Red Eye ASMPH LEC Group 6 Abad and Imperial

Red Eye ASMPH LEC Group 6 Abad and Imperial
Ophthalmology Clerkship Rotation: TMC

Outline Reference Pathophysiology Evaluation Common Causes of Red Eye
Subconjunctival Hemorrhage Blepharitis Conjunctivitis Pterygium Phylctenulosis Episcleratis Keratitis Corneal Abrasion Acute Angle Glaucoma Uveitis Reference

Pathophysiology Dilatation of blood vessels in the eye
conjunctival (superficial) ciliary (deeper)

Evaluation Chief complaint: RED EYE HPI Past Ocular History
Past Medical History Ocular Exam

Common Causes of Red Eye

Subconjunctival hemorrhage
Causes: Idiopathic, Trauma, Valsalva, Bleeding disorders, Drugs: Blood-thinners, steroids, contraceptives, Severe febrile systemic disease: Dengue, typhoid, malaria, etc. Extravasation of blood between the conjunctiva and sclera from broken or ruptured conjunctival or episcleral blood vessels Appears as bright red patch with normal surrounding tissue Usually benign and self- limiting Usually without pain and discharge; unilateral

1) Anterior Blepharitis 2) Posterior Blepharitis
Condition Clinical Findings Treatment 1) Anterior Blepharitis Lid margin erythema, ulceration, fibrin, collarettes (fibrin coating lashes), crusts at base of lashes, sty (pustules forming at the base of hair follicles) Lid hygiene, warm compresses, bactericidal ointment, anti-staphylococcal antibiotics 2) Posterior Blepharitis Chronic burning, foreign body sensation, conjunctival redness, filmy vision, tearing, crusting of eyelids Warm compress, oral tetracycline, doxycycline or erythromycin, topical corticosteroids Two types of lacrimal glands: Apocrine glands Zeiss and Moll affected in Anterior Blepharitis (Kuliti and Muta); Meibomian glands affected in Posterior Blepharitis (Meibomitis). The duct of the Meibomian gland drains posterior to the anterior lacrimal glands. Anterior blepharitis: Staphylococcal blepharitis Primarily: Staphylococcus aureus Infection of lid margin, lash bases, associated glands Infection occurs through: Exogenous ie. Direct contact via infected fingers Local spread from neighboring infected structures such as lacrimal sac, lids and nasopharynx Results in lid inflammation, burning, foreign body sensation, redness, mattering of lashes Underyling problem: Stasis of secretions eventually get infected. Posterior blepharitis: Meibomian gland dysfunction Meibomian glands: Sebaceous glands with unique lipid content without the high triglyceride level of sebum Dysfunction implies abnormal lipid composition and abnormal secretion Characterized by enlargement, irregularity, inspissation, and plugging of meibomian orifices Foamy, thick, yellowish oil can be expressed Symptoms: Chronic burning, foreign body sensation, conjunctival redness, filmy vision, tearing, crusting of eyelids Component of ocular surface disease: Dry Eye which causes chronic type of red eyes. Treatment: Warm compress

Anterior Blepharitis

Posterior Blepharitis

Conjunctivitis inflammation of the conjunctiva
dilatation of the superficial conjunctival blood vessels hyperemia and edema with discharge

Common Types of Conjunctivitis
Clinical Findings and Cytology Viral Bacterial Chlamydial Allergic Itching Minimal Severe Hyperemia Generalized Tearing Profuse Moderate Exudation In- stained scrapings and exudates Monocytes Bacteria, PMNs PMNs, plasma cells, inclusion bodies Eosinophils Associated sore throat and fever Occasional Occasionally Never

Adenoviral Conjunctivitis
Usually self- limiting The common sore eye

Epidemic keratoconjunctivitis
Common sequelae of adenoviral conjunctivitis. Serotypes 8, 11, 19 most common Copious watery discharge Often eyelid edema, preauricular lymphadenopathy, chemosis (bulging of the conjunctiva) Occasionally, severe temporary loss of vision Punctate pattern on fluorescein staining Keratitis- inflammation of the cornea Treatment: artificial tears, cold compress, topical corticosteroids (controversial)

