CONJUNCTIVA DR PRADNYA DESHMUKH ANATOMY Thin mucous membrane

CONJUNCTIVA DR PRADNYA DESHMUKH

ANATOMY • Thin mucous membrane lining the eyelids and ocular surface. • Divided into- PALPEBRAL – adherant to the lid • -ORBITAL-loosely attached to sclera • -FORNICES- cul de sac connecting • INTERMARGINAL STRIP- from anterior to posterior margin of the lid edge. Transitional zone covered with stratified epithelium. •

ANATOMY • Layers of conjunctiva • EPITHELIUM -2 layers of epithelium in palpebral area becoming progressively thicker near the limbus with stratified non keratinized epithelium. • ADENOID- loose connective tissue with leucocytes • FIBROUS – dense passing into the lid and sclera

Ocular surface • TEAR FILM LAYER • 1) LIPID LAYER – secreted by meibomian glands and limits the evaporation of tears. • 2)AQUEOUS LAYER- secreted by lacrimal and accessory conjunctival glands • 3) MUCINOUS LAYER- secreted by goblet cells

Tear film function • 1) maintains smooth ocular surface • 2) nourishes the cornea due to oxygen dissolved in it • 3)wash away debris • 4) immunological protection of ocular surface by enzyme lysozyme and secretory immunoglobin A.

MICROBIOLOGY • Bad propagating medium for organisms due to low temperature, evaporation of lacrimal fluid and moderate blood supply • Tears also help in decreasing the bacteriological load • NON PATHOGENIC COMMENSALS – STAPH ALBUS, DIPTHEROIDS, PROPIONIBACTERIU M ACNES, NEISSERIA CATARRHALIS, CORYNEBACTERIUM XEROSIS

symptoms • ) HYPEREMIA( REDNESS)- transient, acute, recurrent or chronic. Causes irritation or grity sensation. • Causes of red eye • 1) CONJUNCTIVITIS-INFECTIOUS • -NONINFECTIOUS • 2)KERATITIS-INFECTIOUS • -NON INFECTIOUS • 3)UVIETIS • 4)GLAUCOMA •

CLINICAL FEATURES CONJUNCTIVI TIS ACUTE IRIDOCYCLITI S ACUTE CONGESTIVE GLAUCOMA ONSET ACUTE RAPID SUDDEN VISION GOOD FAIR POOR PAIN MILD MODERATE SEVERE RADIATING TO TRIGEMINAL AREA SECRETION MUCOPURULEN T WATERY PHOTOPHOBIA ABSENT USUALLY PRESENT USUALLY ABSENT COLOURED HALOES ABSENT USUALLY PRESENT

CLINICAL FEATURES CONJUNCTIVI TIS ACUTE ANGLE IRIDOCYCLITI CLOSURE S GLAUCOMA CONJUNCTIVAL SUPERFICIAL CONGESTION DEEP CILIARY PUPIL NORMAL SMALL IRREGULAR LARGE VERTICALLY OVAL TENDERNESS ABSENT PRESENT DEPTH OF ANTERIOR CHAMBER NORMAL USUALLY NORMAL SHALLOW IOP NORMAL USUALLY NORMAL RAISED SYSTEMIC NIL VOMITING

SYMPTOMS • DISCHARGE-prominent feature in conjunctivitis. • 1) PURULENT/ MUCOPURULENT- bacterial conjunctivitis • 2) WATERY/ MUCOID-VIRAL /ALLERGIC CONJUNCTIVITIS • 3) ROPY- ALLERGIC CONJUNCTIVITIS • May be mild, matting of eyelashes, copius discharge

SYMPTOMS • • FOREIGN BODY SENSATION OR GRITINESS 1)DRY EYE 2)EYE STRAIN 3)CONTACT LENS INDUCED PAPILLARY REACTION • 4)TRICHIASIS • 5)FOREIGN BODY • 6) KERATITIS

EXAMINATION • LOWER FORNIX easily exposed • Upper palpebral conjuntivitis- eversion of eyelid • Upper fornix-double eversion of upper eyelid with DESMARRE retractor

