Exogenous material on, under, or embedded within the conjunctiva or sclera; commonly dirt, glass, metal, or cilia. Patients usually note foreign body sensation and redness; may have corneal staining, particularly linear vertical scratches due to blinking with a foreign body trapped on the upper tarsal surface. Good prognosis.

• Remove foreign body; evert lids to check tarsal conjunctiva.

• Topical broad-spectrum antibiotic (polymyxin B sulfate-trimethoprim [Polytrim] drops or bacitracin ointment qid).

Laceration

Partial-thickness or full-thickness cut in conjunctiva with or without partial-thickness cut in the sclera; very important to rule out open globe (see below); good prognosis.

• Seidel test for suspected open globe (see below).

• Topical broad-spectrum antibiotic (gatifloxacin [Zymar] or moxifloxacin [Vigamox] qid).

• Conjunctival and partial-thickness scleral lacerations rarely require surgical repair.

Open Globe

Full-thickness defect in eye wall (cornea or sclera), commonly from penetrating or blunt trauma; the latter usually causes rupture at the limbus, just posterior to the rectus muscle insertions, or at previous surgical incision sites; double penetrating injuries are called perforations; an open globe may also be due to corneal or scleral melting.

Associated signs include lid and orbital trauma, corneal abrasion or laceration, wound dehiscence, positive Seidel test (see Laceration section in Chapter 5), low intraocular pressure, flat or shallow anterior chamber, anterior chamber cells and flare, hyphema, peaked pupil, iris transillumination defect, sphincter tears, angle recession, iridodialysis, cyclodialysis, iridodonesis, phacodonesis, dislocated lens, cataract, vitreous and retinal hemorrhage, commotio retinae, retinal tear, retinal detachment, choroidal rupture, intraocular foreign body or gas bubbles, and extruded intraocular contents. Guarded prognosis.

Figure 4-1 (A) Conjunctival foreign body, demonstrating a fragment of corn husk embedded in the conjunctiva. (B) Conjunctival foreign body, demonstrating a grasshopper leg embedded in the conjunctiva. (C) Same patient as in (B), demonstrating multiple vertical corneal abrasions from a grasshopper leg in the superior tarsal conjunctiva. Such a pattern of linear abrasions suggests a foreign body under the upper eyelid, and therefore the examiner should always evert the eyelid to inspect for this.

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Figure 4-2 Conjunctival laceration with gaping edges.

Figure 4-3 Full-thickness corneoscleral limbal laceration with wound gape. Note discontinuity of slit-beam as it crosses the wound edge (arrowhead).

Figure 4-4 Penetrating injury with foreign body (nail) protruding from globe.

Figure 4-5 Open globe. There is a temporal full-thickness scleral laceration with uveal prolapse. Also note the extensive subconjunctival hemorrhage and upper and lower eyelid lacerations.

OPHTHALMIC EMERGENCY

• Admit for surgical exploration and repair; protect eye with metal eye shield; minimize ocular manipulations; examine globe only enough to verify the diagnosis of an open globe; remainder of examination and exploration should be performed in the operating room. Postoperatively, start antibiotics and steroids.

• Consider B-scan ultrasonography if unable to visualize the fundus.

• Consider orbital computed tomography (CT) scan or orbital radiographs to rule out intraocular foreign body; magnetic resonance imaging (MRI) is contraindicated if foreign body is metallic.

• Subconjunctival antibiotics and steroids:

Vancomycin (25 mg).

Ceftazidime (50–100 mg) or gentamicin (20 mg).

Dexamethasone (12–24 mg).

• Topical fortified antibiotics (alternate every 30 minutes):

Vancomycin (25–50 mg / mL q1h).

Ceftazidime (50 mg / mL q1h).

• Topical steroid (prednisolone acetate 1% q1–2 h initially) and cycloplegic (scopolamine 0.25% or atropine 1% tid).

• Systemic intravenous antibiotics for marked inflammation or severe cases:

Vancomycin (1 g IV q12h).

Ceftazidime (1 g IV q12h).

• Small corneal lacerations (< 2 mm) that are self-sealing or intermittently Seidel positive may be treated with a bandage contact lens, topical broad-spectrum antibiotic (gatifloxacin [Zymaxid] or moxifloxacin [Vigamox] q2h to q6h), cycloplegic (cyclopentolate 1% bid), and an aqueous suppressant (timolol maleate [Timoptic] 0.5% or brimonidine [Alphagan-P] 0.15% bid); observe daily for 5–7 days; consider suturing laceration if wound has not sealed after 1 week.