Gonococcal keratoconjunctivitis
Neisseria gonorrhoeae: Hyper-acute, purulent conjunctivitis Rapid progression, copious purulent discharge, chemosis, lid edema Systemic IV/IM ceftriaxone (Cephalosporin) Topical antibiotics

Chlamydial (Inclusion) keratoconjunctivitis
Chlamydia oculogenitalis Most common form of neonatal conjunctivitis and adult STD conjunctivitis Treatment: Oral doxycycline, topical erythromycin

Allergic conjunctivitis
Hallmark: Itching! Type I hypersensitivity reaction (IgE-mediated) Treatment: Topical antihistamines, mast cell stabilizers and avoidance of allergen

Vernal conjunctivitis
Common profile: Male, brown skin, under 20, lives at equatorial region. accumulation of eosinophil On palpebral conjunctiva, especially upper conjunctiva; Diffuse papillary hypertrophy: Giant (cobblestone) papillae Treatment: Topical antihistamines, mast cell stabilizers, corticosteroids FOR SHORT TERM; self-limiting

Giant Papillary Conjunctivitis
Usually occurs in soft contact lens wearers: Contact lens material, solution, debris Reversible chronic inflammatory condition affecting the upper tarsal conjunctiva; most commonly associated with soft contact lens wear. Other causes: protruding suture ends and ocular prostheses. Clinical features: Symptoms: itching, tearing, mucus secretion, foreign body sensation, and contact lens intolerance. Signs: Upper tarsal conjunctival hyperemia Enlarged papillae (ranged from < mm) Mucus discharge, lid swelling and pseudoptosis Management: Remove offending agents such as stopping contact lens wear, changing lens solutions or suture removal. Encourage the patients to replace lenses frequently, use preservative-free lens solution, and increase lens hygiene. Medical treatment with mast cell stabilizers (i.e. sodium cromolyn eyedrops) and / or corticosteroids may be required in more advanced cases. Treatment: Discontinuation of contact lens, topical antihistamine, mast cell stabilizers, shift to disposable lenses.

Pterygium The redness is confined largely to a raised, yellowish, fleshy lesion that is usually located on the nasal side of the bulbar conjunctiva Benign fibrovascular proliferation covered by conjunctival-like epithelium extending into peripheral cornea Location: Within or Above Bowman’s Line Not infectious or inflammatory. It is degenerative A pterygium usually develops over a period of years and is asymptomatic, but the disorder may be manifested as acute redness of the eye if the lesion becomes inflamed and irritable. Causes the subconjunctival tissue to degenerate and proliferate as vascularized granulation tissue under the epithelium, which ultimately encroaches the cornea. The corneal epithelium, Bowman’s layer and superficial stroma are destroyed. Risk Factors: Chronic Exposure to the Sun, Wind, Dust Treatment: Surgery, Excision with ancillary procedure

Phylctenulosis Symptoms: tearing, ocular irritation, mild to severe photophobia and a history of similar episodes Focal, translucent lymphocytic nodules generally located at limbus Cause: Delayed Cell-Mediated Hypersensitivity (IV) Focal, translucent lymphocytic nodules generally located at limbus (conjunctival and corneal also possible) Usually accompanied by significant inflammation as PMNs enter nodule resulting in necrosis Delayed cell-mediated hypersensitivity (Type IV) to tuberculin, staphylococcal antigen. Corneal phlycten cause neovascularization and scarring: sight-threatening Topical corticosteroids MANAGEMENT Ocular management begins with patient education to improve eyelid hygiene. Lid scrubs two to three times per day along with artificial tears and ointments may soothe and reverse mild cases. Moderate to severe cases require topical steroids or steroid-antibiotic combinations. Cycloplegia is only necessary if there is an associated iritis. In most cases, prednisolone acetate (Pred Forte), one drop, Q2H/QID is sufficient, provided there are no corneal contraindications. If the suspected etiology is Staph. reaction or acne rosacea, prescribe 250mg of oral tetracycline QID or 250mg erythromycin QID PO, along with topical antibiotic ointments such as bacitracin or erythromycin at bedtime. Topical metronidazole (Metrogel) applied to the skin TID is also effective. Because tetracycline can damage and discolor the teeth of children, it is contraindicated in patients under age 10. In these cases, substitute doxycycline 100mg TID or erythromycin 250mg QID PO. Continue treatment for two to four weeks. In suspicious cases, order a chest X-ray and PPD to rule out tuberculosis. Treatment: Improve Eyelid Hygiene, Topical Corticosteroids

