Viral Conjunctivitis (Pharyngoconjunctival Fever & Epidemic Keratoconjunctivitis) A Pseudomembrane in EKC Severe Follicular Reaction SIGNS AND SYMPTOMS Most

viral infections produce a mild, self-limiting conjunctivitis, but some have the potential to produce severe, disabling visual difficulties. The two most common selflimiting forms of viral conjunctivitis are epidemic keratoconjunctivitis and pharyngoconjunctival fever. Pharyngoconjunc-tival 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. PATHOPHYSIOLOGY 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 hyperemia and follicle formation. Lymphoid follicles are elevated, with avascular lesions ranging from 0.2 to 2mm in size. They have lymphoid germinal centers that have responded to an infectious agent. Adenovirus type 8 can proliferate in the corneal epithelial tissues, producing the characteristic keratitis and subepithelial infiltrates. This, along with the immune response to viral antigens, causes lymphocytes to collect in the shallow anterior stroma, just beneath the epithelium. Sometimes, a conjunctival membrane will form. These are made

and you may also see papillae of the palpebral conjunctiva. Also instruct them not to share utensils. linens or wash cloths with others. patients will report a history of seasonal or other allergies. there has been a breakthrough in the management of adenoviral keratoconjunctivitis. Allergic Conjunctivitis &Vernal Keratoconjunctivitis (VKC) SIGNS AND SYMPTOMS Itching and conjunctival injection are the two hallmarks of an allergic reaction.. cotton-tipped applicator or forceps. MANAGEMENT Because EKC and PCF are contagious and self-limiting. This topical anti-viral is also possibly effective against herpes simplex and zoster. it is most likely VKC rather than a seasonal allergy. . and that the infection won’t completely go away for three to six weeks. or recalcitrant cases. In most cases. The topical form creates a faulty viral DNA structure. since palpable preauricular nodes signify viral infection. Twice daily instillation is recommended. Cidofovir (Vistide). Onset is typically between the ages of three and 25 years. Medical management can range from cold compresses and artificial tears to topical vasoconstrictors (e.g. CLINICAL PEARLS Keep your equipment. peel it off with a wet. VKC’s prevalence is higher in the warmer climates. After removal. Seasonal allergies typically produce a thin. Flarex. Recently.up of fibrin and leukocytes. prescribe a topical antibiotic-steroid combination such as Tobradex or Maxitrol q. the primary treatment once again is patient education. watery discharge and do not involve the cornea. Instruct patients to stay home from work or school until there is absolutely no discharge. appears to be effective in adenoviral keratoconjunctivitis. “Pseudomembranes” are much easier to remove than “true” membranes.d. If the patient exhibits thick. ropy discharge with severe itching and corneal involvement. an anti-viral drug used intravenously to treat cytomegalovirus retinitis. Remember to always taper steroids slowly as the condition recedes. glasses. of fibroblast and collagen deposits. If a membrane is present. for example). and Epstein-Barr virus. Also definitive is a lack of palpable preauricular lymph nodes. Males are typically more affected than females. EKC infiltrates resolve without scarring the cornea. naphazoline) and steroids (Vexol. Tell patients to expect the symptoms to get worse for about seven to 10 days before getting better. Pred Forte) two to four times daily. and in prolonged cases. instruments and chair area meticulously clean to avoid contaminating your patients and staff.i. The eyelids may be swollen and red. Anti-viral drugs such as Viroptic are ineffective against adenovirus. Most practitioners reserve topical steroidal therapy for severe cases (if the infection is on the visual axis and affecting acuity.