Subconjunctival Hemorrhage

Diffuse or focal area of blood under the conjunctiva. Appears bright red, otherwise asymptomatic. May be idiopathic, associated with trauma, sneezing, coughing, straining, emesis, aspirin or anticoagulant use, or hypertension, or due to an abnormal conjunctival vessel. Excellent prognosis.

• Reassurance if no other ocular findings.

• Consider blood pressure measurement if recurrent.

• Medical or hematology consultation for recurrent, idiopathic, subconjunctival hemorrhages, or other evidence of systemic bleeding (ecchymoses, epistaxis, gastrointestinal bleeding, hematuria, etc.).

Figure 4-6 Subconjunctival hemorrhage demonstrating bright red blood under the conjunctiva. As the hemorrhage resorbs, the edges may spread, become feathery, and turn yellowish (arrowhead).

Telangiectasia

Definition

Abnormal, dilated conjunctival capillary formation.

Symptoms

Asymptomatic red spot on eye; patient may have epistaxis and gastrointestinal bleeding depending on etiology.

Signs

Telangiectasia of conjunctival vessels, subconjunctival hemorrhage.

Figure 4-7 Conjunctival telangiectasia appearing as dot-like, corkscrew, irregular vessels near the limbus.

Differential Diagnosis

Idiopathic, Osler–Weber–Rendu syndrome, ataxia–telangiectasia, Fabry’s disease, Sturge–Weber syndrome.

Evaluation

• Complete ophthalmic history and eye exam with attention to conjunctiva, cornea, lens, and ophthalmoscopy.

• Consider CT scan for multisystem disorders.

• Medical consultation to rule out systemic disease.

Management

• No treatment recommended.

Prognosis

Usually benign; may bleed; depends on etiology.

Microaneurysm

Definition

Focal dilation of conjunctival vessel.

Symptoms

Asymptomatic; may notice red spot on eye.

Signs

Microaneurysm; may have associated retinal findings.

Differential Diagnosis

Diabetes mellitus, hypertension, sickle cell anemia (Paton’s sign), arteriosclerosis, carotid occlusion, fucosidosis, polycythemia vera.

Evaluation

• Complete ophthalmic history and eye exam with attention to conjunctiva and ophthalmoscopy.

• Check blood pressure.

• Lab tests: Fasting blood glucose (diabetes mellitus), sickle cell prep, hemoglobin electrophoresis (sickle cell).

• Medical consultation.

Management

• No treatment recommended.

• Treat underlying medical condition.

Prognosis

Usually benign.

Dry Eye Disease (Dry Eye Syndrome, Keratoconjunctivitis Sicca)

Definition

Sporadic or chronic ocular irritation with visual disturbance due to a tear film and ocular surface abnormality.

Etiology

Any condition that causes a deficiency or imbalance in the aqueous, lipid, or mucin components of the tear film. Dry eye can be classified by mechanism (decreased tear production or increased tear evaporation), category (lid margin disease [i.e., blepharitis, meibomitis], no lid margin disease, altered tear distribution/clearance), or severity (Table 4-1). It is usually multifactorial with an inflammatory component; tear hyperosmolarity and tear film instability create a cycle of ocular surface inflammation, damage, and symptoms.

Table 4-1

Dry Eye Severity and Treatment (DEWS recommendations)

Aqueous-Deficient Dry Eye

Characterized by abnormal lacrimal gland function causing decreased tear production.

Sjögren syndrome

Dry eye, dry mouth, and arthritis with autoantibodies (to Ro (SSA) and / or La (SSB) antigens) and no connective tissue disease (primary, > 95% female) or with connective tissue disease, including rheumatoid arthritis and collagen vascular diseases (secondary).

Non-Sjögren

Hypofunction of the lacrimal gland due to other causes:

Primary lacrimal gland deficiencies

Age-related (historically labeled KCS), congenital alacrima, familial dysautonomia (Riley Day syndrome).

Secondary lacrimal gland deficiencies

Lacrimal gland infiltration, lymphoma, sarcoidosis, amyloidosis, AIDS, graft-versus-host disease, lacrimal gland ablation or denervation.

Obstruction of the lacrimal ducts

Cicatrizing conjunctivitis (Stevens–Johnson syndrome, ocular cicatricial pemphigoid, trachoma, chemical burns, radiation).

Neurosecretory block

Sensory (corneal surgery, contact lens wear, diabetes, neurotrophic keratopathy), motor (cranial nerve VII damage, systemic medications (β-blockers, antimuscarinics, antidepressants, diuretics)).