CONJUNCTIVAL CONGESTION CIRCUMCILIARY CONGESTION POSITION SUPERFICIAL DEEP COLOUR BRIGHT RED DUSKY LILIAC HUE CONDITIONS CONJUNCTIVITIS INFLAM MATION OF IRIS OR SCLERA PRESSURE ON LID BLANCHES DOES NOT BLANCH 10% PHENYLEPHRINE REDUCES DOES NOT REDUCE FILLING OF VESSELS FILL FROM FORNIX INWARDS FILL FROM FORNIX OUTWARDS

SIGNS • CONJUNCTIVAL INFLAMMATORY REACTION • 1) FOLLICLES- yellowish- white round elevations , 1 -2 mm. • Aggregations of lymphocytes in the adenoid layer • Seen in allergic conjunctivitis, viral conjunctivitis, long term pilocarpine use, trachoma, local lid infection

• 2) PAPILLARY REACTION-hyperplasia of normal vascular system with glomerulus like branches. Seen in inflammatory conditions. • 3) GRANULOMA- foreign body

Subconjunctival haemorrhage • • Due to rupture of small vessels Causes-1) TRAUMA 2)eye surgery 3)systolic hypertension 4)eldery patients with fragile vessels. 5) severe conjunctivitis- small 6)severe vomiting, straining 7)systemic diseases- scurvy, malaria, blood dyscrasia

SUBCONJUNCTIVAL HMGHE • INVESTIGATIONS- BP • - RECURRENT BLEEDS SEE COMPLETE HEAMOGRAM • IN CASE OF HEAD INJURIES WITH LARGE BLEEDS SEED FOR FRACTURE OF BASE OF SKULL. • USUALLY SELF LIMITING. • ARTIFICIAL TEAR SUPPLEMENT

CHEMOSIS • EDEMA OF CONJUNCTIVA DUE TO EXTRAVASATION FROM PERMEABLE CAPPILARIES • MUCOUS MEMBRANE BECOMES SWOLLEN AND GELATINOUS IN BULBAR AREA. • CAUSES • 1)Acute inflammationconjunctivitis, panophthalmitis, insect bite, stye • 2)obstruction to outflow-orbital tumour, proptosis • 3)abnormal blood circulation-nephritis, urticaria

CONJUNCTIVITIS • CLASSIFICATION • A) BASED ON ONSET -ACUTE(>4 WEEKS) • -SUBACUTE • -CHRONIC • B)BASED ON TYPE OF EXUDATE • -SEROUS-VIRAL, ALLERGIC • -CATARRHAL-ALLERGIC • -PURULENT-BACTERAIL • -MUCOPURULENTBACTERIAL • MEMBRANOUS/PSEUDOMEMBRANOUS

CONJUNCTIVITIS • C) BASED ON CONJUNCTIVAL RESPONSE • FOLLICULAR, PAPILLARY, GRANULOMATOU S • D)BASED ON ETIOLOGY • 1) INFECTIOUSBACTERIAL(STAPH, HEAMOPHILUS, NEISSERIA, SREPTOCOCCUS) • VIRAL(HERPES SIMPLEX, ADENOVIRUS) • CHYLAMADIAL(TRACHOMA • FUNGAL • PARASITIC

• • 2)NON INFECTIOUS ALLERGIC IRRITANTS ENDOGENOUS DRY EYE TOXIC SELF INFLICTED IDIOPATHIC

ACUTE CONJUNCTIVITIS • BACTERIAL CONJUNCTIVITIS • CONTAGIOUS BY DIRECT CONTACT WITH DISCHARGE. • AETIOLOGICAL ORGANISM-STAPH AURES, • SYMPTOMS- REDNESS, WATERING MUCOPURULENT/ PURULENT, IIRITATION • SIGNS- HYPEREMIA • -MATTING OF EYELASHES

HAEMOPHILUS AEGYPTIUS CONJUNCTIVITIS • GRAM NEGATIVE ORGANISM causes epidemics • may range from mild attack to sever corneal involvement. • Mild attack –hyperemia with mucus discharge which gums the lids in morning. • Severe case-fiery red eye with marked conjunctival vessel congestion. • Flakes of pus and mocopus are seen with matting of eyelashes with yellow crusts. May give rise to haloes.

