epi.: sclera: conjunctiva

7/28/2019 Epi.: Sclera: Conjunctiva

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CONTINUING EDUCATION AND TRAINING

Differential Diagnosis of Ocular Disease Module 9 Part 2 SPECIALISTS IN EYECARE

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topical phenylephrine blanches the conjunc-tival vessels, and some of the vessels con-fined to Tenons capsule. By contrast, thoseassociated with the deep vascular plexusremain unaltered. Furthermore, the samevasculature cannot be manually moved overthe avascular scleral stroma.

EpiscleritisEpiscleritis is a benign, self-limiting condi-tion which typically presents with an acuteonset of hyperaemia and mild pain, withsome degree of lacrimation in one or botheyes. It is frequently recurrent and has apredilection for young adults. It is further

classified into either diffuse (simple)(Figure 1) or nodular forms (Figure 2).With the former, which is the most com-mon, the hyperaemia may be either sector-ial or diffuse and usually resolves withinseven to 10 days. Depending on the degreeof co-existing lacrimation, the patientsvision is usually unaffected. The moreaggressive nodular form is characterised bya localised, raised congested nodule. It istypically associated with more pain andadopts a longer time course. Followingrecurrent episodes, the superficial scleramay appear more translucent a conse-quence of fibre rearrangement within the

superficial sclera.

About the authorGreg Heath works both

as a part-time

optometrist in independ-

ent practice and, after

qualifying in medicine

last year, is undertakingrotations in Barnet and

Chase Farm Hospitals,

London

Whereas the last article in this module (OT 13/01/06) concentrated on the

ocular adnexa, this article will highlight those ocular maladies pertaining

to the episclera, sclera and conjunctiva. A sound knowledge of the ocular

anatomy, and its relevance to ocular disease, is essential for diagnosing

and providing an appropriate management plan for the patient.

Greg Heath BSc, MBBS, MCOptom, DipClinOptom

Module 9 Part 2Differential Diagnosis

of Ocular Disease

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Episclera and sclera

AnatomyThe sclera consists of two main layers namely the lamina fusca, which lies adja-cent to the supraciliary and suprachoroidallamellae of the uveal tract, and the episcle-ral layer anteriorly. The latter, which liesbetween the superficial scleral stroma andTenons capsule, consists of dense vascularconnective tissue.

Essentially, the vascular layers may becompartmentalised into the conjunctivalvessels, the vessels within Tenons capsule,and those confined to the deep vascular

plexus. The most superficial vessels theconjunctival vessels can be easily manual-ly moved over the underlying sclera, andconsist of tortuous arteries and straightveins. The vessels within Tenons capsule areentirely straight and adopt a radial configu-ration; these vessels can also be movedmanually over the sclera. In episcleritis, it isthese vessels which become engorged. Inepiscleritis, the episclera and Tenons cap-sule become infiltrated with inflammatorycells. The sclera, however, is spared. Thevessels confined to the deep vascularplexus, which are located in the superficialsclera, adopt maximum dilatation in scleritis.

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The episclera, sclera and conjunctivaAn overview of relevant ocular anatomy

Course code: c-2688

Figure 1Diffuse episcleritis. Note dilated bloodvessels with preservation of thenormal radial pattern of the episcleralvessels

Figure 2Nodular episcleritis. Note a whiteinflammatory nodule is present withinthe inflamed area while the rest of theepisclera is uninvolved


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Although treatment is seldom institutedapart from topical unguents or artificialtears, the nodular form may require topicalcorticosteroids in order to ameliorate thepatients symptoms.

Despite the recurrent nature of this condi-tion, a cause is seldom found. Occasionally,it may be associated with systemic diseasesuch as rheumatoid arthritis or gout.

Differential diagnosisThe main differential diagnoses are scleritis(see later), conjunctivitis (see later) and ante-

rior uveitis (Figure 3).Unlike anterior uveitis, episcleritis is not

associated with cells or flare in the anteriorchamber, and the patients vision is rarelyaffected. In addition, the degree of photo-

phobia experienced by the patient harbour-ing uveitis is far greater than those sufferingfrom episcleritis.

ScleritisScleritis is associated with oedema and infil-

tration of the entire sclera and, if leftuntreated, its effects on the patients visionare met with far more deleterious conse-quences than its benign counterpart, epis-cleritis. Typically, the patient experiencessevere eye pain, which is deep and boring innature and frequently radiates to the fore-head, brow or jaw. It is noteworthy that thepain is not acute in the majority of cases,but gradual in onset.

In approximately 50% of cases, the aeti-ology may be ascribed to a systemic dis-ease. The most common systemicprogenitor is rheumatoid arthritis. Othersystemic maladies associated with scleritisinclude Wegeners granulomatosis (a sys-temic condition that has a predilection forsmall and medium sized vessels), relapsingpolychondritis (affecting cartilage) and pol-yarteritis nodosa (collagen vascular diseaseaffecting small and medium sized vessels).