Evaporative Dry Eye

Characterized by normal lacrimal gland function but increased tear evaporation.

Intrinsic causes

Meibomian gland dysfunction (MGD)

Primary, secondary, simple, or cicatricial (see Meibomitis and Acne Rosacea sections in Chapter 3).

Lid / globe abnormalities

Conditions that result in a malposition, lagophthalmos, or proptosis with exposure of the ocular surface (see Exposure Keratopathy in Chapter 5).

Reduced blink rate

Reading/computer work (decreases blink rate by up to 60%), Parkinson’s disease.

Medications

Systemic retinoids (Accutane).

Extrinsic causes

Vitamin A deficiency

Malnutrition or malabsorption causes conjunctival xerosis and night blindness (nyctalopia) with progressive retinal degeneration; major cause of blindness worldwide.

Topical drugs

Anesthetics, preservatives (BAK – benzalkonium chloride).

Contact lens wear

Approximately 50% of contact lens wearers have dry eye symptoms.

Ocular surface disease

Cicatrizing conjunctivitis (see above), allergic conjunctivitis.

Epidemiology

Dry eye disease is estimated to affect 5–30% of the population ≥ 50 years old and is more common in women. Associated factors include age, hormone levels (menopause, androgen deficiency), environmental conditions (low humidity, wind, heat, air-conditioning, pollutants, irritants, allergens), and smoking.

Symptoms

Irritation, dryness, burning, stinging, grittiness, foreign body sensation, tearing, red eye, discharge, blurred or fluctuating vision, photophobia, contact lens intolerance, increased blinking; symptoms are variable and exacerbated by wind, smoke, and activities that reduce the blink rate (i.e., reading and computer work).

Signs

Conjunctival injection, decreased tear break-up time (< 10 seconds), decreased tear meniscus height (< 0.20 mm), excess tear film debris, corneal filaments, dry corneal surface, irregular and dull corneal light reflex, corneal and/or conjunctival staining with lissamine green, rose bengal, and fluorescein (typically in the interpalpebral space or on the inferior cornea); may have Bitot’s spot (white, foamy patch of keratinized bulbar conjunctiva [pathognomonic for vitamin A deficiency]), conjunctivochalasis (loosened bulbar conjunctiva resting on lid margin); severe cases can cause corneal ulceration, descemetocele, or perforation. May also have signs of an underlying condition (i.e., rosacea, blepharitis, lid abnormality).

Figure 4-8 Keratoconjunctivitis sicca demonstrating superficial punctate keratitis (SPK) and filaments stained with fluorescein dye.

Figure 4-9 Dry eye due to vitamin A deficiency, demonstrating diffuse staining of cornea, inferior limbus, and interpalpebral conjunctiva with rose bengal.

Figure 4-10 Dry eye demonstrating lissamine green staining of the interpalpebral conjunctiva.

Differential Diagnosis

See above; also allergic conjunctivitis, medicamentosa, contact lens overwear, trichiasis.

Evaluation

• Complete history with attention to severity, duration, exacerbating factors, prior treatment, contact lens wear, previous eye/eyelid surgery, systemic diseases and medications. Consider using a questionnaire such as the Ocular Surface Disease Index (OSDI), Dry Eye Questionnaire (DEQ), National Eye Institute Visual Function Questionnaire (NEI VFQ-25), or McMonnies questionnaire.

• Complete eye exam with attention to lids, tear film (break-up time and height of meniscus), conjunctiva, and cornea (staining with lissamine green or rose bengal [dead and degenerated epithelial cells], and/or fluorescein [only dead epithelial cells]).

• Schirmer’s test: Two tests exist, but they are usually not performed as originally described. One is done without and one is done with topical anesthesia. The inferior fornix is dried with a cotton-tipped applicator, and a strip of standardized filter paper (Whatman #41, 5 mm width) is placed in each lower lid at the junction of the lateral and middle thirds. After 5 minutes, the strips are removed and the amount of wetting is measured. Normal results are 15 mm or greater without anesthesia (basal + reflex tearing), and 10 mm or greater with topical anesthesia (basal tearing). Schirmer’s test often produces variable results so its usefulness may be limited.

• Alternatively, consider the phenol red thread test: Similar to the Schirmer’s test but uses a special cotton thread that changes color as tears are absorbed for 30 seconds; less irritating and may be more reproducible.

• Lab tests: Consider tear lactoferrin and lysozyme (decreased), matrix metalloproteinase 9 (MMP-9) (> 40 ng/mL), tear osmolarity (> 316 mOsm / L), and impression cytology (detects reduced goblet cell density and squamous metaplasia; rarely used clinically).

