The lids are composed of skin, cartilage, connective tissue, and muscle. The lid muscles not only enable blinking, but also, as a component of the mimetic musculature, communicate the emotional state of the individual. Normal lid function is very important in contactology. With each blink, the surface of the eye is covered with the salt-rich aqueous secretion of the lacrimal glands, and with the fatty secretion of the Meibomian glands that are found at the lid margins.

Normal blinking is involuntary and rhythmic when the eyes are adequately wetted, and more frequent when they are dry. Tear flow increases in response to irritation. Chronic excessive tear flow is due to partial or total obstruction of the lacrimal pathway or to an abnormal position of the lid.

The most important tasks of the lid are to prevent drying, visual glare, and ocular injury. These tasks depend upon normal lid function, especially in the contact lens wearer. Each blink distributes the tear fluid over the anterior surface of the contact lens and simultaneously slides the contact lens up and down over the cornea, thus enabling exchange of tear fluid in the space between the corneal surface and the posterior surface of the contact lens, the so-called tear lens. Lid closure also cleans the contact lens of any particulate foreign matter deposited on its surface through the tear fluid, or from the ambient environment.

The skin of the lid may suffer from any ailment known to dermatology. The most common in contact lens wearers is eczema, which tends to take the form of squamous blepharitis in patients suffering from allergic or ectopic dermatitis. Allergic reactions can be induced both by the lens itself and by the chemicals in lens care products.

Symptoms: Uncontrollable bilateral lid contraction.

Clinical findings: Lid opening, whether active or passive, is difficult or even impossible.

Every contact lens fitter is familiar with the reflex increase in lid pressure and spasmodic lid closure that are often encountered during the initial fitting phase. Failure to improve over time may make the further wearing of contact lenses impossible. These problems are less likely to occur with soft lenses.

Symptoms: The upper lid cannot be adequately elevated.

Clinical findings: The upper lid overlaps the limbal area of the cornea regardless of the direction of gaze. Severe ptosis may impair vision.

Ptosis is usually easy to recognize because of the narrowing of the palpebral fissure, which is most often unilateral, though of variable extent. The diagnosis is made by observing that the midpoint of the upper lid is not contiguous with the upper edge of the pupil, but partially or completely overlaps the pupil when the patient looks straight ahead. If more than half of the pupil is covered, vision will be considerably impaired and treatment will be required, perhaps involving a surgical procedure.

Ptosis occasionally occurs as a complication after hard contact lenses are worn for many years. Levator function is impaired by chronic irritation due to the contact lens. This form of ptosis is thus often accompanied by decreased tearing, chronic conjunctivitis, or conjunctival scarring. Scarring is usually seen in the setting of advanced giant papillary conjunctivitis (GPC) and is easy to observe when the lids are ectropionized.

Occasionally, supposedly lost contact lenses, or fragments thereof, can burrow into the subtarsal lid tissue and cause a ptosis, appearing months later.

Differential diagnosis: Neurological disorders, particularly myasthenia gravis, should be included in the differential diagnosis. Pseudoptosis due to blepharospasm can be tested for by instillation of local anesthetic, which abolishes it.

Prophylaxis: Ptosis can be prevented by changing the lenses regularly, and by not wearing them during periods of seasonal allergy.

Symptoms: Swelling of upper and lower lids, discomfort, and fatigue.

Clinical findings: Swollen, thickened lids.

In contrast to inflammatory or traumatic lid swelling, primary allergic lid edema in contact lens wearers is not accompanied by hyperemia. The upper and lower lids are markedly swollen, and the skin of the lids is devoid of its normal wrinkles. Gentle pressure with a fingertip produces an indentation that lasts for several minutes.

Lid edema has both internal and external causes; in contact lens wearers, it is usually caused by allergy to the lens or to lens care products. Artificial tears may soothe the discomfort of lid edema but are often themselves responsible for it.

