1.Diagnostic, emmergency, prophylaxis of eyelids
2.lachrymal organ.
3.orbit inflammations (hordeolum,preseptal cellulitis, dacryocyctitis, periostitis, orbital cellulitis).
A primary care physician frequently encounters patients who complain of a red eye. The condition causing the red eye is often a simple disorder such as a subconjunctival hemorrhage or an infectious conjunctivitis. These conditions either will resolve spontaneously or can be treated easily by the primary care physician. Occasionally, the condition causing a red eye is a more serious disorder, such as intraocular inflammation, corneal inflammation, or acute glaucoma. A patient with one of these vision-threatening conditions requires the immediate attention of an ophthalmologist, whose specialized skills, knowledge, and examining instruments are needed in order to make correct therapeutic decisions.
DISORDERS ASSOCIATED WITH A RED EYE. Any patient who complains of a red or painful eye should be examined to diagnose the condition as one of the following.
Acute Angle-Closure Glaucoma. Acute angle-closure glaucoma is an uncommon form of glaucoma due to sudden and complete occlusion of the anterior chamber angle by iris tissue (Figure 4.1). The condition is serious. The more common chronic open-angle glaucoma causes no redness of the eye.
Iritis or Iridocyclitis. Iritis (more strictly iridocyclitis) is an inflammation of the iris alone or of the iris and ciliary body, often manifested by ciliary flush (Figure 4.2). The condition is serious.Herpes Simplex Keratitis. Herpes simplex keratitis is an infection of the cornea caused by the herpes simplex virus (Figure 4.3). This form of keratitis is common, potentially serious, and can lead to corneal ulceration or scarring. Characteristic dendrites can often be seen in the corneal epithelium.
Conjunctivitis. Conjunctivitis is hyperemia of the conjunctival blood vessels (Figure 4.4). Causes fall into several categories including bacterial, viral, or allergic; exposure to chemical irritants (including eye drops); or mechanical irritation (eg, eyelashes or foreign bodies). Conjunctivitis is common and ofteot serious.
Episcleritis. Episcleritis is an inflammation (often sectoral) of the episclera, the vascular layer between the conjunctiva and the sclera. The condition is uncommon and has the following features: no discharge, not serious, possibly allergic, and often tender over the inflamed area.
Associated With Soft Contact Lenses. A red eye associated with soft contact lenses can be due to poor fit or inadequate lens hygiene. Symptoms can range from mild conjunctival or superficial corneal irritation to a more serious, vision-threatening infection of the cornea. Referral to an ophthalmologist is advised to interpret the subtle slit-lamp findings.
Scleritis. Scleritis is an inflammation (localized or diffuse) of the sclera (Figure 4.5) that is uncommon, often protracted, and usually accompanied by pain, which may be severe. A violaceous hue of sclera may indicate serious systemic disease such as a collagen vascular disorder.
Adnexal Disease. Adnexal disease affects the eyelids, lacrimal apparatus, and orbit and includes dacryocystitis, stye, and blepharitis. A red eye can also occur secondary to lid lesions (such as basal cell carcinoma, squamous cell carcinoma, or molluscum contagiosum), thyroid disease, and vascular lesions in the orbit.Subconjunctival Hemorrhage. A subconjunctival hemorrhage is an accumulation of blood in the potential space between the conjunctiva and the sclera (see Figure 5.10); it is rarely serious.Pterygium. Pterygium is an abnormal growth consisting of a triangular fold of tissue that advances progressively over the cornea, usually from the nasal side (Figure 4.7). It is usually not serious. Localized conjunctival inflammation may be associated with pterygium. It is associated with ultraviolet exposure and occurs more frequently in tropical climates. Surgical excision is indicated if the pterygium starts to encroach on the visual axis.Keratoconjunctivitis Sicca. Keratoconjunctivitis sicca, commonly called dry eye, is a disorder involving the conjunctiva and sclera resulting from lacrimal deficiency. It is usually not serious. Abrasions and Foreign Bodies. Hyperemia can occur in response to corneal abrasions or foreign-body injury.