Horner-Trantas dots (gelatinous. Virtually all cells contain a phospholipid layer within their cell walls. and the other by the production of arachidonic acid and its conversion into so-called “newlyformed” mediators such as prostaglandins (see “Tracing the Complex Path of Allergic Reactions. one caused by the release of so-called “pre-formed” inflammatory mediators such as histamine from mast cells. they easily reach the conjunctival surface by moving through the dilated and highly permeable capillaries. other mediators released from mast cells send out chemical signals that attract both red and white blood cells to the area. referred to as the arachidonic acid cascade. creating the sensation of itching. then adheres to mast cells and causes them to degranulate. immediately begin to stimulate nerve endings called nociceptors. white clumps of degenerated eosinophils at the superior limbus). superiorly located corneal shield ulcers. and also increase vascular permeability and vasodilation. Much like histamine and bradykinin. which the body wrongly perceives as a potential threat. PATHOPHYSIOLOGY An allergic response is an unwarranted over-reaction of the body’s immune system to foreign substances known as allergens. Once these cells arrive. The body’s other defense mechanism. indirect or a combination of the two. This discharges the pre-formed mediators. Their effects can be either direct. Leukotrienes primarily attract macrophages (white blood cells).” on next page). Pre-formed mediators are released immediately upon exposure. it is metabolized into eicosanoids. newly-formed mediators are delayed roughly eight to 24 hours. like a key opening a lock. The presence of an allergen on the conjunctiva initiates two simultaneous immune responses. . In mast cell degranulation. produces three newly-formed inflammatory mediators—prostaglandins. areas of superficial punctate keratitis (SPK) and. prostaglandins directly stimulate nerve endings to produce sensations of itching and pain. The response can be innate or acquired. Meanwhile. the allergen attracts and binds to an antibody known as immunoglobulin E (abbreviated as “IgE”). histamine and bradykinin.The important clinical signs of VKC include large conjunctival papillae on the back of the superior tarsus. this causes the clinical signs of redness and conjunctival injection. When arachidonic acid interacts with two enzymes known as cyclooxygenase and lipoxygenase. An allergen’s presence initiates the arachidonic acid cascade both within conjunctival epithelial cells and also within mast cells as they degranulate. sterile. Both also increase vascular permeability and vasodilation. Any disruption or threat signals the cell to convert phospholipids into arachidonic acid. thromboxanes and leukotrienes—which are collectively known as eicosanoids. in severe cases. Two important mediators released from mast cells. well demarcated.

i. This reduces hyperemia. such as chalazia. homatropine 5% or scopolamine 0. b. But because steroids inhibit the production of arachidonic acid itself. The most effective but least practical treatment is to prevent exposure to the allergen.d. This is why we must use steroids to treat any inflammatory conditions characterized by a build-up of immune cells. A recently developed steroid.MANAGEMENT Management of both allergic conjunctivitis and VKC is primarily aimed at alleviating symptoms. is specifically marketed for the management of allergic conjunctivitis. Patanol (olopatadine 0. The effects last eight hours. as well as emedastine difumarate 0. Flarex or Alrex q.d. have been seen to be very effective.i. provide a low-water content soft lens as a bandage lens. When the corneal lesion has re-epithelialized. use a topical steroid such as Vexol.1%) combines mast cell stabilization with an antihistamine to offer therapy that is for both acute and chronic symptoms.i. These drugs cause vasoconstriction.d.d. used from two to four times per day as needed: a topical medication such as Patanol or Livostin. thus they have virtually no effect on the production of leukotrienes. begin topical steroid therapy. uveitis or corneal infiltrates.i. rather than q. Non-steroidal drugs prevent the formation of cyclooxygenase but not lipoxygenase. This leads to an interesting distinction in anti-inflammatory treatment. Mast cell stabilizers such as Alomide and Crolom help prevent the onset of allergic reactions by blocking the adherence of the IgE-allergen compound to the mast cell. oral antihistamines such as Benadryl. non-steroidals are useful in reducing itching and conjunctival injection but not very helpful in ridding the eye of excess immune cells. VKC patients who present with shield ulcers also need aggressive cycloplegia (atropine 1%. To reduce the interaction between the lid and cornea. are produced from the break-down of arachidonic by lipoxygenase. lubricate and wash away the allergens. Treat patients with a history of recurrent seasonal allergies using a mast cell stabilizer q.5% (Emadine) q. recommend one or more of the following.) and a topical antibiotic (Tobrex.d. Ciloxan Ocuflox or Polytrim) q4-6h. Also recommend that patients use a topical decongestant such as naphazoline or phenylephrine as needed. by contrast. Since this is not usually possible. loteprednol etabonate (Alrex) q.i. In moderate to severe cases.d. Newer anti-histamines. artificial tears and ointments to soothe. or a topical non-steroidal anti-inflammatory drug (Acular.i.i. dosing.1% (Patanol) b.25%. they reduce the production of all three eicosanoids. for four weeks in advance of allergy season.d. CLINICAL PEARLS . chemosis and other symptoms.d. such as dual-action olopatadine hydrochloride 0. In extremely symptomatic cases. Only prostaglandins and thromboxanes are produced when cyclooxygenase interacts with arachidonic acid. instruct patients to frequently use cold compresses. As a result. Leukotrienes.i. Voltaren or Profenal). allowing for b. retarding the release of the chemical mediators into the tissues from the blood stream.