Differential diagnosis: Aside from allergy to the lens and lens care products, lid edema may be caused by cardiovascular disease, renal failure, generalized allergy, and other systemic illnesses, and usually calls for general medical evaluation and treatment. Hyperacute lid swelling (Quincke’s edema) is due to generalized allergy or to poisoning.

Prophylaxis: Persons suffering from allergies should not wear contact lenses during critical seasons or in allergen-rich environments.

Fig. 34 Pseudoptosis due to chronic irritation after many years of wearing moderately well-tolerated hard lenses; an associated finding in a patient with GPC.

Fig. 35 Upper lid edema, soft contact lens, allergy to quaternary ammonium bases.

Fig. 36 Ectopic dermatitis of the lids; allergy to cobalt, nickel, synthetic materials, mercurial compounds and solutions.

Symptoms: Itching of the upper lid, especially the lid margins.

Clinical findings: Reddening and swelling of the lid skin; scaling, loss of lashes.

Infectious and allergic lid changes are usually seen in combination among contact lens wearers. Infectious blepharitis is usually secondary to a preceding allergic reaction. Squamous blepharitis is classically characterized by reddening, swelling, and scaling of the lid margins. Its causes and course are identical to that of localized eczema occurring elsewhere on the skin. Squamous blepharitis is sometimes restricted to the lid margins, in the spaces between the lashes. The lashes are brittle, poorly developed, or absent, and they may grow in an abnormal direction.

Fig. 37 Squamous blepharitis of unknown cause; mild form.

Fig. 38 Squamous blepharitis caused by chlorhexidinecontaining lens care solution.

Fig. 39 Marked allergic blepharitis; wrinkling of the corner of the lid due to HEMA allergy.

Fig. 40 Eczema of the upper lid; allergy to PVP.

Fig. 41 Eczema of upper and lower lids; allergy to benzalkonium chloride (BAC) and chlorhexidine.

Fig. 42 Matting of the upper lid cilia due to recurrent blepharitis.

Fig. 43 Marked upper and lower lid eczema caused by allergy to chlorbutanol, thiomersal, and BAC.

Fig. 44 Blepharoconjunctivitis; purulent crusting on the lashes; typical problem caused by bad hygiene.

Fig. 45 Bacterial blepharoconjunctivitis with staphylococcal superinfection.

Fig. 46 Swelling of upper and lower lids; allergic blepharitis; allergy to thiomersal and BAC; bacterial superinfection.

Fig. 47 Marked lower lid dermatitis in gel lens wearer with severe diabetes mellitus; epithelial scaling; superinfection with Candida.

Fig. 48 Allergic blepharoconjunctivitis in an aphakic eye; superinfected with Haemophilus; intraocular inflammation.

Fig. 49 Ectopic dermatitis; scaling along the lid margin; allergy to cosmetics and contact lens products.

Fig. 50 Bacterial blepharitis; conjunctivitis; purulent material seeping through the lashes on the upper lid.

Fig. 51 Typical squamous blepharitis with scaly deposits on the lashes; allergy to penicillin and thiomersal.

Fig. 52 Bacterial infection of the lid margins; purulent deposits on the lashes; staphylococcal infection in contact lens wearer with AIDS.

Fig. 53 Severe blepharitis with loss of lashes; nodular concretions of the lipid-secreting glands on the lid margin, caused by allergy to lens care products. Further testing revealed a nickel allergy (intolerance to piercing).

Fig. 54 Ulceration of the lower lid at the inner canthus; severe allergy to multiple preservative agents and lens materials, cobalt allergy, intolerance to piercing.

Symptoms: Lid pain. When the lid margin is involved, there is a foreign-body sensation on opening or closing of the lids.

Clinical findings: Tissue defect, bleeding.

The inner surface of the lid and the tarsal conjunctiva are often injured by the edges of defective lenses. These injuries, though usually superficial, may nevertheless cause permanent scarring that impairs the function of the lid, leading to chronic corneal erosion or recurrent keratitis.