Corneal Ulcerations. Loss of the integrity of the corneal epithelium accompanied with infection or inflammation can result in an ulcer with associated hyperemia. Often the normally clear cornea appears hazy or white in the area of the ulcer. Mucus secretions in the eye (called mattering) and pain are common as well as photophobia.
Secondary to Abnormal Eyelid Function. Bell palsy, thyroid ophthalmopathy, or other conditions can cause ocular exposure and corneal breakdown and may present with a red eye. Lagophthalmos, or poor lid closure, is also commonly seen in comatose patients and can result in exposure keratitis, corneal ulceration, and blindness. Eyelids that do not appose the eye well can cause exposure problems and a red eye. An eyelid that turns in toward the eye with the lashes contacting the globe surface can result in pain, photophobia, tearing, and redness of the eye.
SYMPTOMS OF A RED EYE.
In the symptoms of a red eye that follow, a symbol (!) by the heading indicates a danger signal.
Blurred Vision (!) Blurred vision often indicates serious ocular disease (see “Reduced Visual Acuity” in the following section, “Signs of a Red Eye”). Blurred vision that improves with blinking suggests a discharge or mucus on the ocular surface.
Severe Pain (!) Pain may indicate keratitis, ulcer, iridocyclitis, scleritis, or acute glaucoma. Patients with conjunctivitis may complain of a scratchiness or mild irritation but not of severe pain.
Photophobia (!) Photophobia is an abnormal sensitivity to light that accompanies iritis, either alone or secondary to corneal inflammation. Patients with conjunctivitis have normal light sensitivity.
Colored Halos (!) Rainbow-like fringes or colored halos seen around a point of light are usually a symptom of corneal edema, often resulting from an abrupt rise in intraocular pressure. Therefore, colored halos are a danger signal suggesting acute glaucoma as the cause of a red eye.
Exudation. Exudation, also called mattering, is a typical result of conjunctival or eyelid inflammation and does not occur in iridocyclitis or glaucoma. Patients will often complain that their lids are “stuck together” on awakening from sleep. Corneal ulcer is a serious condition that may or may not be accompanied by exudate.
Itching. Although it is a nonspecific symptom, itching usually indicates an allergic conjunctivitis.
Reduced Visual Acuity (!) Reduced visual acuity suggests a serious ocular disease, such as an inflamed cornea, iridocyclitis, or glaucoma. It never occurs in simple conjunctivitis unless there is associated corneal involvement.
Ciliary Flush (!) Ciliary flush (see Figure 4.2) is an injection of the deep conjunctival and episcleral vessels surrounding the cornea. It is seen most easily in daylight and appears as a faint violaceous ring in which individual vessels are indiscernible to the unaided eye. Ciliary flush is a danger sign often seen in eyes with corneal inflammation, iridocyclitis, or acute glaucoma. Usually, ciliary flush is not present in conjunctivitis.
Conjunctival Hyperemia. Conjunctival hyperemia (see Figure 4.4) is an engorgement of the larger and more superficial bulbar conjunctival vessels. A nonspecific sign, it may be seen in almost any of the conditions causing a red eye.
MANAGEMENT OR REFERRAL. The following conditions either require no treatment or may be appropriately treated by a primary care physician. Patients with chronic, unilateral blepharitis should be referred to an ophthalmologist to rule out a malignant process such as sebaceous cell carcinoma or squamous cell carcinoma. Cases requiring prolonged treatment or those in which the expected response to treatment does not occur promptly should also be referred to an ophthalmologist. (See Table 4.3 for a summary of instructions for patients to follow.)
BLEPHARITIS. Response to the treatment of blepharitis, or inflammation of the eyelid, is often frustratingly slow, and relapses are common. The inflammation of the eyelid can primarily be in the anterior aspect of the lid such as in staphylococcal blepharitis or posterior aspect of the lid as in rosacea blepharitis. Treatment should address the following considerations.
Lid Hygiene. Warm compresses (tap water on clean washcloth) can be applied for 3 to 5 minutes, each morning and before bedtime. If lids are oily, follow with lid scrubs using dilute baby shampoo (2 drops shampoo in 2 oz. water).