Scleritis may be secondary to a wholehost of infectious agents ranging from bac-terial organisms, such as pseudomonasaeruginosa and staphylococcus aureus, toviruses such as varicella zoster. That said,scleritis secondary to fungal agents isexceedingly rare.

Surgically induced scleritis is a well-docu-

mented complication, which characteristi-cally affects females and occurs six monthsfollowing the initial procedure. Thus, a fullocular history should be sought in at riskpatients. Patients who have also receivedbeta irradiation or mitomycin C followingremoval of a pterygium are also at risk.

Anatomically, scleritis may be subdividedanteriorly and posteriorly. The former is themost common mode of presentation,accounting for over 95% of cases. Theanterior form may be further subdividedinto either non-necrotising (Figure 4) andnecrotising (Figure 5). Recognising theform is essential, as the gravity associated

with the latter is such that high doseimmunosuppressants are required in orderto abrogate the signs and symptoms.

Anterior non-necrotising scleritis may beeither diffuse or nodular. Although thisform of scleritis is similar in appearance toepiscleritis, it can be readily differentiatedby the fact that the engorged vasculaturecannot be entirely constricted with topicalphenylephrine; the pain is typically moresevere and the onset is more gradual thanepiscleritis. Moreover, the scleral nodulecannot be moved over the underlying tissuein the nodular form of the disease.

Necrotising scleritis with inflammation is

characterised by avascular patches as aresult of vascular occlusion. The surround-ing vascular network is engorged. Leftuntreated, scleral necrosis ensues resultingin overlying conjunctival ulceration.

Extensive necrosis may result in the scleraadopting a blueish hue, due to theenhanced visualisation of the underlyinguvea secondary to scleral thinning.

Further ocular sequelae associated withthis form of scleritis include staphyloma for-

mation and anterior uveitis, with concomi-tant spread into further uveal tissues. Thus,practitioners should be aware that whileanterior uveitis may be one of the conditionsthat must be differentially diagnosed withscleritis, it may actually co-exist. The pres-ence of a co-existing uveitis compounds therisk to the eye owing to attendant sequelae,namely cataract, glaucoma and macularoedema.

As mentioned earlier, management of thenecrotising form requires far more potenttherapy than its non-necrotising counter-part. Therapy ranges from oral corticos-teroids alone to the use of other specialisedimmunosuppressive agents, such ascyclophosmamide or cyclosporin. For thosepatients in whom the degree of necrosis isextensive, an intravenous regimen may berequired in order to salvage the eye.

Although unlikely to be encountered ineveryday optometric practice, scleromalaciaperforans (an anterior, necrotising scleritiswithout inflammation), which is associatedwith a painless extension of scleral thinningsuch that the whole sclera adopts a bluehue, is frequently bilateral and is associatedwith patients who suffer from rheumatoidarthritis. The prognosis is poor in these

patients for two reasons: first, there is noeffective ocular treatment; and second, thepresence of scleromalacia perforans conferswidespread vascular disease with a con-comitant high mortality risk.

Owing to the gravity associated with thisocular malady, it remains incumbent on allpractitioners to be cognisant with the signsand symptoms of this disease. It is impera-tive that patients suspected of sufferingfrom scleritis are referred to a hospital eyedepartment that same day, so that a treat-ment regimen can be started.

Conjunctiva

AnatomyThis mucous membrane may be subdividedinto three compartments the palpebral,forniceal and bulbar conjunctivae. Whilstthe palpebral component is firmly adheredto the tarsal plate, the tarsal conjunctiva israther loose in comparison. The bulbar con-junct iva envelopes the anter ior sclera.Although it is tightly bound to the underly-ing Tenons capsule at the limbus, its attach-ments to the structure elsewhere are looser.

Histologically, the conjunctiva consists ofan epithelium and stroma. The rich vascularnetwork is confined to the stromal layer and

is separated from the epithelium via a base-ment membrane. The superficial region ofthe stroma contains adenoid tissue and isnot present at birth. In fact, it takes threemonths to develop. The significance of this

Figure 3Anterior uveitis keratic precipitatesseen on lower half of cornea

Figure 4Non-necrotising (diffuse) anterior scleritis.Note the vascular engorgement has a darkviolaceous colour, with loss of the normalradial pattern of the episcleral vessels(pupil is dilated)

Figure 5Necrotising anterior scleritis. Note largearea where the sclera is ulcerated and theoverlying conjunctiva and episclera are

missing


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is that neonates and infants below this ageare not able to elicit a follicular response inthe presence of conjunctival inflammation.

The conjunctiva contains numerousglands consisting of mucin secretors, suchas goblet cells, and the accessory lacrimal

glands of Krause and Wolfring. In the con-text of conjunctival disease, it is importantto appreciate that chronic inflammatory dis-orders may result in augmentation of thegoblet cells, whereas destructive lesions,such as chemical burns, are associated withreduction of the same said secretors.

