14.10.10-scleral and conjunctival disease kuliah international class finish
TRANSCRIPT
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dr. Marlyanti N. Akib, Sp.M
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Conjunctiva is a translucent mucousmembrane which lines the posterior surfaceof the eyelids and anterior aspect of eyeball.
Conjunctiva can be divided into three parts :Palpebral conjunctiva.Bulbar conjunctiva.Conjunctival fornix.
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Inflammation of the conjunctiva(conjunctivitis ) is classically defined asconjunctival hyperaemia associated with a
discharge which may be watery, mucoid,mucopurulent or purulent. Infective conjunctivitis
Bacterial
ChlamydialViral
Allergic conjunctivitis Granulomatous conjunctivitis
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EtiologyResult of bacterial overgrowth and infiltration ofthe conjunctival epithelial layer.Caused by a wide range of organisms :
Staphylococcus aureusStaphylococcus epidermidisStreptococcus pneumoniae (pneumococcus)Streptococcus pyogenes (haemolyticus)Haemophilus influenzaeEtc
Conjunctiva may get infected from threesources, via exogenous, local surroundingstructures and endogenous.
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PathologyVascular response, congestion and increasedpermeability of the conjunctival vessels .Cellular response, exudation ofpolymorphonuclear cells and other inflammatorycells into the substantia propria of conjunctiva .Conjunctival tissue response, conjunctivabecomes edematous. The superficial epithelialcells degenerate, become loose and evendesquamate.Conjunctival discharge. It consists of tears,mucus, inflammatory cells, desquamatedepithelial cells, fibrin and bacteria.
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1. ACUTE MUCOPURULENT CONJUNCTIVITISMost common type of acute bacterialconjunctivitis. It is characterized by markedconjunctival hyperemia and mucopurulentdischarge from the eye.Commonly caused by Staphylococcus aureus,Koch-Weeks bacillus, Pneumococcus andStreptococcus.
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SIMPTOMS :Discomfort and foreignbody sensationMild photophobia Mucopurulent discharge
Sticking together of lidmarginsSlight blurring of visiondue to mucous flakesConjunctival congestion .
Flakes of mucousCilia are usually mattedtogether with yellowcrusts.
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TreatmentTopical antibioticsIrrigation of conjunctival sacDark gogglesNo bandageNo steroids
Anti-inflammatory and analgesic drugs
Complications.Occasionally the disease may be complicated bymarginal corneal ulcer, superficial keratitis,blepharitis or dacryocystitis.
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2. ACUTE PURULENT CONJUNCTIVITISAlso known as acute blenorrhea or hyper acuteconjunctivitis is characterized by a violentinflammatory response.Two forms:
Adult purulent conjunctivitisOphthalmia neonatorum in newborn
Commonest causative organism is Gonococcus; butrarely it may be Staphylococcus aureus orPneumococcus.
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2a. Adult purulent conjunctivitisClinical feature :
Stage of infiltration. It lasts for 4-5 daysPainful and tender of eye ballBright red chemosed conjunctivaLids are tense and swollenDischarge is watery or sanguinous
Pre-auricular lymph nodes are enlargedStage of blenorrhea. It starts about fifth day and lastfor several days.
Purulent, copious, thick discharge trickling down thecheeks
Stage of slow healingPain is decreasedSwelling of the lids subsidesConjunctiva remains red and discharge diminishedslowly.
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Complications :Corneal ulcer, corneal PerforationIridocyclitis
Systemic complication (GO arthritis, Endocarditis andSepticemia).
Treatment :Acute nonsevere bacterial conjunctivitis :
Topical agents : Polymixin, aminoglycoside orfluoroquinolone (ciprofloxacin, ofloxacin, levofloxacin,moxifloxacin or gatifloxacin) 4 times daily for 5-7 daysHaemophylus species : Polymixin B-trimethoprim.Definitive treatment : culture result
Gonococcal Conjunctivitis :
Systemic antibiotics : Ceftriaxone.Without corneal ulceration : 1 i.m injection (1 g)With Corneal Ulceration : Ceftriaxone iv 1 gr/12 daysfor 3 days.