Episcleritis Simple: intermittent bouts of moderate-to-severe inflammation that often recur at 1- to 3-month intervals Nodular: prolonged attacks of inflammation that are typically more painful than simple episcleritis Inflammation and vasodilatation of episclera Self-limited, not associated with systemic disease Usually monocular and focal, but can be bilateral and generalized No significant pain or tenderness Can resolve without treatment Topical vasoconstrictors, mild corticosteroids The episclera lies beneath the conjunctiva and over the sclera. Episcleritis which occurs much less often than conjunctivitis, is a self-limited, recurrent, presumably autoimmune inflammation of the episcleral vessels. It is characterized by the rapid onset of redness, a dull ache, and tenderness on palpation. Vision is unaffected. Discharge, if present, is watery. There are focal areas of redness present within which white sclera may be observed between radially coursing, dilated episcleral vessels. An oral nonsteroidal antiinflammatory drug (e.g., aspirin) may relieve the symptoms, but reassurance that the condition is self-limited and will clear spontaneously is often all that is required. Persistent or recurrent disease warrants a referral to an ophthalmologist. The pathophysiology is poorly understood. The inflammatory response is localized to the superficial episcleral vascular network, and histopathology shows nongranulomatous inflammation with vascular dilatation and perivascular infiltration. The 2 clinical types are simple and nodular. The most common type is simple episcleritis, in which there are intermittent bouts of moderate-to-severe inflammation that often recur at 1- to 3-month intervals. The episodes usually last 7-10 days, and most resolve after 2-3 weeks. Prolonged episodes may be more common in patients with associated systemic conditions. Some patients note that episodes are more common in the spring or fall. The precipitating factor is rarely found, but attacks have been associated with stress and hormonal changes. Patients with nodular episcleritis have prolonged attacks of inflammation that are typically more painful than simple episcleritis. Many patients with nodular episcleritis have an associated systemic disease. Inflammatory condition affecting the episcleral tissue Symptoms: Rapid onset of redness, dull ache, and tenderness on palpation Treatment: Topical Vasoconstrictors, Mild Corticosteroids

Bacterial Keratitis Inflammation of the cornea due to infection
Symptoms Pain and foreign body sensation due to mechanical effects of lids Watering from the eye due to reflex hyperlacrimation Photophobia from stimulation of nerve endings Blurred vision from corneal haze Redness of eyes due to congestion of circumcorneal vessels Interruption of an intact corneal epithelium and/or abnormal tear film permits entrance of microorganisms into the corneal stroma, where they may proliferate and cause ulceration. Virulence factors may initiate microbial invasion, or secondary effector molecules may assist the infective process. Many bacteria display several adhesins on fimbriated and nonfimbriated structures that may aid in their adherence to host corneal cells. During the initial stages, the epithelium and stroma in the area of injury and infection swell and undergo necrosis. Acute inflammatory cells (mainly neutrophils) surround the beginning ulcer and cause necrosis of the stromal lamellae. Diffusion of inflammatory products (including cytokines) posteriorly elicits an outpouring of inflammatory cells into the anterior chamber and may create a hypopyon. Different bacterial toxins and enzymes (including elastase and alkaline protease) may be produced during corneal infection, contributing to the destruction of corneal substance. The most common groups of bacteria responsible for bacterial keratitis are as follows: Streptococcus,Pseudomonas, Enterobacteriaceae (including Klebsiella, Enterobacter, Serratia, and Proteus), andStaphylococcus species. Up to 20% of cases of fungal keratitis (particularly candidiasis) are complicated by bacterial coinfection.