Defective soft corneoscleral lenses are particularly likely to injure the sclera or cornea, in addition to the lid. The problem usually arises because the lenses are worn for longer periods than recommended (whether they are of the disposable or brief-wear variety, or are part of a system of exchangeable lenses).

The wearing of hard PMMA lenses for many years can also chronically traumatize the tarsal conjunctiva, leaving scars that may make further lens wearing intolerably uncomfortable.

The conjunctiva reacts promptly to endogenous and exogenous irritants and is thus a sensitive indicator of contact lens complications. Practically any problem caused directly or indirectly by contact lenses is associated with conjunctival changes (though not all conjunctival changes are due to contact lenses). Lid disease caused by contact lenses is associated with changes of the tarsal conjunctiva, and corneal disease caused by contact lenses is associated with changes of the bulbar conjunctiva.

Changes of the lids and cornea should be sought whenever a contact lens wearer presents with conjunctivitis, because, in contact lens wearers, the lids, cornea, and conjunctiva constitute a functional unit. The complications that arise are generally due to a disturbance of the physiological, metabolic, and toxicological interrelationship of these three structures. This interrelationship is the central theme of contactological research and accounts for a major part of the ophthalmologist’s work in caring for the contact lens-wearing patient.

The conjunctiva is a mucous membrane that extends from the lid margins to the limbal region of the globe. It is a well vascularized, translucent membrane with two portions, tarsal (palpebral) and bulbar. The tarsal conjunctiva is tightly bound to the underlying tissue on the inner surface of the lid, while the bulbar conjunctiva is more loosely applied to the sclera, except in the limbal area. The fornix (zone of transition between the tarsal and bulbar conjunctiva) lies at the most remote area of the surface of the eyeball and forms the base of the conjunctival sac (cul-de-sac).

The conjunctiva is a mucous membrane containing many secretory cells; the most important of these for contact lens wearers are the goblet cells. When their function is impaired, lacrimation becomes deficient, the eye dries out, and a foreign body sensation ensues that makes lens-wearing intolerable.

Symptoms: Severe itching while wearing lenses; burning; increased secretions; impaired visual acuity (VA).

Clinical findings: Hyperemia, follicular swelling; papillary hypertrophy of the tarsal conjunctiva; recurrent deposition of hydrophobic material on lens surfaces.

Hyperemia, follicular swelling, and papillary hyper-trophy of the tarsal conjunctiva are the classic signs of GPC in contact lens wearers, a complication that is not at all rare in wearers of hard or soft lenses. This condition is becoming significantly more common, not least because of air pollution.

Both in etiology and in phenotype, GPC resembles vernal conjunctivitis (vernal catarrh), a condition seen in the springtime in patients with an allergic predisposition. GPC is caused by proteins from the lacrimal fluid that are presumably denatured by lens-hygiene solutions and thereby become immunologically active. Deposited on the surface of the lens, these proteins act as antigens, to which antibodies then bind. The sandwich of lens, antigen, and antibody rubs on the tarsal conjunctiva, causing increased conjunctival swelling and secretions—the vicious cycle of GPC.

The hallmark of GPC is the coating of the contact lens surface with a strongly adherent protein layer, which pierces the film of tear fluid over the lens within seconds of insertion, leading to diminished visual acuity and increased glare. The case history generally points to the diagnosis: The patient wears lenses without complications for weeks or months and then, suddenly, a problem develops. A few minutes after lens insertion the patient experiences burning, chafing, and itching in the eyes. Tears and a film deposited on the surface of the lens impair visual acuity within a few seconds after the eyes are opened, and until the next blink. Conjunctival secretions cause the eyelids to stick together and limit the mobility of the contact lens during blinking and eye movements.

Fig. 55 Scarring of the tarsal conjunctiva of the lower lid after decades of wearing hard PMMA lenses.