Topical antibiotics : Erythromicin EO, Bacitracin EO,Gentamicin EO or Ciprofloxacin ED.
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2b. Neonatal Gonococcal ConjunctivitisClinical features :
Bilateral conjunctival discharge 3-5 days afterparturition.Discharge may be serosanguineous during first severaldays and a copious purulent exudate may developlater.Corneal ulceration, corneal perforation and
endoftalmitis can occurTreatment :
First-line : Ceftriaxone injection (up to 125 mg or adosage 25-50 mg/kg) or cefotaxime single dose of 100mg/kg IV or IMHourly saline IrrigationIf corneal involvement suspected : Topicalerythromycin or gentamicin EO or frequentapplication of topical fluoroquinolone.
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3. ACUTE MEMBRANOUS CONJUNCTIVITIScharacterized by formation of a true membrane on theconjunctiva.
caused by Corynebacterium diphtheria and occasionallyby virulent type of Streptococcus haemolyticus.Clinical features :
Stage of infiltrationConjunctival discharge and severe pain in the eye
Lids are swollen and hardConjunctiva is red, swollen and covered with a thick grey-yellow membrane.Pre-auricular lymph nodes are enlarged
Stage of suppurationPain decreases and the lids become softThe membrane is sloughed off leaving a raw surface.
Stage of cicatrisationThe raw suface covered with granulation tissue .Healing occurs by cicatrisation, which may causetrichiasis.
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TreatmentTopical therapy
Peniccilin ED (1:10000 units per ml) every half hourlyAtropine sulfate 1% EO if cornea involveBroad spectrum antibiotic EO at bed time.
Systemic therapy
Crystalline peniccilin 5 lac units i.m twice a day for 10days.ADS i.m
Prevention of symblepharon
Prophylaxis Isolation of patient will prevent family membersfrom being infected.Proper immunization against diphtheria is veryeffective and provides protection to the community.
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4. PSEUDOMEMBRANOUS CONJUNCTIVITIS
It is a type of acute conjunctivitis, characterized byformation of a pseudo membrane on theconjunctiva.It may be caused by following varied factors:
Bacterial infection ; Corynebacterium diphtheria of lowvirulence, staphylococci, streptococci, H. influenza and N.gonorrhea. Viral infections such as herpes simplex and adenoviralChemical irritants such as acids, ammonia, lime, silver nitrate and copper sulfate.
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PathologyThese agents produce inflammation ofconjunctiva associated with pouring of fibrinnousexudate on its surface which coagulates andleads to formation of pseudomembrane.
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Clinical features :Acute mucopurulent cinjunctivitisPseudomembrane formation which is thinyellowish-white membrane seen in the fornicesand on the palpebral conjunctiva.Pseudomembrane can peeled off easily anddoesnt bleed.
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5. CHRONIC CATARRHAL CONJUNCTIVITISAlso known as simple chronic conjunctivitis ischaracterised by mild catarrhal inflammation ofthe conjunctiva.Etiology
Predisposing factors ; Chronic exposure, Localcause of irritation, Eye strain, Abuse of alcohol insomnia and metabolic disorders.Causative organisms ; Staphylococcus aureus, Gramnegative rods
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Symptoms : Burning and grittiness in the eyes Mild chronic redness in the eyes. Feeling of heat and dryness on the lid margins. Difficulty in keeping the eyes open. Mild mucoid discharge.
Feeling of sleepiness and tiredness in the eyesTreatment
Predisposing factors when associated should betreated and eliminated.
Topical antibiotics (Chloramphenicol or gentamycin 3-4 times a day for 2 weeks) Astringent eye drops
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TRACHOMAchronic keratoconjunctivitis, primarilyaffecting the superficial epithelium ofconjunctiva and cornea simultaneously.characterised by a mixed follicular andpapillary response of conjunctival tissue.caused by Chlamydia trachomatis.