Bacterial Keratitis Streptococcus pneumoniae
Very painful! Serpiginous, gray-white stromal infiltrate and hypopyon characteristic of Gram-positive bacteria Suppuration does not usually extend over entire corneal surface Bacterial keratitis: Streptococcus pneumoniae Streptococcus pneumoniae: Relatively distinct borders, with overhanging edges; usually with epithelial defect (ulcer) Corneal epithelial damage is a prerequisite for most infecting organism to produce corneal ulceration such as in corneal abrasion, epithelial drying/xerosis Suppuration does not usually extend over entire corneal surface Sterile hypopyon common: Perforates in a week or so and causes white material in anterior chamber (Hypopyon: Pus in the eye. It is a leukocytic exudate, seen in the anterior chamber, usually accompanied by redness of the conjunctiva and the underlying episclera. It is a sign of inflammation of the anterior uvea and iris, i.e. iritis, which is a form of anterior uveitis. The exudate settles at the bottom due to gravity.). Very painful becasue of disruption of epithelium (where you have most of your corneal nerves) and contraction of ciliary body. Produces a deeper duller pain. Lancet-shaped, encapsulated, G(+) diplococci Treatment: Topical erythromycin, chlorampheicol, 4th generation fluoroquinolones (moxiflocxcin, gatifloxacin) Oral cephalosporin, erythromycin Also give cycloplegic to relax the ciliary body. Fig. 25: Bacterial keratitis Streptococcus pneumoniae Usually produce an oval, yellowish white densely opaque ulcer surrounded by relatively clear cornea. Treatment: Topical erythromycin, chloramphenicol, 4th generation fluoroquinolones (moxiflocxcin, gatifloxacin), Oral cephalosporin, erythromycin, Cypoplegics

Bacterial Keratitis Pseudomonas aeruginosa
Common in immunocompromised patients, contact lens wearers with faulty hygiene Typical Gram-negative corneal ulcer: Rapid evolution, marked tendency to spread. Can perforate in 48 hours. Typical Gram-negative corneal ulcer: Rapid evolution, marked tendency to spread Can perforate in 48 hours. Upon perforation, the condition is more dangerous. Spreads laterally. Common in immunocompromised patients, contact lens wearers with faulty hygiene Tenacious mucopurulent discharge adherent to ulcer surface Opacification and edema of corneal stroma surrounding ulcer Rapid stromal necrosis as result of proteolytic enzymes from Pseudomonas and PMNs Pseudomonas releases collagenases that melt stroma very rapidly. Blunt Gram-negative rods Treatment: Topical tobramycin, ciprofloxacin, moxifloxacin, gatifloxacin Fig. 26: Bacterial keratitis: Pseudomonas Most common cause is contact lens Patient presents with painful eye upon waking up, with blurred vision and history of casual handling of contact lenses and a habit of wearing it while sleeping. Think Pseudomonas infection! There is a 13x greater risk of infection if you sleep with contact lenses on. So if keratitis occurs in a contact lens wearer, think Pseudomonas. Treatment: Topical tobramycin, ciprofloxacin, moxifloxacin, gatifloxacin

Fungal Keratitis Intense suppuration, progressive hypopyon
Modes of infection: Injury by vegetative material such as crop, leaf, branch of tree, straw, hay or decaying vegetable matter. Common sufferers are field workers especially during harvest season Therapeutic problem: No effective topical agent Debridement: Scrape it off and reduce load of organism or perform keratectomy. Candida: Natamycin; ketoconazole, voriconazole, amphotericin B Fungal keratitis Leads to intense suppuration, progressive hypopyon, anterior chamber membranes Modes of infection: Injury by vegetative material such as crop, leaf, branch of tree, straw, hay or decaying vegetable matter. Common sufferers are field workers especially during harvest season. Therapeutic problem: No effective topical agent Debridement: Scrape it off and reduce load of organism or perform keratectomy. Candida: Natamycin; ketoconazole, voriconazole (Good but very expensive), amphotericin B