Staphylococcal Infection. Staphylococcal infection (Figure 4.15) may be present. If so, it should be treated with application of appropriate antibiotic ointment (bacitracin or erythromycin) to the lid margin at night for 1 week.
Associated Acne Rosacea/Meibomian Gland Dysfunction. These symptoms should be treated with doxycycline 100 mg twice a day and tapered to once a day for 2 months or longer. Artificial tears may be applied 4 to 8 times a day as needed for symptoms of dryness.
Scalp Seborrhea. Treatment with antidandruff shampoos can improve symptoms of seborrheic blepharitis (Figure 4.16).
Contact Dermatitis.Contact dermatitis (Figure 4.17) can masquerade as blepharitis. A careful history of the lid redness associated with application of medication helps make the diagnosis. For example, the glaucoma medication brimonidine can produce a red eye with erythematous, swollen lids that have a dry “leathery” texture. Any ocular medication or cosmetics can be associated with similar clinical findings. Discontinuing the offending product should result in improvement in symptoms within 48 hours, but healing may take up to 2 weeks.
STYE AND CHALAZION. A stye, or hordeolum, is an acute, usually sterile, inflammation of the glands or hair follicles in the eyelid. Hordeola can be categorized as external or internal, according to where the inflammation is located in the lid (Figures 4.18 and 4.19). A chalazion is a chronic inflammation of a meibomian gland in the eyelid that may develop spontaneously or may follow a hordeolum (Figure 4.20).
A persistent or recurring lid mass should undergo biopsy because it may be a rare meibomian gland carcinoma or squamous cell carcinoma of the lid rather than a benign chalazion. The mainstays of treatment are the following:
Apply warm compresses to the eyelid 4 times a day for 3 to 5 minutes. Massage the lid and lash line to encourage the glands to open up and drain. Apply topical ocular antibiotic ointment to the lash line and over the area if there is tenderness and infection is suspected. Rarely, oral antibiotics may be indicated if there is a secondary bacterial infection. Refer the patient for incision and curettage of the lesion if there is no resolution in 3 to 4 weeks.
SUBCONJUNCTIVAL HEMORRHAGE. In the absence of blunt trauma, hemorrhage into the subconjunctiva, the potential space between the conjunctiva and the sclera, requires no treatment and, unless recurrent, no evaluation (see Figure 5.10). Causes include a sudden increase in ocular venous pressure, such as occurs with coughing, sneezing, vomiting, or vigorous rubbing of the eye. Many subconjunctival hemorrhages occur during sleep. If recur-rent, an underlying bleeding disorder should be considered. Blood pressure should be measured, as marked elevation can result in subconjunctival hemorrhage.
CONJUNCTIVITIS. There is no specific medicinal treatment for viral conjunctivitis, although patients should be instructed in proper precautions to prevent contagion. Here are some treatments often recommended: Apply cool compresses periodically throughout the day.
Use artificial tear drops if irritation occurs. Apply antibiotic eye drops 4 to 6 times a day if bacterial infection is suspected (sulfacetamide, gentamicin, or any broad-spectrum topical antibiotic). Minimize spread to other family members and co-workers (eg, washing hands after touching eye secretions, no sharing of towels).
It cannot be emphasized too strongly that corticosteroids have limited use in treatment of infectious conjunctivitis. Eye drops containing a combination of antibiotics and corticosteroids should be used only under the close observation of an ophthalmologist.
Disease of the Conjunctiva. CONJUNCTIVAL SPOROTRICHOSIS.
Ocular sporotrichosis is a chronic infection caused by Sporothrix schenckii, a fungus found in soil and vegetative material. Sporotrichosis may be localized to the conjunctiva as a primary infection or may be secondary to involvement of the lid and face. The first evidence of infection in the skin of the eyelid is the appearance of a hard, spherical, elastic movable, nontender nodule that later becomes attached to the skin. The nodule is initially pink, then purple, and finally black and necrotic. This lesion has been described as a sporotrichotic chancre. Multiple subcutaneous nodules appear along the course of the lymphatics draining the area. Numerous soft, yellow, granulomatous nodules, which may ulcerate, develop in the palpebral or bulbar conjunctiva of the involved eye. The conjunctival ulcers usually discharge a small amount of purulent material. The preauricular and submandibular lymph nodes are grossly enlarged and may suppurate. There are few other findings, and the patient does not usually appear systemically ill.