Fig. 56 Tarsal conjunctiva 1 hour after test wear of a rigid contact lens for myopia; injection of conjunctival vessels.

Fig. 57 Isolated hyperemia of the upper lid conjunctiva caused by protein deposits on the anterior surface of a soft contact lens.

Fig. 58 Mild hyperemia of the tarsal conjunctiva; mechanical irritation of the conjunctiva on the initial fitting of a hard lens.

Fig. 59 Injection of the upper lid conjunctiva; focal conjunctival atrophy after 18 years of wearing hard lenses for keratoconus; tear deficiency.

Fig. 60 Upper-lid hyperemia and edema; allergic reaction to chlorhexidine.

Fig. 61 Upper-lid hyperemia; mild cockscomb swelling of the conjunctiva indicating chronic irritation; hard contact lens worn for 6 years.

Fig. 62 Early GPC, characterized by hyperemia and moderate papillary hypertrophy; soft hydrophilic lens.

Fig. 63 GPC reaction on upper lid; marked hypertrophy of the papillae; hyperemia.

Fig. 64 GPC stage 1–2; isolated tarsal conjunctival hyperemia; papillary hypertrophy in the region of the fold.

Fig. 65 GPC stage 2–3; papillary hypertrophy; identical picture to vernal conjunctivitis.

Fig. 66 GPC in a CAB lens wearer; stage 2; fluorescein staining.

Fig. 67 GPC follicular swelling in the region of the lower conjunctival fold; soft contact lens worn for 3 months.

Fig. 68 GPC stage 3; fluorescein staining; PMMA lens worn for 11 years.

Fig. 69 Marked GPC, stage 3; fluorescein staining; gel contact lens worn for 4 months.

Fig. 70 GPC; scarring; 9 months of wearing a fluorosilicone carbonate lens.

Differential diagnosis: Other conditions resembling GPC include other allergic reactions of the conjunctiva, auto-immune conditions, and (typically in the springtime) primary vernal conjunctivitis independent of the wearing of contact lenses.

Prevention: Meticulous daily lens hygiene, frequent use of protein removers, and a temporary cessation of lens wearing during critical seasons will reduce the risk of GPC.

Symptoms: Severe itching and tearing; difficulty closing the lids.

Clinical findings: Marked swelling of the conjunctiva that may project beyond the lid margin, with clear or sanguineous secretion. Mild proptosis.

Conjunctival edema in contact lens wearers is usually due to lens-cleaning solutions, or to wetting solutions or artificial tears that are supposed to enhance wearing comfort. Acute conjunctival edema may occur as early as the fitting phase, particularly when relevant details of the case history are not obtained or disregarded, such as a previous episode of allergic blepharitis or conjunctivitis requiring treatment. Patients with certain types of allergies, for example to thiomersal, a common constituent of eye drops and contact lens solutions, also tend to develop acute conjunctival reactions when contact lenses are fitted.

Acute chemosis is a complication that usually appears within a few minutes of the initial insertion of a lens or the initial use of a lens care product or variety of eye drops. Most of the affected patients were previously treated at some time with eye drops or ointments and were presumably sensitized in this way. An adequate history helps to identify and prevent this problem: patients should be asked at the initial prefitting visit whether they have ever had complications from the use of eye drops or ointments, or difficulty tolerating them. If so, the risk is high that the initial insertion of contact lenses will cause marked conjunctival swelling within minutes, so that the fitting will have to be terminated.

Fig. 71 Acute chemosis 45 seconds after insertion of a soft contact lens stored in Polyquad; known allergy to quaternary ammonium bases.

Fig. 72 Acute hemorrhagic chemosis after the application of an artificial tear solution to a dry eye; hard lens; BAC allergy.

Fig. 73 Acute bulbar conjunctival injection; immediate reaction to PMMA lens; because of the pressure exerted by the contact lens, the edema is limited to the area not covered by the lens.

Fig. 74 Acute bulbar conjunctival injection; immediate reaction to chlorhexidine and thiomersal; the lens contact zone remains visible for a few minutes after the lens is removed.