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SIMPTOMS : In the absence of secondary infection,
symptoms are minimal and include mildforeign body sensation in the eyes, occasionallacrimation, slight stickiness of the lids andscanty mucoid discharge.
In the presence of secondary infection,typical symptoms of acute mucopurulentconjunctivitis develop.
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Conjunctival signs :Congestion of upper tarsal and fornicalconjunctivaConjunctival follicles.Papillary Hyperplasia. Papillae are reddish, flattopped raised area which give red and velvetyappearance to the tarsal conjunctiva.Conjunctival scarring
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Corneal signs :Superficial keratitisHerbert follicels : typical follicles present in thelimbal area.Pannus : Infiltration of the cornea associatedwith vascularization is seen in upper part.Herbert pits : left after healing of herbertfollicles in the limbal area.Corneal opacity, it is the end result oftrachomatous corneal lesions.
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Sequelae of trachomaSequelae in the lids may be trichiasis, entropion,tylosis (thickening of lid margin),
ptosis,madarosis and ankyloblepharon.Conjunctival sequelae includeconcretions, pseudocyst, xerosis andsymblepharon.Corneal sequelae may be corneal opacity,ectasia, corneal xerosis and total corneal pannus(blinding sequelae).Chronic dacryocystitis, and chronicdacryoadenitis.
ComplicationsThe only complication of trachoma is cornealulcer which may occur due to rubbing byconcretions, or trichiasis with superimposedbacterial infection.
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DiagnosisMade from its typical signs;
Conjunctival follicles and papillaePannus progressive or regressiveEpithelial keratitis near superior limbusSigns of cicatrisation or its sequelae
Laboratory diagnosis ;
Conjunctival cytology.Detection of inclusion bodiesEnzyme-linked immunosorbent assay (ELISA) forchlamydial antigens.Polymerase chain reaction (PCR) is also useful.
Isolation of chlamydiaSerotyping of TRIC agents is done by detectingspecific antibodies usingmicroimmunofluorescence (micro-IF) method
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ManagementTreatment of active trachoma
Topical therapy regimes. (1% tetracycline or 1%erythromycin EO 4 times a day for 6 weeks)Systemic therapy regimes (Tetracycline orerythromycine 250 mg orally 4x1 for 3-4 weeks orsingle dose 1 gm azithromycinCombined topical and systemic therapy regimes.
Treatment of trachoma sequelae
Concretions should be removed with a hypodermicneedle.Trichiasis may be treated by epilation, electrolysis orcryolysis .Entropion should be corrected surgically
Xerosis should be treated by artificial tears.ProphylaxisHygienic measures.Early treatment of conjunctivitis.Blanket antibiotic therapy (intermittent treatment).
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ADULT INCLUSION CONJUNCTIVITIStype of acute follicular conjunctivitisassociated with mucopurulent discharge.
caused by serotypes D to K of Chlamydiatrachomatis.swimming pool conjunctivitis.
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Symptoms :Similar to acute mucopurulentconjunctivitis and include:
Ocular discomfort, foreign bodysensation, Mild photophobia, and Mucopurulent discharge.
Sign :Conjunctival hyperaemia, moremarked in fornices. Acute follicular hypertrophypredominantly of lower palpebral
conjunctiva Superficial keratitis in upper halfof cornea.Pre-auricular lymphadenopathy
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TreatmentTopical therapy (tetracycline 1% EO 4x1 for 6weeks)Systemic therapy (Tetracycline, Erythromycine,doxicycline)
ProphylaxisImprovement in personal hygiene and regularchlorination of swimming pool water.Patient's sexual partner should be examined andtreated.