The organism grows in 3 to 5 days on Sabouraud agar. Biopsy of the nodules may also reveal the organism if special stains are used. Cutaneous and subcutaneous sporotrichosis responds to orally administered iodides. Therapy begins with a saturated solution of potassium iodide, 1 ml in a glass of water three times daily. The dose is increased by 0.5 to 1 ml/day until a daily dose of 9 to 12 ml is reached. To avoid recurrence, iodides should be continued for 4 to 6 weeks after clinical resolution. Since the dosage of iodide is large and can cause thyroid dysfunction, it is best to consult an internist or endocrinologist.
CONJUNCTIVAL SYPHILIS
This photograph depicts a child with a bilateral eye condition known as interstitial keratitis (IK), a stigma related to congenital syphilis. This photograph depicts a child with a bilateral eye condition known as interstitial keratitis (IK), a stigma related to congenital syphilis. Conjunctival syphilis is caused by Treponema pallidum and may occur during the primary, secondary, or tertiary stages of the disease. In primary syphilis the conjunctival lesion is an indolent ulcer with an indurated margin and a gray base. The lid may be involved and is markedly swollen. Healing of the ulcer is followed by a dense scar. Secondary syphilis of the conjunctiva is characterized by multiple granulomatous nodules or a diffused, rose red, jelly-like thickening of the tarsal conjunctiva. An acute granulomatous iridocyclitis is usually present in the early secondary stage of dissemination accompanied by other secondary manifestations in the skin and mucous membranes. In tertiary syphilis (gumma), the conjunctiva may be involved as a result of syphilitic tarsitis. Regional lymph nodes are often enlarged in all three stages of syphilis. Complications such as uveitis, pannus, perforation, and panophthalmitis may occur. Diagnosis is confirmed by darkfield examination of scrapings or exudates and serologic tests (VDRL and fluorescent treponemal antibody-absorption testing). Treatment is the systemic administration of penicillin; the dose depends on the stage of the disease. In addition, use of topical tetracycline and warm compresses is appropriate for the conjunctival and subconjunctival lesions.
Viral conjunctivitis. Although either herpes simplex virus type 1 (HSV-1) or type 2 (HSV-2) can cause neonatal conjunctivitis, up to 70% of neonatal herpetic infections have been attributed to the genital strain, HSV-2.34 Most neonatal HSV-1 infections seem to be related to contact with active infections (“fever blister” or “cold sores”) in the immediate family during the perinatal period. HSV-2 is usually transmitted during passage through the birth canal or by transplacental mechanisms. Fortunately, virus shedding from the cervix at time of delivery is a rare event, occurring in only 0.1% to 0.4% of deliveries. Even if a mother with an active herpetic genital infection delivers vaginally, there is only a 40% to 60% chance that her child will become infected.37 Culturing for herpes is recommended as a routine antenatal screening test. In as many as 60% of neonatal infections, the mother has no antecedent herpetic symptoms. Approximately 12% of women with antecedent genital herpes shed virus asymptomatically. Mothers with histories of genital herpes should be watched closely and cultured frequently for herpes throughout pregnancy. If there is a positive culture in the immediate prepartum period, serious consideration should be given to cesarean section delivery to reduce the chance of exposure to HSV during delivery. Neonatal conjunctivitis related to HSV typically occurs within the first 2 weeks postpartum and may be unilateral or bilateral. It may be the first presentation of a herpes infection, or it may follow vesicular lesions on the skin or lid margins.