Signs and symptomsInflammation of the conjunctiva (conjunc-tivitis) may be due to a multitude of causes,including bacteria, viruses, allergens andchlamydia. Although the definitive diagno-sis relies on positive laboratory identificationof the contagion, such a methodologicalapproach is seldom adopted in the clinicalsetting. Rather, recognition of co-existingsigns and symptoms is utilised by the practi-tioner to determine the appropriate treat-ment regimen.

Conjunctivitis per se may be associatedwith non-specific symptoms irrespective ofthe causative agent. These include lacrima-tion, photophobia and generalised ocularirritation. However, a patient complaining ofpain implies co-existing corneal involve-ment. Although itching may be associatedwith keratoconjunctivitis sicca, it is virtuallypathognomonic of allergic eye disease.

Discharge, resulting from exudates fromthe dilated conjunctival vasculature, mayvary in consistency depending on thecausative agent. Whereas a purely mucoiddischarge is typically seen in patients suffer-ing from vernal conjunctivitis or keratocon-junctivitis sicca, a mucopurulent form isobserved in chlamydial and mild bacterialcases. A thick purulent discharge isobserved in severe bacterial infections. Thedischarge associated with viral and allergiceye disease, by contrast, is watery in nature.

Subconjunctival haemorrhages, whenassociated with generalised conjunctivalinflammation, are frequently associated

with viruses. That said, bacteria such asstreptococcus (strep.) pneumoniae may alsoproduce such a haemorrhagic reaction.

Conjunctival oedema, known as chemo-sis, is associated with allergic eye diseaseand severe inflammation of any cause and isdue to exudation of protein rich fluidthrough the inflamed blood vessels.

Follicles, which consist of hyperplasticlymphoid tissue, characteristically appear asslightly elevated lesions encircled by bloodvessels. They are typically seen in medica-mentosa (reaction to topical agents) andviral or chlamydial conjunctivitis.Interestingly, folliculosis may occur especial-

ly in children despite a paucity of conjuncti-val inflammation.

Papillae consist of hyperplastic conjuncti-val tissue with central vessels that arereplete with inflammatory cells, such as

polymorphonuclear leukocytes, eosinophils,plasma cells and lymphocytes. They aremost commonly observed in the palpebralconjunctiva. Unlike follicles, the presence ofpapillae is far less effective diagnosticallyand is associated with a plethora of oph-

thalmic conditions such as allergic eye dis-ease, bacterial conjunctivitis and, of course,contact lens wear.

Pseudomembranes, consisting of coagu-lated exudates adherent to the conjunctivalepithelium, may be associated with severeadenoviral and gonococcal infections. Truemembranes, which infiltrate the superficiallayers of the conjunctiva, are rarely encoun-tered in practice as their presence is indica-tive of severe infections such as diphtheria.Pseudomembranes may be differentiatedfrom their deeper counterpart clinically,since they can be peeled off with relativeease. Moreover, bleeding is not typicalunlike the attempted removal of a truemembrane.

As mentioned in the previous article,knowledge of the lymphatic drainage sys-tem is important. To reiterate, the upper lidand lateral canthus drain to the preauricularnode, whilst the lower lid and medial can-thus drain to the submandibular nodes. Thepresence of lymphadenopathy frequentlyco-exists with viral and chlamydial infec-tions. A marked lymphadenopathy is alsoseen in a rare condition, known as Parinaudoculoglandular syndrome a granuloma-tous conjunctivitis with very painful ipsilat-

eral lymphadenopathy that is associatedwith numerous causes.

Investigation of conjunctivitisAlthough laboratory investigations remainthe diagnostic method par excellence inidentifying the aetiology of conjunctivitis,they are seldom used in everyday practice.That said, the use of such techniques is rec-ommended in the following cases: first, inpatients suspected of harbouring chlamydi-al infections, owing to the fact that referralto a genitourinary clinic has to be madetogether with notification of sexual part-ners; second, in patients with fulminant

purulent conjunctivitis in order that themost appropriate antibiotic may be pre-scribed; and third, in all cases of neonatalconjunctivitis.

Conjunctival manifestationsSince it is beyond the scope of this article toprovide a definitive description of conjuncti-val pathology, various conditions of thoselikely to be encountered by optometrists willbe described with their relevant differentialdiagnoses. The following should thereforeact as a trustworthy reference for those con-ditions likely to be encountered in everydaypractice. Notwithstanding the fact that con-

junctival tumours are rare, the inclusion ofsome is necessary as they may easilybecome confused with their benign, com-mon, degenerative counterparts such aspterygium and pingueculae.

Acute conjunctivitis

Hyperacute onsetA conjunctivitis which rapidly develops intoa fulminant inflammatory state within a 12-hour period is usually referred to as hypera-

cute. The pathogen most likely to beresponsible is the gram negative bacteria,neisseria gonorrhoea. Recognition of thiscondition is imperative as the organism iscapable of penetrating an intact cornea.Therefore, failure to treat this condition maylead to corneal perforation and endoph-thalmitis.