Fig. 75 Jelly-like swelling of the tarsal and bulbar conjunctiva after many years of astringent eye drop abuse while wearing soft contact lenses.

Fig. 76 Acute chemosis in a gel lens wearer with known allergies to various plant species, after a brief stay in a garden. Remnants of organic foreign matter in the cul-de-sac, pollen dust on the lens surface.

Prophylaxis: Acute chemosis can often be prevented by meticulous history-taking.

Symptoms: Usually no pain or discomfort, but patients are highly distressed by the prominently visible abnormality.

Clinical findings: Deep-red hematoma under the conjunctiva, which is usually somewhat raised.

Multiple microhemorrhagic spots are often present in the conjunctiva of contact lens wearers, usually in the perilimbal region where the lens rests, but occasionally in the tarsal conjunctiva. These easily visible lesions appear spontaneously, often sending the highly distressed patient to the emergency service of the eye clinic. There is usually no pain or impairment of visual acuity.

Blood begins to pool under the bulbar conjunctiva shortly after lens insertion, usually arising from a site of injury near the limbus and spreading out evenly under the conjunctiva of the lower half of the eye. When a soft lens is still on the eye, the hematoma in the area covered by the lens is somewhat compressed and thus paler than elsewhere. There is no pain, discomfort, or corneal edema, unless the eyes are rubbed.

Fig. 77 Hyperacute, severe conjunctival edema; hemorrhagic form; immediate reaction after the initial insertion of a hard contact lens wetted with an artificial tear solution; longstanding abuse of astringent eye drops, known thiomersal allergy.

Fig. 78 Perilimbal hemorrhage of the bulbar conjunctiva caused by wearing a soft lens with edge defects.

Fig. 79 Conjunctival lesion caused by wearing a disposable soft lens with an edge defect for several months longer than the recommended time.

Fig. 81 Extensive bleeding into the conjunctiva at the 6 o’clock position caused by an edge defect of a gel contact lens.

Fig. 82 Massive conjunctival bleeding after wearing a hard contact lens with edge defects; 42-year-old patient with coagulopathy. Further wearing of contact lenses is contraindicated.

Fig. 83 Cutting injury of the bulbar conjunctiva from a defective lens edge; disposable gel contact lens; prescribed wearing time exceeded.

Fig. 84 Cutting injury of the conjunctiva and cornea; 8-year-old soft hydrophilic corneoscleral lens in situ; large, sharp-edged defect.

Fig. 85 Perilimbal, superficial conjunctival bleeding caused by improperly processed edge of a PMMA lens.

Fig. 86 Conjunctival hemorrhage in the sulcus region; mechanical irritation due to poor fitting.

Conjunctival hyperemia in contact lens wearers has a variety of causes, which can often be distinguished from one another by the location and appearance of hyperemia. Focal conjunctival hyperemia is most often due to mechanical irritation of the conjunctiva in a circumscribed area from a dried-out, ill-fitted, defective, or deposit-coated lens; annular perilimbal injection is usually of toxic or allergic etiology. Generalized conjunctival hyperemia (i.e., of the entire conjunctiva, including the area under the contact lens) is usually caused by mechanical irritation or infection; other causes include inadequate lacrimation, allergic or toxic processes, and radiation injury. Whether focal or generalized, the hyperemic area is superficially discolored (brick-red); the reactively dilated vessels of the conjunctiva are always bright red and freely mobile over the scleral surface. (This is not so in cases of conjunctival hyperemia secondary to underlying deep or scleral infection.)

Mechanical Irritation and Injury

Symptoms: Eye-rubbing; foreign body sensation; tearing.

Clinical findings: The entire bulbar conjunctiva is injected and appears brick-red.

Conjunctival vasodilatation as a rapidly occurring response to a foreign body is routinely observed when a patient first starts to wear contact lenses. Surface vessels of the bulbar conjunctiva are greatly enlarged during this period. This response is normal in the initial phase of contact lens wear, but pathological at later times.