• Consider corneal topography (computerized videokeratography): Irregular or broken mires with resulting abnormal topography and blank areas due to poor-quality tear film and dry spots. Surface regularity index (SRI) value correlates with severity of dry eye.

• Electroretinogram (reduced), electro-oculogram (abnormal), and dark adaptation (prolonged) in vitamin A deficiency.

• Consider medical consultation for systemic diseases.

Management

• Reduce/eliminate associated factors.

• The mainstay of therapy is topical lubrication with artificial tears up to q1h and gel or ointment qhs. Preservative-free tear formulations should be used if the frequency of administration is greater than qid.

• Additional treatment is performed in a stepwise fashion and includes: hydroxypropyl methylcellulose (Lacrisert), topical cyclosporine 0.05% (Restasis) bid for at least 3 months, short course (1–2 weeks) of topical steroid (Lotemax, Alrex, Pred Mild, or FML) bid to qid, punctal occlusion (with plugs or cautery), nutritional supplements (i.e., oral flaxseed / fish oils [omega-3 fatty acids]), bandage contact lens, moisture chamber goggles, lid taping at bedtime, and tarsorrhaphy for more severe cases. Recommendations of the 2007 Dry Eye Workshop (DEWS) are based on severity (1–4) of symptoms (discomfort, fatigue, visual disturbance) and signs (lid, tear film, conjunctiva, cornea) (see Table 4-1).

• Consider acetylcysteine 10% (Mucomyst) qd to qid for mucus strands or filaments.

• Consider autologous serum drops or Boston ocular surface prosthesis (PROSE lens) in severe cases.

• Consider oral cholinergic agonists (pilocarpine, cevimeline) to increase tear production, especially in patients with Sjögren syndrome.

• Treat underlying condition:

• Acne rosacea/blepharitis: see Chapter 3.

• Vitamin A deficiency: Vitamin A replacement (vitamin A 15,000 IU po qd).

• Androgen deficiency: Consider treatment with transdermal testosterone cream (3%) to closed eyelids, and/or topical DHEA (compounded eye drops).

• Lid malposition: Consider surgical repair.

Prognosis

Depends on underlying condition; severe cases may be difficult to manage.

Inflammation

Definition

Chemosis

Edema of conjunctiva; may be mild with boggy appearance or massive with tense ballooning.

Figure 4-11 Chemosis with extensive ballooning of conjunctiva and prolapse over lower lid nasally. Temporally, the edges of the elevated conjunctiva are delineated by the light reflexes from the tear film.

Follicles

Small, translucent, avascular mounds of plasma cells and lymphocytes found in epidemic keratoconjunctivitis (EKC), herpes simplex virus, chlamydia, molluscum, or drug reactions.

Figure 4-12 Follicular conjunctivitis demonstrating inferior palpebral follicles with the typical gelatinous bump appearance.

Figure 4-13 Large, gelatinous, tarsal follicles in a patient with acute trachoma.

Granuloma

Collection of giant multinucleated cells found in chronic inflammation from sarcoid, foreign body, or chalazion.

Hyperemia

Redness and injection of conjunctiva.

Figure 4-14 Hyperemia. The dilated conjunctival vessels produce a diffuse redness (injection).

Membranes

A true membrane is a firmly adherent, fibrinous exudate that bleeds and scars when removed; found in bacterial conjunctivitis (Streptococcus species, Neisseria gonorrhoeae, Corynebacterium diphtheriae), Stevens–Johnson syndrome, and burns. A pseudomembrane is a loosely attached, avascular, fibrinous exudate found in EKC and mild allergic or bacterial conjunctivitis.

Figure 4-15 Pseudomembrane evident as a thick yellow coating in a patient with epidemic keratoconjunctivitis.

Papillae

Vascular reaction consisting of fibrovascular mounds with central vascular tuft; nonspecific finding in any conjunctival irritation or conjunctivitis; can be large (“cobblestones” or giant papillae).

Figure 4-16 Large papillae in a patient with vernal keratoconjunctivitis. The central vascular cores are clearly visible as dots within the papillae.

Phlyctenule

Focal, nodular, vascularized infiltrate of polymorphonuclear leukocytes and lymphocytes with central necrosis due to hypersensitivity to Staphylococcus species, Mycobacterium species, Candida species, Coccidioides, Chlamydia, or nematodes; located on the bulbar conjunctiva or at the limbus; can march across the cornea, causing vascularization and scarring behind the leading edge.