Typically, the discharge is purulent innature and there is marked chemosis, con-junctival papillae and preauricular lym-phadenopathy. Owing to the direconsequences of this condition, patients areusually admitted to hospital and, once cul-tures of the eye have been taken, areadministered antibiotics intravenously. Thus,any patient presenting to practice with adense purulent discharge should be referredimmediately to the hospital eye depart-ment.

Acute onset

Simple bacterial conjunctivitis

Simple bacterial conjunctivitis is frequentlyseen in children and arises from direct con-tact of infected secretions. Commonpathogens include strep. pneumoniae andstaph. epidermidis. Classically, the eyelids

are stuck together in the morning as a resultof overnight accumulation of exudates.Although the degree of hyperaemia is max-imal in the fornices, the conjunctivae arediffusely hyperaemic. The discharge trans-forms from a watery consistency to a moreviscous mucopurulent form several dayslater. The fact that the condition will resolvewithout any treatment, application ofbroad-spectrum antibiotics, in combinationwith a daily eyelid hygiene regimen servesto expedite resolution of the condition.

Viral conjunctivitis

The most common type of virus to affect

the conjunctiva is adenovirus. Althoughthere are numerous strains of the virus, sixare notable with regard to conjunctival dis-ease. Serotypes 3, 4, 5 and 7 are responsi-ble for pharyngoconjunctival fever. Childrenare predisposed to this infection and fre-quently present with a co-existing upperrespiratory tract infection. Serotypes 8 and19 cause the more ominous epidemic kera-toconjunctivitis. It is highly contagious andis spread easily by hand to eye contact,inadequate disinfection of instruments (e.g.applanation tonometer prisms) and solu-tions. Whilst systemic features are commonand keratitis rare in pharyngoconjunctival

fever, the keratitis associated with the epi-demic form, by contrast, is common andsevere.

The presentation consists of acute hyper-aemia, photophobia and watery discharge.


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Owing to the contagious nature of this con-dition, the conjunctivitis is frequently bilat-eral. The eyelids are frequently oedematousand the discharge watery in nature.Conjunctival follicles are observed in thepalpebral conjunctiva and fornices.

Although not diagnostic, lymphadenopathy,which is frequently tender, may be present.In severe cases, pseudomembranes and sub-conjunctival haemorrhages may also occur.The keratitis associated with the conditiondevelops approximately eight to 10 days fol-lowing the onset of symptoms. Althoughthe lesions are confined to the epitheliuminitially, they soon become subepithelial andthen anterior stromal. It has been suggestedthat the deeper opacifications represent theimmune response to the virus.

Unfortunately, the quest for an effectivetopical anti-adenoviral agent remains elu-sive. As such, treatment is usually merelysupportive with topical lubricants. However,topical steroids and non-steroidal anti-inflammatories may be administered inpatients with severe symptoms or poorlyresolving keratitis.

Allergic conjunctivitis

Allergic rhinoconjunctivitis is the most com-mon form of ocular and nasal allergy. It isessentially a type I hypersensitivity reactioninvolving the cross-linking of immunoglobu-lin E (IgE) bound to mast cells that results inthe release of histamine and other pro-inflammatory mediators. It may be further

classified into a seasonal form (also knownas hay fever conjunctivitis) and a perennialform. Although the latter is invariably milderin nature, it is more persistent. Patients whosuffer from the perennial form are usuallyallergic to fungal spores and the house dustmite. Although it is difficult to avoid fungalspores, abrogation of the house dust mitemay be achieved through daily hoovering athome especially the bed sheets.

The conjunctiva may not appear tremen-dously hyperaemic due to the concomitantconjunctival oedema. The lids are also fre-quently oedematous, and small papillae areinvariably present on the tarsal conjunctivae.

Fortunately, the condition is innocuousand is amenable to both conservative andtopical treatment. Indeed, the optometrist is

well placed to deal with this form of allergiceye disease. Conservative measures includethe frequent application of cold compress-es, together with eye baths in order todilute the allergen. The optometrist canmanage this ocular malady with topical

mast cell stabilisers, such as sodium cromo-glycate and nedocromil sodium, topicalantihistamines such as levocabastine oremedastine, or combination mast cell sta-biliser and antihistamine agents, such asolopatadine.

Vernal and atopic conjunctivitis

Both conditions are the result of Type I andType IV hypersensitivity reactions combined.In other words, their pathology incorporatesboth IgE and a cell mediated immuneresponse involving T-lymphocytes.

Patients with vernal conjunctivitis are fre-quently atopic, suffering from conditionssuch as asthma and eczema. The conditiontypically develops after five years of age andrarely persists after 25 years. Indeed, it fre-quently resolves around the age of puberty.Despite the condition adopting a perennialtimescale, there are frequent exacerbationsin the Spring and Summer months. Cornealectatic conditions, such as keratoconus andpellucid margin degeneration, are more fre-quently encountered in those suffering fromvernal conjunctivitis.