Fig. 87 Severe conjunctival hemorrhage after a punch in the eye; the gel lens remained intact.

Fig. 88 Conjunctival hyperemia; mechanical irritation from a hard contact lens characterized by an even, brick-red discoloration of the entire bulbar conjunctiva.

Fig. 89 Focal lateral bulbar conjunctival hyperemia from a foreign body reaction; hard contact lens; typical brick-red color.

Fig. 90 Focal lateral conjunctival hyperemia from a foreign body reaction; rigid contact lens.

Fig. 91 Focal limbal conjunctival hyperemia from a foreign body reaction; gel contact lens.

Fig. 92 Focal conjunctival hyperemia with accentuation near the limbus, due to a foreign body reaction; soft contact lens.

Fig. 93 Diffuse conjunctival injection from a foreign body reaction to a rigid contact lens; tear deficiency.

Fig. 94 Severe conjunctival swelling; erythema from a foreign body reaction in a patient wearing gel contact lenses. Eversion of the lower lid reveals an insect wing as the cause.

Fig. 95 Diffuse conjunctival injection as a foreign body reaction to a hard contact lens worn for many hours.

Fig. 96 Diffuse conjunctival irritation after test wear of a gel contact lens for 4 hours; tear deficiency.

Fig. 97 Mild, diffuse conjunctival hyperemia; tear deficiency; gel contact lens with desiccated anterior surface.

Fig. 98 Marked, deep-red conjunctival discoloration due to both superficial and deep vasodilatation; mechanical irritation; soft, hydrophilic contact lenses.

Fig. 99 Marked, diffuse brick-red coloration of the conjunctiva in bacterial conjunctivitis.

Fig. 100 Bacterial conjunctivitis due to Haemophilus in a patient wearing gel contact lenses.

Fig. 101 Massive conjunctival injection, mildly accentuated in the area contacted by the (soft, hydrophilic) contact lens; bacterial conjunctivitis due to Pseudomonas.

Fig. 102 Bacterial conjunctivitis; gel contact lens; diffuse conjunctival hyperemia without accentuation in the area contacted by the lens.

Fig. 103 Bacterial conjunctivitis; soft contact lens; streptococcal infection.

Fig. 104 Toxic hyperemia, most severe in the perilimbal area; thiomersal reaction; standard aphakic fitting.

Fig. 105 Mechanical hyperemia; perilimbal white ring of compression from steeply fitted lens; tear deficiency.

Fig. 106 Bacterial conjunctivitis; pus in the lower cul-de-sac; staphylococcal infection.

Fig. 107 Diffuse conjunctival infection and hemorrhage; viral conjunctivitis; hard contact lens.

Fig. 108 Viral conjunctivitis; diffuse brick-red to deep-red discoloration of the conjunctiva, with hemorrhage; soft contact lens wearer.

Fig. 109 Fungal conjunctivitis; diffuse vasodilatation with mild paralimbal accentuation; soft contact lens; candidiasis in a diabetic patient.

Symptoms: Burning; itching; foreign body sensation; tearing.

Clinical findings: Marked injection; microhemorrhages; swelling of the plicae; minimal secretion.

Unlike bacterial conjunctivitis, viral conjunctivitis is rarely related to contact lens wearing; it is usually a manifestation of systemic viral infection, for example influenza. Nonetheless, though primary viral conjunctivitis is the most common type, fitters of contact lenses must be aware that poor hygiene on their part may cause an outbreak of iatrogenic epidemic keratoconjunctivitis (EKC).

Differential diagnosis: Viral conjunctivitis is distinguished from bacterial conjunctivitis by the watery secretion in the cul-de-sac, and by the swollen plicae (particularly in EKC). Signs of infection often involve the cornea as well. Cases that fail to improve with treatment should arouse suspicion of another type of infection, such as fungal or parasitic. Foreign body reactions as well as toxic and allergic processes must be excluded.