Unless the patient has herpetic keratitis, there is no specific diagnostic clue. Findings include nonspecific lid edema, moderate injection of the bulbar conjunctiva, and usually nonpurulent, often serosanguineous, discharge. Microdendrites or geographic ulcers, rather than typical herpetic dendrites, are the most typical signs of corneal involvement iewborns. The exudate contains mononuclear cells or, if there is a conjunctival membrane, polymorphonuclear leukocytes.
Clinical suspicion is enhanced by a maternal history of herpetic infection, the presence of a dendrite, or evidence of herpetic infection elsewhere on the body.
FOLLICULOSIS. Folliculosis describes a condition, usually in children, in which follicles occur in the conjunctiva, without other signs of inflammation, such as hyperemia or discharge. This lymphoid tissue in the conjunctiva is analogous to the lymphoid hyperplasia of tonsils in children. In children with underlying folliculosis, the occurrence of a bacterial conjunctivitis can sometimes be interpreted as follicular conjunctivitis. Marked folliculosis is most common in children from the age of 4 or 5 until adolescence. However, the presence of a few follicles in the conjunctiva of adults is not unusual. Folliculosis occurs in both the upper and lower conjunctiva. On the upper tarsus, clinically insignificant follicles are frequently found at the superior border of the tarsus, which corresponds to the lowermost portion of the visible evened upper lid. Follicles on the central part of the upper tarsal plate suggest a pathologic process.
In chronic folliculosis in young children it has not been possible to identify any infective agent. However, it is possible that chronic folliculosis may be a response to a chronic viral infection similar to that seen in tonsillar tissue in some children.
ACUTE FOLLICULAR CONJUNCTIVITIS. Acute follicular conjunctivitis usually has an acute onset, often unilateral at first, with involvement of the second eye within a week. It is frequently accompanied by preauricular lymphadenopathy on the side of the affected eye. The syndromes to be considered in patients with acute follicular conjunctivitis include:
· Pharyngoconjunctival fever (PCF). Epidemic keratoconjunctivitis (EKC). Herpesvirus hominis (herpes simplex) keratoconjunctivitis. Newcastle disease virus conjunctivitis. Inclusion conjunctivitis. Other chlamydial infections (zoonoses). Acute hemorrhagic conjunctivitis. Rubella.
Among the points to be considered in the differential diagnosis of acute follicular conjunctivitis are accompanying skin lesions, upper respiratory infections, keratitis, discharge, accompanying systemic illness, age, and occupation.
Acute follicular conjunctivitis occurs at all ages. Although newborns do not develop conjunctival follicles readily, they are susceptible to the organisms that cause these syndromes, including adenoviruses, chlamydial agents, and herpesvirus.
Epidemic Keratoconjunctivitis. Epidemic keratoconjunctivitis (EKC) presents as an acute follicular conjunctivitis that is not accompanied by respiratory symptoms and only rarely by low-grade fever. It is usually unilateral at onset with ipsilateral preauricular lymphadenopathy. The patient often complains of a foreign body sensation and occasionally, in the more severe cases, of periorbital pain. The conjunctivitis usually runs a 7- to 16-day course. However, it is the corneal involvement that sets EKC apart from the other forms of adenovirus conjunctivitis (Fig. 2).
In the first week of the disease a patient may have a diffuse superficial epithelial keratitis. However, after the fifth day many patients develop slightly elevated focal epithelial lesions that stain with fluorescein; the development of these lesions is associated with a marked foreign body sensation. Subepithelial opacities then form under these focal epithelial lesions. The epithelial component then gradually fades, and usually disappears by the 30th day. The subepithelial opacities may linger, slowly disappearing within 3 months in some patients, but persisting for 2 years or longer in others.
Herpes Zoster and Epstein-Barr Virus Infections.Other viruses in the herpes group that involve the conjunctiva include the varicella-zoster agent and the Epstein-Barr virus (EBV). In varicella, pustules and phlyctenlike lesions occur in the conjunctiva or at the limbus and are probably sites of virus proliferation. The varicella-zoster virus localizes in the dorsal root ganglia of the spinal cord and the extramedullary ganglia of the cranial nerves. In herpes zoster, the recurrent skin disease occurs by proliferation of the virus in the distribution of the affected peripheral nerves.