The hallmark sign of vernal conjunctivitisare giant cobblestone papillae on the uppereyelid. In time, although the papillae dimin-

ish in size and become more separated, theymay remain indefinitely. The limbal form ischaracterised by raised, white, mucoid nod-ules, known as Trantas dots. These nodulesare composed of degenerative eosinophils.The keratopathy affiliated with this condi-tion ranges from superficial punctuate ero-sions, which may progress to shieldulceration, and the formation of cornealplaques. The latter occurs when the base ofthe ulcer becomes coated with dessicatedmucus, making it refractory to wetting andre-epithelialisation.

Although mast cell stabilisers may beemployed prophylactically, their use during

acute exacerbations is futile. Topical steroidsor cyclosporin in steroid resistant cases areadministered in order to quell the signs and

symptoms. Indeed, subtarsal steroid injec-tions are administered in recalcitrant cases.Owing to the potential severity of the con-dition, patients should be referred to anophthalmologist during acute exacerba-tions.

Atopic conjunctivitis shares similarities toits vernal counterpart except that, unlikevernal conjunctivitis which resolves sponta-neously, it may persist for many years.Owing to the chronic nature, the visualmorbidity associated with this condition ishigh. The patient is typically male and suf-fers from atopic dermatitis. Other ocularmanifestations of this dermatological condi-tion include presenile anterior and posteriorsubcapsular cataracts, keratoconus and reti-nal detachment.

The lids are usually indurated and oedma-tous. The conjunctivitis has a predilectionfor the inferior fornices and tarsal conjunc-tivae. The tarsal conjunctivae may appearfeatureless due to the degree of infiltration.As the disease progresses, chemosis andpapillae may ensue. In extreme cases, cica-trisation occurs with the formation of sym-blepharon. It is not uncommon for thesepatients to possess bacterial eyelid margindisease and since the corneal complicationsare similar to those described for vernal dis-ease, such patients are at risk of acquiringmicrobial keratitis.

The treatment regimen for atopic kerato-conjunctivitis is similar to that recommend-ed for vernal disease. Owing to the

protracted timescale of the condition andthe co-existing bacterial eyelid margin dis-ease, treating these patients is an arduoustask. They can, therefore, be most appropri-ately managed by an ophthalmologist witha special interest in external eye disease.

Chronic conjunctivitis

Chronic conjunctivitis is usually reserved foreyes with a discharge, hyperaemia and ocu-lar irritation of four weeks duration or more.The aetiology may be due to toxicity to top-ical medications, eyelid conditions such asmolluscum contagiosum or chlamydia. In

view of the seriousness associated with thelatter, further elaboration of this condition ismerited.

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Chlamydial inclusionconjunctivitisAdult chlamydial conjunctivitis is a sexuallytransmitted disease due to chlamydialserotypes D-K (serotypes A-C cause tra-choma). While female patients usually have

a concomitant cervicitis, males have a ure-thritis. Despite the presence of active infec-tion, the patient may be asymptomatic.Transmission of the organism isfrom autoinoculation from genital secre-tions.

The presentation is subacute and is asso-ciated with a stringy mucous discharge. Thecondition maybe either unilateral or bilater-al. The follicles tend to be prodigious andhave a tendency to reside in the inferior for-niceal conjunctiva. There may be plicaloedema. Corneal infiltrates typically occurtwo to three weeks after the onset of theconjunctivitis. As mentioned previously,chlamydial disease is associated with tenderlymphadenopathy.

Patients suspected of suffering fromchlamydia should be referred to the hospi-tal eye department, as they would requirelaboratory investigations and treatment at agenitourinary clinic together with contacttracing of partners. Treatment includes sys-temic oral antibiotic such as azithromycin asa single dose, together with topical tetracy-cline ointment for at least one month.

Subconjunctival haemorrhageThis is commonly encountered in optomet-

ric practice and usually develops acutely. It ispainless and does not interfere withpatients vision. Most cases are idiopathic inorigin. Valsalval manoeuvres are commonprogenitors and the history should incorpo-rate questions about sneezing, vomiting,coughing or constipation. Other causesinclude trauma, systemic disease such ashypertension and the use of anticoagulantdrugs such as warfarin. It may co-exist withconjunctivitis.

If a clear, benign cause can be establishedfrom the history then the patient should bereassured and advised that the blood stain-ing will resolve over several weeks.

Conjunctival degenerationsand their differential diagnoses

Pingueculum

This common condition is slow growing andappears as a yellow-white, flat or slightlyraised conjunctival lesion in the interpalpe-bral fissure adjacent to the limbus. Thecornea is spared. Treatment is only initiatedfor those lesions, which are abnormallyraised and, as such, are causing symptomsdue to the resultant inability to wet the eyeor for those patients who develop a pingue-culitis. A short course of topical steroids can

ameliorate the inflammation and assuagethe patients symptoms, whereas surgicalexcision is required to remove those thatdisrupt the tear film.