3. Fungal Infection

Symptoms: Foreign body sensation; eye-rubbing; sensation of heat and dryness.

Clinical findings: Marked surface injection accompanied by marked, generally livid, deep injection; whitish secretions in the cul-de-sac.

Fungal infection is rare in healthy contact lens wearers and is usually seen in those suffering from immune compromise, diabetes, or other metabolic disorders. Candida albicans and Aspergillus niger are often the cause. Fungal infections are difficult to treat. Corneal involvement or infiltration into the interior of the globe poses a major threat to vision.

Fungal infections are much more common in soft lens wearers than in hard lens wearers, as the soft lens is an ideal fungal culture medium. The organisms take the water they need from the aqueous compartment of the lens, and nutrients and electrolytes from the lacrimal fluid.

Fungal infections are best diagnosed by microbial culture of the secretions from the cul-de-sac. Microscopic examination of secretions and of the contact lens itself may reveal fungal hyphae. Demonstration of the responsible fungal organism serves to exclude other possible causes of conjunctivitis, for example GPC.

Differential diagnosis: Fungal infections of the anterior segment are not always readily distinguishable from bacterial or viral infections, particularly because mixed flora may be present. Microbial culture is required.

Prophylaxis: In general, patients at risk of fungal infection should not wear contact lenses. Those who do wear lenses must comply rigidly with the recommended lens-care routine.

Focal conjunctival hyperemia is due to a spatially restricted process; thus, in contact lens wearers, it is usually found in the limbal area, (i.e., at the periphery of the contact lens). The etiology of hyperemia in contact lens wearers (as in other persons) may be toxic, allergic, metabolic, mechanical, or inflammatory.

3-O’Clock and 9-O’Clock Limbal Hyperemia

Symptoms: Increased foreign body sensation; increased tear flow.

Clinical findings: Marked dilatation of the vessels at the 3-o’clock and 9-o’clock positions. These sites are often covered with a mildly raised, yellowish deposit.

Conjunctival injection near the limbus at the 3-o’clock and 9-o’clock positions in a hard lens wearer implies an inadequate cushion of tear fluid between the lens and the eye. The lens mechanically irritates the conjunctiva and cornea during horizontal saccades. The problem may be caused by inadequate lacrimation or by poor fitting. Diagnostic assessment includes quantitative tear analysis, inspection of the sit of the lens, and slit-lamp examination of the cornea after staining.

Differential diagnosis: Conjunctival injection near the limbus can also result from local lesions of the conjunctiva and cornea.

Fig. 110 Marked deep-red discoloration of the conjunctiva due to candidiasis in a soft contact lens wearer with AIDS.

Fig. 111 Marked conjunctival vasodilatation at the 3-and 9-o’clock positions in a hyperopic wearer of hard contact lenses with tear deficiency.

Fig. 112 Focal conjunctival hyperemia at the 4-to 5-o’clock position; injury of the edge of the cornea through improper fitting.

Fig. 113 Isolated perilimbal conjunctival hyperemia under a hard corneoscleral contact lens. Mechanical irritation by excessively tight fitting in the haptic zone.

Symptoms: The discomfort is rarely severe and is usually limited to itching and a feeling of dryness.

Clinical findings: Markedly dilated vessels in the paralimbal or perilimbal region.

Isolated, superficial perilimbal injection is a pathological finding seen almost exclusively in wearers of soft contact lenses. It is easily mistaken for ciliary injection, which indicates an intraocular process. The affected vessels in ciliary injection are livid in color, more deeply situated, and more finely reticulated.