Fungal Keratitis Yeast Fungi Filamentous Fungi
Presentation differs according to etiologic agent Filamentous fungi Gray-white infiltrate with feathery border; occasionally with “satellite” infiltrates Deep lesions: Endothelial plaque; Hypopyon Yeast fungi (Candida sp.) Focal, dense suppuration similar to pneumococcus keratitis Yeast produces characteristic creamy, opaque, pasty colonies on the surface of culture media. Candida is the most representative pathogen in this group, primarily affecting those corneas already compromised by topical steroids, surface pathology, or both. A feathery or powdery growth on the surface of culture media is produced by septate filamentary fungi, which are the most common cause of fungal keratitis.

Herpes simplex keratitis
Coalesces in a few days into branching or dendritic lesion Mode of infection: HSV1 - Through kissing or coming in close contact with patient suffering from herpes labialis. HSV2 - Transmitted to eyes of neonates through infected genitalia of the mother. Herpes simplex keratitis Begins as discrete punctate epithelial keratitis Mode of infection: HSV1 - Through kissing or coming in close contact with patient suffering from herpes labialis. HSV2 - Transmitted to eyes of neonates through infected genitalia of the mother. Coalesces in a few days into branching or dendritic (Pathognomonic) lesion consisting of swollen, opaque epithelial cells Characteristic branch morphology: “terminal bulbs” Ulcer develops in center of dendrite due to lysis and desquamation of infected cells If it progresses, there is centrifugal spread of virus from central dendrite toward peripheral cornea leading to “geographic” ulcer appearance Mild stromal edema, subeptihelial infiltrates Self limited but recurrent. Topical/systemic acyclovir, ganciclovir, debridement Symptoms: Injection, Irritation, Mucoid discharge, Pain, Mild photophobia Treatment: Self limited but recurrent. Topical/systemic acyclovir, ganciclovir, debridement

Corneal abrasion Symptoms: Acute pain after ocular trauma
Photophobia, excessive tearing, blepharospasm, foreign body sensation, blurred vision Follows Occular Trauma May be superficial or deep Symptoms of acute pain after ocular trauma, Photophobia, pain, excessive tearing, blepharospasm, foreign body sensation, blurred vision May be superficial (not involving Bowman's) and deep (penetrate Bowman's) Superficial: no scarring Adjacent cells expand and fill defect in hours; basal epithelial cell undergo mitosis; producing new cells Patching or bandage contact lens, topical antibiotic, cycloplegic Corneal abrasion is probably the most common eye injury and perhaps one of the most neglected. It occurs because of a disruption in the integrity of the corneal epithelium or because the corneal surface scraped away or denuded as a result of physical external forces. Corneal epithelial abrasions can be small or large, but they usually heal without serious sequelae. However, deep corneal involvement may result in facet formation in the epithelium or scar formation in the stroma Treatment: Patching, Topical Antibiotics, Cycloplegics

Acute Angle Closure Glaucoma
Angle closure occurs when peripheral iris physically opposes the trabecular meshwork and impedes aqueous outflow Pupillary block: flow of aqueous from posterior to anterior chamber is inhibited causing the peripheral iris to balloon forward Genetic predisposition: short eye Posterior synechiae: adhesion of pupillary border to anterior lens surface Enlargement of lens Plateau iris: peripheral iris unusually lax, comes into contact with angle Angle closure may occur via 2 mechanisms. The iris may be pushed forward into contact with the trabecular meshwork, as in pupillary block or plateau iris, or it may be pulled anteriorly, as occurs with other inflammatory conditions. In either case, the position of the iris causes the normally open chamber angle to close. Aqueous humor that should drain out of the anterior chamber is trapped inside the eye. Pain, blurred vision, and nausea may occur if the ensuing rise in pressure is sudden. Glaucomatous damage to the optic nerve also may occur due to the increased IOP, either in a sudden attack or in intermittent episodes over a long period of time