Although pingeuculae are readily identi-

fied, several lesions may be confused withthis innocuous lesion such as early pterygia,gouty tophi (crystallisation) and xanthelas-ma associated with Type IIa hypercholes-terolaemia.

PterygiumA pterygium is a triangular fibrovasculargrowth of conjunctival tissue that invadesthe cornea. The term pterygos literallytranslates as wing. The invading pterygiumconsists of: a cap at the apex of the lesionthat penetrates Bowmans layer and as suchremains firmly adherent to the cornea; ahead which is firmly attached to both thecornea and limbus; and finally the bodywhich is located on the conjunctiva. Thetrue aetiology of this lesion has yet to bemade, suffice to say that ultraviolet radia-tion is the primary insult. It is noteworthythat pterygia only occur at interpalpebralnasal or temporal limbus, more commonlyat the former. This distribution has led to theconjecture that of pterygia may be theresult of localised stem cell damage.

Complications associated with pterygiaare relatively common and include ocularirritation secondary to disruption of the tearfilm, visual disturbance either secondary toinvolvement of the visual axis or frominduced astigmatism and, finally, the ptery-gium itself may become inflamed.

Unfortunately, simple excision of theselesions leads to a high rate of recurrence.Numerous studies have shown the recur-

rence rate to be in the region of 90% aftersix months. This has led to the introductionof adjunctive agents such as beta radiationand mitomycin C. However, these agentsare not without their own ocular complica-tions. Other techniques employed includeconjunctival autografts and amniotic mem-brane transplantation.

The differential diagnosis of pterygiainclude pseudopterygia, which are folds ofconjunctiva adherent to a corneal lesion.The lesion may be an ulcer or area ofperipheral thinning. However, unlike truepterygia where the conjunctiva is adherentto the whole cornea, their pseudo counter-

parts are only adherent to the corneal lesionin question.Another important lesion that must be

recognised in the differential diagnosis isconjunctival and corneal intraepithelial neo-plasia (CCIN). Essentially, this is a dysplasticlesion with a low potential for malignanttransformation. Histologically, there is dys-plasia (abnormal cellular changes) of theepithelium, ranging from the basal third toits full thickness. Once the whole epitheliumbecomes dysplastic, it is known as carcino-ma in situ as the basement membrane is notbreached.

The appearance of CCIN may adopt vari-

ous guises that include a raised gelatinouslesion, one that is papillomatous in appear-ance and a diffuse non-descript area of con-junctival thickening.

Patients suspected of acquiring CCIN

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should be referred urgently as there still is arisk, albeit low, of the lesion transforminginto a squamous cell carcinoma. Treatmentusually involves excision with adjunctivecryotherapy or the use of topical anti-metabolites, such as mitomycin C or

5-fluorouracil. The lesion is usually slowgrowing and is rare in young patients(except patients suffering from AIDS).A history of ultraviolet exposure iscommon.

Other tumours that may be confusedwith either pterygia or CCIN includesessile papillomata and amelanoticmelanoma.

Pigmented lesions

Pigmented lesions of the conjunctiva arecommon, especially in dark skinned individ-uals. Conjunctival epithelial melanosis isthe term used to describe the pigmentationobserved in such patients. Although thepigmentation is bilateral, it is not uncom-mon for the degree to be asymmetrical.Since the pigmentation is confined to theepithelium, it will move freely over theglobe when manually displaced. Sometimesthe pigmentation may extend into theperipheral cornea.

Common pigmented lesions that may beconfused with melanosis include axenfeldloops, which is an area of melanosis sur-rounding a intrascleral nerve, conjunctivalfreckles and adrenochrome deposits. Thelatter should be rarely encountered now, as

it is representative of clumps of pigmentassociated with the use of adrenaline drugs(now seldom employed) in the treatment ofglaucoma.

Primary acquired melanosis (PAM) isinvariably a unilateral condition, whichaffects middle aged caucasian individuals.Unlike conjunctival epithelial melanosis,PAM may be a pre-malignant condition.Indeed, the risk of transformation intomalignant melanoma may be as great as50% in patients who demonstrate cellularatypia (atypical cells) on biopsy andimmuno-histochemistry. Since PAM, with orwithout atypia, maybe indistinguishableclinically, an ophthalmological opinionshould be sought for any melanotic lesionin a caucasian individual acquired later inlife. Ominous signs include melanosis in thecaruncle and the appearance of nodules.It is imperative that the optometristeverts both lids to exclude intraepithelialspread.

Conclusion

This article has outlined the various conjunc-tival, episcleral and scleral lesions, togetherwith their aetiologies and differentials,which might present to the ophthalmic

practitioner. A brief referral guide has beenincluded where appropriate in order tohighlight the most appropriate, manage-ment plan.

Further reading

Kanski JJ (2003) Clinical Ophthalmology.Fifth Edition. Butterworth Heinemann,Oxford.