An arc-shaped, superficial perilimbal area of injection (sometimes accompanied by fine microhemorrhages) is usually due to faulty lens fitting. If the edge of the lens is too steep or too firmly applied to the conjunctival surface, it can compress the bulbar conjunctiva in the region of the corneal sulcus. On the other hand, if the lens is too flat, its edges can scrape the perilimbal conjunctiva. The differential diagnosis is straightforward: If the perilimbal redness disappears within 10 minutes of lens removal, the lens was too flat; if in the same period of time a reactive hyperemia appears, the lens was too steep.

Redness from wearing lenses with abrasive edges or edge defects disappears within 1–2 hours after the lenses are removed. Hyperemia of this type is only rarely associated with corneal injury.

Deep perilimbal vasodilatation indicates an entirely different situation. Deep-red or livid vessels, located below the surface and parallel to the limbus, are a definite indication of corneal damage or an intraocular process. The usual cause in contact lens wearers is toxic keratopathy in reaction either to the lens material or to a lens care product.

A finding of deep and livid (rather than superficial and brick-red) vasodilatation limited to the limbal region is classically termed “ciliary injection.” The dilated vessels are located in the perilimbal sclera and are an indication of deep corneal and intraocular changes, such as iritis or uveitis, which are very rarely related to the wearing of contact lenses. It may prove difficult to determine by examination whether the finding is superficial (perilimbal) or deep (ciliary), particularly in protracted cases. A rule of thumb for the crucial differentiation of primary intraocular problems from contact lens complications is that the latter, unlike the former, generally resolve after the lenses are removed.

Fig. 114 Focal conjunctival hyperemia at the limbus; hard contact lens; tear deficiency.

Fig. 115 Marked, diffuse conjunctival hyperemia; tear deficiency; soft contact lens; marked drying of the anterior surface of the lens.

Fig. 116 Diffuse vasodilatation of the bulbar conjunctiva with accentuation at the limbus; dry eye; gel contact lens.

Fig. 117 Diffuse bulbar conjunctival vasodilatation with accentuation at the limbus at the area of contact of the soft contact lens; deposits on the lens surface; tear deficiency.

Fig. 118 Brick-red perilimbal injection from poorly seated soft contact lens; hyperopia + 6.5 D.

Fig. 119 Limbal hyperemia; diffuse bulbar conjunctival vasodilatation due to a toxic keratopathy; gel lenses; PMMA intolerance.

Fig. 120 Limbal injection in toxic keratopathy; hyperemia of the bulbar and tarsal conjunctiva. Soft hydrophilic contact lens.

Fig. 121 Firered limbal hyperemia in toxic keratopathy; reaction to lens cleaning agents; gel contact lens.

Fig. 123 Toxic conjunctival hyperemia, especially marked at the limbus, caused by PMMA allergy.

Fig. 124 Perilimbal hyperemia from toxic damage to the conjunctiva and cornea; thiomersal allergy; soft contact lens.

Fig. 125 Pseudoepiscleritic irritation after several weeks of wearing a defective contact lens.

The sclera, the stabilizing outer layer of the eye, is almost entirely composed of strong, interwoven, opaque collagen fibers; at the limbus, it makes a seamless transition to the transparent cornea. The sclera is completely shielded from the outside world by the conjunctiva. It is only loosely bound to the inner layer of the conjunctiva and to Tenon’s capsule, with enough slack to ensure that saccadic eye movements in any direction are not hindered. Isolated pathological changes of the sclera are only rarely the result of wearing contact lenses.

Symptoms: As in conjunctival inflammation: itching, foreign body sensation; rarely tearing; a sensation of pressure on the globe.

Clinical findings: Scleral vessels are a deep, livid color; concomitant conjunctival injection.

Pseudoepiscleritis can be caused by the haptic of hard or soft corneoscleral lenses rubbing against the surface of the eyeball, or by the wearing of lenses with defective edges. Vasodilatation indicates mechanical irritation or infection of the sclera; scleral infection is usually secondary to conjunctivitis or keratitis. The deep-seated, livid discoloration that typifies these scleral changes is clearly distinct from the intense, brick-red color of the overlying conjunctiva and its vessels.