The EB virus is the main cause of infectious mononucleosis, a disease characterized by extensive lymphadenopathy, fever, lymphocytosis, hepatitis, pharyngitis, and occasional conjunctivitis, which is sometimes follicular. These responses are probably due to widespread proliferation of the virus in affected organs, and in circulating lymphoctyes. The EB virus is probably responsible for systemic diseases other than mononucleosis, and can be incriminated in ocular disease by antibody studies. Ocular manifestations attributed to EB infection include nummular keratitis, stromal keratitis, severe vitritis, punctate retinitis, and multifocal choroditis with panuveitis.
Rubella and Rubeola. German measles (rubella) is usually accompanied by nondescript, catarrhal conjunctivitis. A mild form of follicular conjunctivitis may also occur and, more rarely, mild superficial punctate epithelial keratitis. Permanent corneal disease due to childhood rubella has not been described. Congenital rubella infection, however, causes microphthalmia, cataract, retinitis, iridocyclitis, corneal clouding, strabismus, nystagmus, nasolacrimal duct obstruction, and viral dacryoadenitis. Rubeola (measles) does not produce follicular conjunctivitis, but it causes a marked catarrhal, papillary conjunctivitis. Patients complain of tearing, pain, discharge, and photophobia. In addition, pale, discreet, avascular spots may appear on the conjunctiva or caruncle that are morphologically identical to the Koplik’s spots seen on the buccal mucosa. Superficial punctate keratitis, superficial pannus, and interstitial keratitis (rarely) are also seen in rubeola. In developing countries, keratomalacia and suppurative keratitis occur frequently after measles. Devastating corneal complications, including perforation of the globe, may occur, especially in the presence of malnutrition, vitamin A deficiency, and concurrent herpes simplex keratouveitis.
CHRONIC FOLLICULAR CONJUNCTIVITIS. Any follicular conjunctivitis that persists for more than 16 days is regarded as chronic follicular conjunctivitis. These disorders may have an acute onset or develop insidiously; they can persist for months or years. Listed below and in Table 3 are the syndromes to be considered in patients with chronic follicular conjunctivitis:
· Trachoma. Inclusion conjunctivitis and other chlamydial infections. Toxic follicular conjunctivitis. Molluscum contagiosum. Drug induced. Ocular cosmetics. Bacterial (Moraxella lacunata and others). Axenfeld’s chronic follicular conjunctivitis. Chronic follicular keratoconjunctivitis of Thygeson. Parinaud’s oculoglandular syndrome. Rosacea blepharoconjunctivitis. Lyme Disease.
Trachoma. In the early stages, trachoma presents as a chronic follicular conjunctivitis with follicles on the upper tarsal plate (Fig. 8) and a varying degree of papillary hypertrophy and inflammatory infiltration of the conjunctiva, often so intense that the follicles are obscured. As the disease progresses, there is scarring of the conjunctiva, with fine linear scars in mild cases and broader confluent scars in more severe cases. There is no evidence that resistance to infection and healing are a result of scarring because severe active trachoma, follicular hypertrophy, and conjunctival infiltration continue to occur in the presence of severe conjunctival scarring (see Fig. 10). In patients with severe scarring, tear deficiency syndromes and dacryostenosis occur as late complications. The major blinding complication, however, is lid deformation with trichiasis and entropion (Fig. 12), usually of the upper lid, which lead to corneal ulceration and scarring.
Corneal involvement in trachoma includes epithelial keratitis, marginal and central infiltrates, superficial vascularization, shallow epithelial (pannus) ulcers, limbal swelling, and limbal follicles and their cicatricial sequelae, Herbert’s pits. The characteristic epithelial keratitis of trachoma occurs on the upper half of the cornea, but it is not limited to this area. Inflammatory infiltrates of the cornea appear most frequently at the limbus and range in size from small lesions seen only with a slit lamp to large trachoma pustules that are actually small corneal ulcers at the site of an infiltrate. Neovascularization in trachoma appears to be a response to the marginal corneal infiltration, which is induced by chlamydial and bacterial infection. The pannus consists of a superficial fibrovascular membrane and associated infiltration and scarring (Fig. 13). With trachoma, the vascular pannus is more extensive at the superior limbus although it is present in all the corneal meridians.