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Tend to affect the epithelium, both of theconjunctiva and cornea.Viral infections of conjunctiva :
Adenovirus conjunctivitis Herpes simplex keratoconjunctivitis Herpes zoster conjunctivitis Pox virus conjunctivitis
Myxovirus conjunctivitis Paramyxovirus conjunctivitis ARBOR virus conjunctivitis
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FOLLICULAR CONJUNCTIVITISCharacterized by formation of follicles,conjunctival hyperaemia and discharge fromthe eyes.Types
Acute follicular conjunctivitis.Chronic follicular conjunctivitis.
Specific type of conjunctivitis with follicleformation e.g., trachomaEtiologically, acute follicular conjunctivitis isof the following types:
1. Adult inclusion conjunctivitis2. Epidemic keratoconjunctivitis3. Pharyngoconjunctival fever4. Newcastle conjunctivitis5. Acute herpetic conjunctivitis.
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Epidemic Keratoconjunctivitis (EKC)caused by adenoviruses type 8 and 19.
markedly contagious and spreads throughcontact with contaminated fingers, solutionsand tonometers.Incubation period after infection is about 8
days and virus is shed from the inflamed eyefor 2-3 weeks.Treatment, usually supportive. Antiviral drugsare ineffective.
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Pharyngoconjunctival fever (PCF)Commonly associated with subtypes 3 and 7Characterized by an acute follicularconjunctivitis, associated with pharyngitis,fever and preauricular lymphadenopathy.Treatment is usually supportive.
Acute herpetic conjunctivitisAccompaniment of the 'primary herpeticinfection. Caused by herpes simplex virus type 1.Usually a unilateral affection with an
incubation period of 3-10 days. It may occurin two clinical forms the typical and atypical.Treatment. Primary herpetic infection isusually self-limiting.
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CHRONIC FOLLICULAR CONJUNCTIVITISBenign folliculosis, also called 'School
folliculosis. follicles are typically arranged in parallelrows in the lower palpebral conjunctivawithout any associated conjunctivalhyperaemia
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Inflammation of conjunctiva due to allergic orhypersensitivity reactions which may beimmediate (humoral) or delayed (cellular).Types
Simple allergic conjunctivitis
Hay fever conjunctivitis (commonly associated with hayfever or allergic rhinitis) Seasonal allergic conjunctivitis (SAC) Perennial allergic conjunctivitis (PAC) : is a response toperenial allergens such as house dust and mite.
Vernal keratoconjunctivitis (VKC)Atopic keratoconjunctivitis (AKC)Giant papillary conjunctivitis (GPC)Phlyctenular keratoconjunctivitis (PKC)Contact dermoconjunctivitis (CDC)
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VERNAL KERATOCONJUNCTIVITISRecurrent, bilateral, interstitial,self-limiting, allergic inflammation
of the conjunctivacharacterised by marked burningand itching sensationMild photophobia, lacrimation,
stringy (ropy) discharge andheaviness of lids.GIANT PAPILLARYCONJUNCTIVITIS (GPC)
localised allergic response to aphysically rough or deposited surface
Itching, stringy discharge andreduced wearing time of contactlens or prosthetic shell.
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Common conjunctival condition that occurstypically at the nasal and temporal anteriorbulbar conjunctiva.
Etiology :Not known exactlyIt has been considered as an age-change, morecommonly in persons exposed to strong sunlight,dust and wind.
Clinical Features :Usually bilateral, stationary conditionYellowish-white triangular patch near the limbus.
Apex of the triangle is away from the cornea.
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TreatmentLubricant to alleviate ocular irritation .No treatment is required, except cosmeticproblem.
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Is a wing-shaped fold of conjunctiva andfibrovascular tissue that has invaded thesuperficial cornea
Pathogenesis :Strongly correlated with UV exposureOther factors : dryness, inflammation exposureto wind and dust or other irritans.UV B is mutagenic for the p53 tumor supressorgene in limbal basal stem cells.Overexpression of TGF and VEGF leads tocollagenase up-regulation, cellular migration andangiogenesis.