albeit much more severe. and patients usually say that their eyelids and eyelashes are matted shut upon awakening. There may be mild photophobia and discomfort. If effective. and non-pathogenic bacteria that colonize the eye and compete against external organisms that try to enter. healthy person the eye will fight to return to homeostasis. However. Follow-up with patients on non-steroidal medicines in one to two weeks after the start of therapy. The most commonly encountered organisms are Staphylococcus aureus. See patients on topical steroids no later than one week after the start of therapy. When any of these defense mechanisms break down. Invading bacteria. and recommend prophylactic treatment with a mast cell stabilizer. and the bacteria will eventually be eradicated. but usually no pain. then soon spreads to the other. episcleral vessels and perhaps papillae of the palpebral conjunctiva. Streptococcus pneumoniae and Pseudomonas aeruginosa. the patient will present with similar signs and symptoms. Haemophilus influenzae. Visual function is normal in most cases. Follow up with patients placed on topical medications after one week. The most common infectious organisms in hyperacute conjunctivitis are Neisseria gonorrhoeae and Corynebacterium diptheroides. Bacterial Conjunctivitis SIGNS AND SYMPTOMS Patients with bacterial conjunctival infections present with injection of the bulbar conjunctiva. causing a conjunctival infection and setting the eye up for potential corneal infection. such as bacterial infection. This induces an antigen-antibody immune reaction and subsequently causes inflammation. but the arachidonic acid cascade occurs after any threatening event. surgery or accidental trauma. . Re-examine patients treated for shield ulceration every one to three days. maintain this therapy for the duration of the season. are considered foreign antigens. the immune system in general. the shearing force of the blink. and the exotoxins they produce.Educate patients with a history of seasonal allergic conjunctivitis about how to avoid exposure to substances that precipitate symptoms. PATHOPHYSIOLOGY The eye has a battery of defenses to prevent bacterial invasion. Mast cell degranulation only occurs in allergic reactions. and monitor their IOP routinely for the duration of the therapy. The infection often starts in one eye. In a normal. pathogenic bacterial infection is possible. These include bacteriostatic lysozymes and immunoglobulins in the tear film. an extra heavy load of external organisms can be too difficult to fight off. There is more danger in hyperacute bacterial conjunctivitis as these organisms can penetrate an intact cornea. with close monitoring thereafter. In cases of hyperacute bacterial conjunctivitis. There will be thick mucopurulent discharge.

those suffering from viral and allergic conjunctivitis will often report that their lids are matted shut in the morning with mucopurulent material. CLINICAL PEARLS Like patients with bacterial conjunctivitis.S. or a steroidantibiotic combination such as Maxitrol (neomycin. prescribe a steroid such as Pred Forte. they will do nothing to suppress the concurrent inflammation. Most clinicians immediately begin treatment with a broad spectrum antibiotic and reserve culturing for hyperacute conditions or those that fail to respond to the initial therapy. Excellent initial broad spectrum antibiotics include Polytrim (polymixin B sulfate and trimethoprim sulfate). and tobramycin 0. Pred-G (gentamicin 0.3%. sticky. Diagnosis of inclusion conjunctivitis is often difficult. Although antibiotics will eradicate the bacteria. dexamethasone 0. if any. Chlamydial & Gonococcal Conjunctivitis SIGNS AND SYMPTOMS Chlamydial (inclusion) conjunctivitis typically affects sexually active teens and young adults and is the most frequent infectious cause of neonatal conjunctivitis in the U.MANAGEMENT Ordering cultures and sensitivity tests is ideal for diagnosis but usually impractical and expensive. estimating approximately three million new cases per year. Many times there are little. prednisolone acetate 0.3%. Therapy should be aggressive. gentamicin 0. However. though the aminoglycosides (gentamicin and tobramycin) have weak activity against Staphylococcal species. Ocuflox and Chibroxin are also excellent options.1%). Remember.3%. due to the excellent defense systems of the eye. Women seem to be more susceptible than men. mucopurulent matting characteristic of bacterial conjunctivitis. The incidence of infection seems to be directly related to sexual activity and geography. symptoms. not the wet.1%). These will give good coverage of gram-positive and gram-negative organisms. Vexol or Flarex along with your antibiotic of choice. Infants whose mothers have untreated chlamydial infection have a 30 to 40 . dexamethasone 0. with urban populations having higher incidences. The Centers for Disease Control (CDC) recognizes chlamydia as one of the major sexually transmitted pathogens. there are also resistant strains of Pseudomonas. There are many antibacterial options.3%. Too often. these patients actually have crusting of the lashes due to drying of tears and serous secretions. acute bacterial conjunctivitis is uncommon. with administration from QID to Q1H for the first few days. polymyxin B. The incidence in pregnant women overall is 4 to 10 percent. If there is no significant corneal disruption. Fluoroquinolones such as Ciloxan. or Tobradex (tobramycin 0.1%). clinicians will consider the crusting of the lashes to be the same as the mucopurulent matting and misdiagnose the condition.