Kanski JJ and Nischal KK (1999)Ophthalmology. Clinical Signs andDifferential Diagnosis. Mosby,Philadelphia.

Parrish II RK (2000) Atlas ofOphthalmology. Butterworth Heinemann,Oxford.

Acknowledgements

Figures 1-5 by courtesy of Professor SusanLightman.

Module questions

1. Which one of the following statements

regarding scleral anatomy is incorrect?a. Episclera contains vascular connective

tissueb. The deep vascular plexus can be easily

manually moved over the overlyingstructure

c. Conjunctival vessels blanch with topicalvasoconstrictors

d. The lamina fusca lies adjacent to the uveallayers

2. Which one of the following statementsregarding episcleritis is correct?

a. The condition primarily affects the elderlyb. Pain typically radiates to the jawc. Urgent referral is mandatoryd. The condition is benign

3. Which one of the following statementsregarding scleritis is correct?

a. It is always associated with acute painb. Relapsing polychondritis is the most

common causec. Ocular surgery is a risk factord. Vision is always spared

4. Which one of the followingstatements regarding scleritisis incorrect?

a. Necrotising scleritis is characterised byavascular patches

b. It is usually treated with topical steroids

c. It may co-exist with anterior uveitisd. Staphyloma is a known complication


regarding the conjunctiva is incorrect?a. The bulbar portion covers the anterior sclerab. It consists of epithelial and stromal tissuec. The goblet cells secrete mucind. The epithelium is highly vascularised

6. Which one of the following statementsregarding signs and symptoms ofconjunctival disease is incorrect?

a. Subconjunctival haemorrhages may beobserved in adenoviral infections

b. Follicles indicate the presence of severeepiscleritis

c. Chemosis may be seen in severeinflammation

d. Papillae are present in allergic eye disease

7. Which one of the following statementsis correct?

a. Vernal keratoconjunctivitis can be managedentirely by the optometrist

b. Atopic keratoconjunctivitis normally resolvesby puberty

c. The most common virus to affect theconjunctiva is herpes simplex

d. Chlamydial conjunctivitis may be unilateral

8. Which one of the following statementsis incorrect?

a. A purulent discharge suggestssevere bacterial infection

b. A watery discharge is observed inviral conjunctivitis

c. Tender lymphadenopathy is characteristicof allergic conjunctivitis

d. Keratitis often co-exists with adenoviralserotype 8 conjunctivitis

Course code: c-2688

Please note, there is only one correct answer. Enter online or by using the form provided.

An answer return form is included in this issue. It should be completed and returned to: CET initiatives (c-2688), OT, Victoria House,178-180 Fleet Road, Fleet, Hampshire, GU51 4DA by March 8, 2006. Under no circumstances will forms received after

this date be marked the answers to the module will have been published in our March 10, 2006 issue.

9. Which one of the following requires

urgent referral to an ophthalmologist?a. Adenoviral conjunctivitisb. gonococcal conjunctivitisc. Episclerit isd. Simple bacterial conjunctivitis

10. Which one of the following isnot an example of conjunctivalpigmentation?

a. Conjunctival epithelial melanosisb. Primary acquired melanosisc. Amelanotic melanomad. Axenfeld loops

11. Which one of the followingstatements regarding pterygiais incorrect?

a. It is a fibrovascular overgrowth of theconjunctiva

b. It is most commonly found encroaching thetemporal limbus

c. Surgery requires adjunctive therapy toreduce recurrence

d. It is a known cause of induced astigmatism

12. Which one of the followingstatements is correct?

a. Primary acquired melanosis is common indark skinned races

b. Pingueculae are pre-malignant lesionsc. Pseudopterygia are adherent to the whole

cornea

d. Conjunctival and corneal intraepithelialneoplasia (CCIN) has malignant potential


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42 | February 10 | 2006 OT



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a

CET answers

1. Which one of the following statementsis correct regarding orbital anatomy?

a. The palatine bone forms part of the floor

b. The zygomatic bone forms part of the

medial wall

c. The ethmoid bone forms part of the roof

d. The lacrimal bone forms part of the lateral

wall

a is correct

The orbit can be compartmentalised into five

structures namely the roof (lesser wing of

sphenoid and orbital plate of the frontal bone),

the floor (zygomatic, maxillary and palatine

bones), the lateral (greater wing of sphenoid

and zygomatic bones) and medial (maxillary,lacrimal, ethmoid and sphenoid bones) walls

and, finally, the superior orbital fissure.


regarding proptosis is correct?

a. Dystopia always occurs in conjunction

with proptosis

b. Axial proptosis is never caused by tumours

c. Ipsilateral enophthalmos is a cause of

pseudoproptosis

d. The degree of proptosis can be measured

with a rule

d is correct

Dystopia may co-exist with proptosis or its reces-sive counterpart. Proptotic eyes that are axial in

nature are usually associated with lesions

confined to the muscle cone, such as optic nerve

tumours. Causes of pseudoproptosis include an

enlarged ipsilateral eye (for example, high

myopia), ipsilateral eyelid retraction or contralat-

eral enophthalmos. Proptosis may be quantified

by measuring from the lateral orbital ridge to

the corneal apex with a transparent rule.