Alterations in the extracellular matrix components and collagen metabolism occur in the conjunctival tissue, with new collagen type V formation in active trachoma and scarred trachoma. The conjunctival tissue from patients with active trachoma contains an increased amount of collagen types I, II, and IV. Scarred trachoma is characterized by a marked increase in basement membrane collagen IV and a marked decrease in types I and III.
Risk factors. Poverty, excessive distance to water, small amounts of water used by the household, the presence of flies, and poor hygiene are risk factors for trachoma. Active trachoma is associated with young age and close contact between people. Discharge from the eyes and nose may be a source of reinfection. It is likely that host factors also play a role in a person’s susceptibility to C. trachomatis disease.
Health education. Interventions to prevent scarring trachoma by reducing active infection include promotion of facial washing. It has been shown that it is possible to increase facial cleanliness through education even where there is a water shortage. Trachoma transmission by flies could be reduced by encouraging the use of latrines and also by insecticides.
MEDICAL TREATMENT. Historically, sulfonamides were found to be effective in controlling trachoma; however, they caused unacceptable side effects in a few cases and thus had to be discontinued. Topical tetracycline ointment was shown to be effective in individual cases when applied once daily for 6 weeks or for 5 days a month for 6 months. However, poor compliance and rapid reinfection when only individual cases were treated meant that this was not successful at the community level. Treatment with azithromycin as a single oral dose (20 mg/kg) is safe and has been shown to be at least as effective as 6 weeks of supervised tetracycline ointment. This has been a major advance, and in 1998, a new international initiative was launched by the Edna McConnell Clark Foundation and Pfizer Inc, in collaboration with the WHO, in which the drug is provided free to national trachoma control programs in selected countries.
Azithromycin is a key component of SAFE and is more successful in curing chlamydia and improving clinical outcome, with the added advantage of ease of treatment. It has been recommended that in areas where trachoma is moderately prevalent (more than 35% of children affected), treatment should be undertaken annually; but in hyperendemic areas (more than 50% of children affected), it should be given biannually. However, azithromycin-resistant pneumococci have been isolated from the nasopharynx of children after two mass treatments, suggesting the need to monitor resistance.
SURGICAL TREATMENT. Preventing blindness from trachoma, even when transmission is stopped, still requires surgery for the irreversible scarring and trichiasis affecting large numbers of the already exposed population. The operation of choice for trachomatous trichiasis is bilamellar tarsal rotation. It is important that this surgery is done before corneal scarring has started to develop, and earlier uptake of surgery requires health education.
To prevent blinding trachoma, it will not be necessary to eradicate ocular chlamydial infection, but only to reduce the frequency of reinfection in endemic populations to such an extent that severe conjunctival scarring, leading to trichiasis and corneal scarring with subsequent visual loss, is prevented.
LYME DISEASE. Ocular findings in Lyme disease were first noted in the original observations of Steere and colleagues in 1977. Animal studies have shown that the Lyme spirochete invades the eye early and may remain dormant. Nonspecific follicular conjunctivitis may occur in up to 10% of patients during the flulike illness of Lyme disease. The conjunctivitis is usually self-resolving and does not lead to long-term sequelae. Associated episcleritis, photophobia, and subconjunctival hemorrhages have beeoted. Other ocular manifestations of the disease include keratitis, which is most common within a few months of the onset of disease. This may be nummular with nonstaining opacities, or it may be interstitial with keratouveitis, neovascularization, scarring, and corneal edema. The corneal effects are likely to be secondary to a delayed hypersensitivity response to the Borrelia burgdorferi antigen.
Inflammatory syndromes, such as vitritis and uveitis, may occur. Neuro-ophthalmic manifestations include neuroretinitis, multiple cranial nerve palsies, optic atrophy, and disc edema. In endemic areas, Lyme disease may be responsible for 25% of new-onset seventh nerve palsy.