Transmission is generally by direct or indirect sexual contact or contact with an infected individual. iritis and follicles (most dense in the inferior cul-de-sac) may all be present. and serotypes D through K produce adult inclusion conjunctivitis. MANAGEMENT . Systemically. Mucopurulent. N. pseudomembrane or true membrane formation and preauricular lymph nodes are usually present. The mode of ocular transmission may be hand contact from a site of genital infection to the eye. polymorphonuclear leukocytes and lymphocytes. Conjunctival papillae. A palpable preauricular node is almost always present. Subconjunctival hemorrhage (hemorrhagic conjunctivitis). PATHOPHYSIOLOGY Chlamydia trachomatis is an intracellular parasite that contains its own DNA and RNA. cervix and rectum. even casual interaction with infected individuals has been reported as a cause. shared cosmetics and occasionally an improperly chlorinated hot tub. Gonococcal conjunctivitis. laboratory accidents. peripheral subepithelial corneal infiltrates may occur. leading to marginal ulceration with anterior uveitis. recalcitrant or severe cases. superficial punctate keratitis. Diagnostic testing for chlamydia is expensive and difficult to interpret. gonorrhoeae’s ability to penetrate an intact corneal epithelium makes the risk of corneal infection and ulceration high. is also a sexually transmitted ocular disease. Ocular signs and symptoms include the chief complaint that an eye infection has persisted for over three weeks despite treatment with topical antibiotics. a gramnegative. The preferred method of identification is to culture the organism. pelvic inflammatory disease or urethritis. stringy or mucus discharge is common. Symptoms vary from nothing to discharge and irritation. In chronic. gonococcal infections are associated with infection of the urethra. intracellular diplococcus capable of invading an intact mucosal membrane. The infectious organism in gonococcal conjunctivitis is Neisseria gonorrhoeae. While sexual contact is the customary route of transmission.percent chance of developing neonatal chlamydial conjunctivitis. The sub-group A causes chlamydial infections. the eye may be “glued” shut with severe purulent discharge. Ba and C cause trachoma. Conjunctival scrapings for Giemsa staining will show intracytoplasmic inclusion bodies in epithelial cells. Systemic signs and symptoms may include a history of vaginitis. superficial punctate keratitis and marked chemosis are almost always present. B. the serotypes A. Conjunctival injection. This unusually contagious ocular disease typically presents as a hyperacute red eye of less than four weeks duration with foreign body sensation. sometimes referred to as hyperacute conjunctivitis. a mother infecting the newborn. The conjunctivitis has an incubation period of two to seven days. superior corneal pannus. Newborn infants may acquire the infection by passing through an infected birth canal. peripheral subepithelial infiltrates.