3. Which one of the following is not

a cause of pseudoproptosis?

a. Nanophthalmos

b. High myopia

c. Ipsilateral eyelid retractiond. Contralateral enophthalmos

a is correct

Nanophthalmos is not a cause of

pseudoproptosis. Causes of pseudoproptosis

include an enlarged ipsilateral eye (for example,

high myopia), ipsilateral eyelid retraction or

contralateral enophthalmos.

4. Which one of the following is a

myogenic cause of ptosis?

a. Oculomotor nerve palsy

b. Marcus Gunn jaw winking syndrome

c. Horners syndrome

d. Myasthenia gravis

d is correct

Oculomotor nerve palsy, Marcus Gunn jaw

winking syndrome and Horners syndrome are allneurogenic causes of ptosis. Myasthenia gravis is

a myogenic cause of ptosis.

5. Which one of the following statements is

incorrect regarding thyroid eye disease?

a. Patients are typically hyperthyroid

b. Eyelid retraction is a manifestation

c. Treatment of the thyroid dysfunction always

corrects the ophthalmic signs

d. Corneal ulceration is a complication

c is correct

Thyroid eye disease or ophthalmic Graves disease

is most commonly associated with

hyperthyroidism. Eyelid retraction and cornealulceration are signs of thyroid eye disease.

6. Which one of the following is suggestive

of orbital rather than preseptal cellulitis?

a. Hyperaemic lid

b. Ophthalmoplegia

c. Tenderness

d. Previous history of infection

b is correct

A hyperaemic lid, tenderness and a previous

history of infection are all signs suggestive of

preseptal cellulitis.

7. Which one of the following statementsregarding eyelid anatomy is correct?

a. Mllers muscle is innervated by the

parasympathetic system

b. The levator is innervated by the

abducens nerve

c. The glands of Zeiss are sweat glands

d. The meibomian glands on the upper

lid out number those on the lower

d is correct

Mllers muscle is innervated by the sympathetic

nervous system. The levator muscle is innervated

by the oculomotor nerve. The glands of Zeiss are

modified sebaceous glands. The meibomian

glands are more numerous in the upper tarsalplate, with approximately 25 in this region

compared to approximately 20 in the lower.

8. Which one of the following signs

are suggestive of malignancy?

a. Normal lid architecture

b. No documented growth

c. Normally directed lashes

d. Bleeding

d is correct

Lesions that have grown over a relatively short

period of time, or have undergone morphological

changes such as spontaneous or prolonged

bleeding, should arouse suspicion of malignancy.

9. Which one of the following is not

a differential diagnosis of ptosis?

Here are the correct answers to Module 9 Part 1 of Differential Diagnosis of Ocular Disease The eyelids and the orbit key signs for differential diagnosis and management Course code c-2686 which appeared in our January 13, 2006 issue.

a. Contralateral hypotropiab. Contralateral eyelid retraction

c. Dermatochalasis

d. Brow ptosis

a is correct

Contralateral eyelid retraction, dermatochalasis

and brow ptosis should all be considered in the

differential diagnosis of ptosis.

10. Which one of the following is

not a cause of ectropion?

a. Dermatit is

b. Lower lid mass

c. Cicatrising lesion of the

palpebral conjunctivad. Horizontal lid laxity

c is correct

Dermatitis, a lower lid mass and horizontal

lid laxity are all causes of ectropion.

11. Which one of the following

is not a cause of madarosis?

a. Anterior eyelid margin disease

b. Psoriasis

c. Hyperthyroidism

d. Malignant lesions

c is correct

Anterior eyelid margin disease, psoriasis andhypothyroidism are the most frequent primary

causes of madarosis to be encountered by the

optometrist. In addition, malignant processes

may cause madarosis.

12. Which one of the following

statements is correct?

a. Distichiasis is always congenital

b. Choroidal folds are always symptomatic

c. Optic neuropathy secondary to orbital

disease is only associated with tumours

d. Thyroid eye disease is the

most common cause of

unilateral proptosis

d is correct

Although distichiasis may be congenital,

acquired cases are usually secondary to

cicatrising lesions such as Stevens-Johnson

syndrome and cicatrising pemphigoid.

Although choroidal folds are contemporaneous

with the onset of severe proptosis, their

presence may, in certain circumstances,

pre-date the onset of orbital signs. Thyroid eye

disease is the most common cause of both

unilateral and bilateral proptosis and as it may

co-exist with optic neuropathy, formal tests to

assess the health of the nerve should be

performed on all patients. In addition, since

the cause of optic neuropathy is compressionsecondary to the enlarged recti muscles,

optic nerve dysfunction may not

correlate with the degree of proptosis.

epi.: sclera: conjunctiva

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