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Clinical features :
It may be unilateral or bilateralTriangular fold of conjunctiva encroaching thecornea in the area of palpebral aperture, usuallyon nasal side.Three stages
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Treatment :Surgical excision :
Indication : Cosmetic reasons, continued progressionthreatening to encroach onto pupillary area anddiplopia due to interference in ocular movements.
Lubricant if symptom persist
DD/Pseudopterygium : fols of bulbar conjunctivaattached to the cornea. It is formed due toadhesions of chemosed bulbar conjunctiva to
the marginal corneal ulcer. Usually occursfollowing chemical burns of the eye.
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NEXT
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dr. Marlyanti N. Akib, Sp.M
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Introduction
Sclera forms the posterior five-sixthopaque part of the external fibrous tunicof the eyeball.
Its inner surface lies in contact withchoroid with a potential suprachoroidalspace in between.sclera consists of following three layers:1. Episcleral tissue.2. Sclera proper.3. Lamina fusca.
INFLAMMATIONS OF THE
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INFLAMMATIONS OF THESCLERA 1. EPISCLERITIS
Benign recurrent inflammation of theepisclera, involving the overlying Tenon's
capsule but not the underlying sclera.Etiology ; unknown
Characterised by redness, mild oculardiscomfort described as gritty, burning orforeign body sensation.
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Episclera is seen acutely inflamed in theinvolved area. In diffuse episcleritis, although whole eyemay be involved to some extent, themaximum inflammation is confined to one ortwo quadrants
In nodular episcleritis, a pink or purple flatnodule surrounded by injection is seen
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TreatmentTopical corticosteroid eyedrops instilled 2-3hourly, render the eye more comfortable and
resolve the episcleritis within a few days.Cold compresses applied to the closed lidsmay offer symptomatic relief from oculardiscomfort.
Systemic non-steroidal anti-inflammatorydrugs (NSAIDs)
INFLAMMATIONS OF THE
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SCLERITISChronic inflammation of the sclera proper.May cause visual impairment and even lossof the eye if treated inadequatelyEtiology : Autoimmune collagen disorders Metabolic disorders Infections Granulomatous diseases Miscellaneous conditions Idiopathic.
INFLAMMATIONS OF THESCLERA
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Moderate to severe painwhich is deep and boring in
character and often wakesthe patient early in themorning .Diffuse redness, mild tosevere photophobia andlacrimation.Diminution of vision.Investigations ;Following laboratorystudies may be helpful inidentifying associatedsystemic diseases
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It can be classified as follows: Anterior scleritis (98%)
Non-necrotizing scleritis (85%)1. Diffuse2. Nodular
Necrotizing scleritis (13%)1. with inflammation2. without inflammation (scleromalacia
perforans)
Posterior scleritis (2%)
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Non -necro t izing anter ior di ffusescleri t is , It is the commonest variety,characterized by widespreadinflammation involving a quadrant ormore of the anterior sclera. The involvedarea is raised and salmon pink to purple
in colorNon-necro t izing anter ior no du larscleri t is , characterised by one or two
hard, purplish elevated scleral nodules,usually situated near the limbus
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A t i t i i l i ti i th
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An ter io r n ec ro t i zing sc ler i ti s w i thinf lammat ion , intense localizedinflammation associated with areas of
infarction due to vacuities.An ter io r n ec ro t i zing sc le r it i s w i thou tinf lammat ion , development of yellowishpatch of melting sclera (due to obliteration
of arterial supply).Pos ter ior sc ler i t is , involving the sclerabehind the equator, features of associatedinflammation of adjacent structures, whichinclude: exudative retinal detachment,macular oedema, proptosis and limitation ofocular movements.
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TreatmentNon-necrot i s in g sc ler i t is . It is treated
by topical steroid eyedrops and systemicindomethacin 100 mg daily for a day andthen 75 mg daily until inflammationresolves.Necr ot is ing sc ler i t is . It is treated bytopical steroids and heavy doses of oralsteroids tapered slowly.
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