Symptoms Signs ocular pain, headache unilateral blurring of vision "iridescent" vision: haloes around lights nausea and vomiting Elevated intraocular pressure (>40 mmHg) deep circumlimbal conjunctival and episcleral injection: "ciliary flush" fixed, mid-dilated pupil edematous or steamy cornea shallow anterior chamber Risk factors include a shallow anterior chamber, older age, female sex, a history of farsightedness, Eskimo or Asian extraction

Treatment: Lower IOP Carbonic anhydrase inhibitors Hyperosmotic agents Pilocarpine Supportive: steroids and analgesics Laser Iridotomy Laser iridotomy: Treatment of choice for pupillary-block ACG is laser iridotomy. Iridotomy with an argon or Nd:YAG laser creates an opening in the iris through which aqueous humor trapped in the posterior chamber can reach the anterior chamber and trabecular meshwork. As aqueous flows into the anterior chamber through the iris defect, pressure behind the iris falls, allowing the iris to recede toward its normal position. This procedure opens the anterior chamber angle and relieves the blockade of trabecular meshwork. If the cornea is extremely cloudy or the patient cannot cooperate, incisional peripheral iridectomy may be performed instead of a laser procedure.

Acute anterior uveitis
Hallmark: Cells and Flare Signs Ciliary flush Sterile hypopyon (severe) Cells and flares Keratic precipitates Posterior synechiae Granulomatous nodules Symptoms Deep, dull pain of involved eye and surrounding orbit Photophobia Tearing Difficulty in reading Cells: leukocytes floating in the convection currents of the aqueous Flare: liberated protein from inflammed iris or ciliary body Uveitis: Inflammation of one or all parts of the uveal tract

Keratic precipitates Posterior synechiae Granulomatous nodules Koeppe (pupil) Brusacca Keratic: Cells (e.g. leukocytes) deposited on the endothelium of the cornea which occur as a result of inflammation of the iris or the ciliary body. They often collect in a triangular pattern with the base down (Arlt's triangle) on the inferior portion of the endothelial surface. They may also be distributed diffusely over the endothelium, as in Fuchs' heterochromic iridocyclitis or anterior uveitis, or concentrated in one area, as in disciform keratitis or herpes simplex keratitis. In granulomatous uveitis they are larger than in nongranulomatous uveitis, greasy in appearance (called 'mutton fat'). Following treatment of the primary cause they usually disappear. Thick pigmented precipitates on endothelium posterior synechian.Adhesion of the iris to the capsule of the lens. Adhesions between the posterior surface of iris and anterior capsule of crystalline lens or anterior hyaloid face. These are formed due to organization of the fibrin-rich exudates. Granulomatous nodules (Sequelae of inflammation in the anterior chamber), Koeppe nodules (Papillary margin) and Busacca nodules (Iris surface or near the collarette )

Systemic causes Infectious causes Ankylosing spondylitis Bechet’s disease Chronic granulomatous disease Enthisitis Inflammatory bowel disease Kawasaki’s disease Multiple sclerosis Polyarteritis nodosa Psoriatic arthritis SLE Vogt-Koyanagi-Harada syndrome Brucellosis Herpes simplex Herpes zoster Leptospirosis Lyme disease Syphilis Toxoplasmosis Tuberculosis

Treatment Immobilize iris, ciliary body to relieve pain (ie. atropine, cyclopentolate) Reduce inflammation (ie. topical steroids) Treat underlying ocular, systemic disease

References Vaughan & Asbury’s General Ophthalmology 17th ed.
ASMPH Ophthalmology Lecture Notes on “Common Causes of Red Eye” by Dr. Victor L. Caparas. January 2010. The Red Eye. The New England Journal of Medicine. Volume 343 Number 5. December 2007.

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Red Eye ASMPH LEC Group 6 Abad and Imperial

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