trabeculum. If this debris builds significantly, and if the ciliary body resumes its normal secretory output, the pressure may rise sharply, resulting in a secondary uveitic glaucoma.
Uveitis, as the name implies, represents an inflammation of the uveal tissues, chiefly the iris and ciliary body. Inflammation may be associated with underlying systemic disease, or it may occur as a direct result of ocular trauma. Occasionally, inflammatory reactions in adjacent tissues (e.g., keratitis), can induce a secondary uveitis.
Uveitis can be either acute or chronic. The chronic form is more often associated with systemic disorders including, but not limited to, ankylosing spondylitis, Beh3et’s syndrome, inflammatory bowel disease, juvenile rheumatoid arthritis, Reiter’s syndrome, sarcoidosis, syphilis, tuberculosis, and T yme disease. Chronic uveitis most likely occurs due to an immunopathological mechanism which is not fully understood.
Management. There are two primary goals when managing anterior uveitis. First, immobilize the iris and ciliary body to decrease pain and prevent exacerbation of the condition. Second, quell the inflammatory response. Begin by cyclopleging the patient with homatropine 5% TID/QID, scopolamine 0.25% BID/QID or atropine 1% BID, depending upon the severity of the reaction. Next, prescribe a topical steroid Q2-3H, or more often if the reaction is severe. If there’s a posterior synechia present, attempt to break the adhesion in the office using atropine 1% and phenylephrine 10%. Treat secondary elevations in IOP using standard anti-glaucoma agents, such as timolol 0.5% BID or dorzolamide 2% TID.
As the uveitis resolves, discontinue the cycloplegics and taper the steroids to QID or TID. Generally, it is better to taper slowly rather than
abruptly, and patients may need to remain on steroid drops daily or every other day for several weeks. In recalcitrant uveitis which is unresponsive to conventional therapy, consider injectible steroids such as methylprednisolone 60mg or even oral steroids such as prednisone 60 to 80mg.
Posterior uveitis
Retinitis typically manifests by toxoplasmic or herpetic infection. Spillover into the adjacent choroid creating a retinochoroiditis or chorioretinitis may occur. Choroiditis may occur with any of the granulomatous uveitides (TB, sarcoid, Lyme, lues), histoplasmosis, or more unusual syndromes, such as birdshot or serpiginous chorioretinitis. Papillitis may occur with toxoplasmosis, viral retinitis, lymphoma, or sarcoidosis.
Diffuse uveitis
Diffuse uveitis, panuveitis, or endophthalmitis generally occur with overwhelming infections such as infantile toxocariasis, postoperative bacterial endophthalmitis, or severe toxoplasmosis. Many of the granulomatous uveitides may produce a highly disseminated pattern especially when delayed diagnosis occurs. Exacerbations of the illness or poor compliance with a treatment regimen may add to the spread of these diseases throughout the choroids.
Management of uveitis
Specific clinical laboratory tests
• Bacterial antibody testing (toxocariasis, toxoplasmosis, B
henselae, brucellosis)
• Viral antibody testing (herpes simplex virus [HSV],
CMV, varicella-zoster virus [VZV], Epstein-Barr virus [EBV],
hepatitis, HIV, human T lymphotrophic virus (HTLV)
• Luetic serology – Treponemal tests (fluorescent
treponemal antibody absorption [FTA-ABS] test,
microhemagghitination-Treponemapallidum [MHA-TP]) and
nontreponemal tests (rapid plasma reagin [RPR], Venereal Disease
Research Laboratory [VDRL] test)
• Connective tissue disease – Rheumatoid factor (RF),
antinuclear antibody (ANA), lupus anticoagulant, complement,
protein electrophoresis, antineutrophil cytoplasmic antibody (ANCA),
and specific antinuclear antibodies (single stranded, Smith,
ribonucleoprotein)
• Nonspecific inflammation – Erythrocyte sedimentation
rate (HSR), C-reactive protein (CRP)
Diagnostic imaging
• Chest x-ray (TB, sarcoidosis, histoplasmosis, tumor)
• Sacroiliac films (HLA-B27, Reiter, ankylosing
spondylitis)
• Orbital films, CT scan, or MRI (tumor, foreign body,
thyroid, scleritis)
• Joint films (rheumatoid, HLA-B27, JRA, lupus,
gonorrhea)
Specialty consultations
• Internal medicine and pediatrics (general evaluation,
medication monitor)
• Oncology (cytotoxic immunosuppressive medication
monitor)
• Infectious disease (diagnostic and therapeutic assistance,
antibiotic medication monitor)
• Dentistry, periodontology (diagnostic assistance with
mucosal lesions)
• Dermatology (diagnostic assistance with cutaneous
lesions)
• Rheumatology (diagnostic and therapeutic collaboration)
Diagnosis and treatment
With a careful history, a directed physical examination, appropriate use of office diagnostic procedures, a tailored approach to laboratory testing, and selective medical consultations, the ophthalmologist can mesh a collection of useful data to obtain a diagnosis in up to 80% of referral uveitis patients and about 50% of uveitis patients in a comprehensive ophthalmology practice. Expeditious and specific treatment based on a complete and organized diagnostic evaluation is best for the patient, physician, and economy.
EJNDOPHTHALMITIS is an inflammatory reaction of the intraocular fluids or tissues caused by microbial organisms.
Pathophysiology: The entry of bacteria to 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.
Bacteria, as foreign objects, incite an inflammatory response. The cascade of inflammatory products occurs resulting in an increase in 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.
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.
General findings: Visual acuity decreased below the level expected, lid edema, conjunctival hyperemia, corneal edema, anterior chamber cells and flare, keratic precipitates, hypopyon, fibrin membrane formation, vitritis, loss of red reflex, retinal periphlebitis if view of fundus possible.