Taken as a 1 gram dose.i. Following discharge..o. topical therapy is usually not indicated. Follow up should be weekly. With the slit lamp. Currently. But since tetracycline must be administered one hour before or after meals to avoid gastrointestinal side effects and interference of dairy products with its efficacy. because gonococcal conjunctivitis does not respond to topical antibiotics. Fluorescein will pool in the area of the laceration under the cobalt filter.i. Ideally.d.i. Patients will present with a history of ocular trauma and complain of mild pain or a scratchy. Follow up with gonococcal conjunctivitis patients every day until you see consistent improvement. conjunctival abrasions and lacerations are less symptomatic than corneal abrasions of the same severity. Topical therapy is adjunctive and includes erythromicin. A topical fluoroquinolone (ofloxacin or ciprofloxacin) is appropriate if corneal infection occurs. resume treatment with either erythromicin 250 to 500mg p. Conjunctival Laceration SIGNS AND SYMPTOMS Because the conjunctiva is far less innervated than the cornea. tetracycline 250 to 500mg p. q. CLINICAL PEARLS Inclusion conjunctivitis should be one of the differential diagnoses any time a patient presents with a chief complaint of chronically red eyes or follicular conjunctivitis that is recalcitrant to topical therapies. Amoxacillin and erythromycin 250 to 500mg q. There may be some tearing and photophobia. for three weeks the treatment of first choice. for one week are acceptable alternatives. tetracycline or sulfacetamide t. the drug of choice is azithromycin (Zithromax). Begin ocular management with saline lavage to clear the mucopurulent debris from the lids and conjunctiva. other oral medications may be more appropriate. Educate the patients regarding the circumstances surrounding the disease and that partners at risk should be informed about the possibility of infection. foreignbody sensation in the affected eye.i. Eventually. the affected region of the conjunctiva will appear torn and the edges may be retracted. 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 1g.d.o. it has been documented as being as effective for the treatment of genital chlamydial infection as doxycycline. or doxycycline 100mg p.i. for three weeks as well. for three weeks or doxycycline 100mg b.In treating chlamydial conjunctivitis.d. contact the Centers for Disease Control for instructions and recommendations.d. Educate patients that the disease is contagious and that partners are at risk and should be examined. vision is rarely impaired.i. revealing the underlying sclera. stain will seep underneath the conjunctiva and produce a generalized "glow" to that part of the . one time. q. The adjacent vessels will be dilated. Finally. by mouth.d. many doctors consider oral tetracycline 250 to 500mg q. b. and there will often be a subconjunctival hemorrhage.d. However. the patient should be hospitalized and given one gram of ceftriaxone intravenously within 12 to 24 hours.i.o.d.

The fact that the eye is very red and often hemorrhaging may be cause for great concern on the patient's part. use a broad spectrum antibiotic (Polytrim solution Q3-4H. While it's important to rule out a penetrating injury. it is important to rule out global perforation. or Polysporin ointment QID) and examine the patient again in three to five days.eye. in which you apply fluorescein to the laceration and look carefully for external leakage of aqueous. If the involved area of conjunctiva is small. CLINICAL PEARLS Conjunctival lacerations are a minor problem that typically resolve with minimal intervention. PATHOPHYSIOLOGY Although the conjunctiva is normally a tough. Then instill an antibiotic ointment and pressure-patch the eye for 24 hours. gentamicin solution or ointment QID. even though there is little pain or other symptoms. MANAGEMENT As with any case of ocular trauma. While most conjunctival lacerations resolve without surgical repair.. Patching is generally not necessary for smaller lesions. the trauma itself acts as an antigen and sets off an inflammatory cascade resulting in vasodilation and edema of the involved and surrounding tissues.e. first apply topical anesthesia and use a forceps or moistened cotton-tipped applicator to manipulate any ragged areas of conjunctiva back into position. and that it will heal in a few days. resilient tissue. Once you are certain that there are no perforations or other complications. Also meticulously inspect the surrounding area to look for subconjunctival foreign bodies. it may be lacerated in cases of ocular trauma with sharp or pointed objects such as fingernails. significantly large (i. . This should only be performed by a qualified optometrist or ophthalmologist. begin treatment. In these cases. Rarely is there significant white cell proliferation to the point of causing an anterior chamber reaction. If the laceration is larger. yet patients often present with great anxiety. you can safely reassure most patients that they have a simple "cut" on their eye. We recommend using the Seidel test. greater than 2cm) wounds may require suturing. Be careful to differentiate this pattern of staining from simple accumulation of fluorescein within the physiologic folds of the conjunctiva. tree branches or the edge of a piece of paper.

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