HAEMOPHILUS AEGYPTIUS CONJUNCTIVITIS • Lid edema, chemosis, small ecchymosis • DIAGNOSIS-HISTOLOGICAL EXAMINATION OF SECRETION BY CONJUNCTIVAL SWAB. • SCRAPINGS OF CONJUNCTI VA STAINED WITH GRAM/ GIEMSA/ PAPANICOLAOU STAIN. • COMPLICATIONS- SUPERFICIAL KERATITIS, RARELY UVIETIS

HAEMOPHILUS AEGYPTIUS CONJUNCTIVITIS • DO NOT BANDAGE • DARK GOGGLES • PREVENTION OF INFECTION BY KEEPING CLEAN HANDS AND AVOIDING FOMITES LIKE TOWELS, PILLOWS, HANDKERCHIEF. • BROAD SRECTRUM ANTIBIOTICS FLUOROQUINOLONE GROUP 6 -8 HOURLY • ANTIBIOTIC OINTMNENT AT NIGHT • NO ROLE OF TOPICAL STEROIDS

GONORRHEAL CONJUNCTIVITIS • RARE SEEN IN PEOPLE WITH POOR HYGIENE • NEISSERIA gonorrhoeae GRAM NEGATIVE COCCI • OPHTHALMIA NEONATURUM IN BABIES AND SEVERE PURULENT CONJUNCTIVITIS IN ADULTS. • ADULTS ACUTE PRESENTATION WITH SEVERE LID EDEMA WITH PUS. • PALPEBRAL AND BULBAR CONJUNCTIVA IS INFLAMMED WITH PAIN. PREAURICULAR LYMPH NODE TENDER. • CORNEA- DIFFUSE HAZINESS WITH YELLOW SMALL ULCERS. MAY INVOLVE THE WHOLE CORNEA • URETHRITIS, ARTHRITIS, SEPTICEMIA, ENDOCARDITIS

GONORRHOEAL CONJUNCTIVITIS • OCULAR TREATMENT • IRRIGATING WITH WARM SALINE • BROAD SPECTRUM ANTIBIOTICSOFLOXACIN, CIPROFLOXACIN, GENTAMICIN. • SYSTEMIC TREATMENT • 1 GM CEFTRIAXONE IM.

Membranous / pseudomembranous conjunctivitis • SEEN IN INFECTIONS WITH CORYNEBACTERIUM diphtheria, STREPTOCOCCUS, HAEMOPHILUS aegyptius, N. gonorrhea, STAPH aureus, • MILD CASES-some eyelid swelling with mucopurulent discharge. White membrane is seen covering the palpebral conjunctiva aesily peeled off-pseudomembranous. • SEVERE CASES-seen in diphtheria • Brawny lid edema.

MEMBRANOUS/PSEUDEMEMBRANOUS CONJUNCTIVITIS • Conjunctiva is permeated with exudates leading to necrosis. • Patchy or full membrane is seen covering the palpebral conjunctiva beginning at the lid margin. • Preauricular lymph node is inflammed • COMPLICATIONS- CORNEAL ULCER, SYMBLEPHARON. • LIGNEOUS CONJUNCTIVITIS- RECURRENT

VIRAL CONJUNCTIVITIS • SEROUS OR WATERY DISCHARGE • FOLLICULAR CONJUNCTIVITIS • CAUSED BY ADENOVIRUS AND HERPES VIRUS RAPIDLY DEVELOPING FOLLICULAR REACTION • WATERY SCANTY EXUDATE WITH MARKED INFLAMMATION. • MAY HAVE MEMBRANOUS CONJUNCTIVITIS • PREAURICULAR LYMPH NODE • CORNEAL INVOVLEMENT WITH SUPERFICIAL PUNCTATE EPITHELIAL INFILTRATES FOLLOWED BY SUBEPITHELIAL INVOLVEMENT. PHOTOPHOBIA IS MARKED.

VIRAL CONJUNCTIVITIS • ACETAMIDE DROPS ARE USED. ANTIVIRALS NOT NEEEDED AS ACYCLOVIR NOT EFFECTIVE AGAINST ADENOVIRUS. • MILD ANTI INFLAMMATORY DRUGS WITH TEAR SUPPLEMENTS • ANTIBIOTIC DRUGS TO PREVENT SECONDARY INFECTION. 20% SULPHA ACETAMIDE DROPS ARE USED. • ANTIVIRALS USED IF THERE IS CORNEAL ULCER OR SKIN INVOLVEMENT

OPHTHALMIA NEONATORUM • MUCOID, PURULENT OR MUCOPURULENT DISCHARGE FROM ONE OR BOTH EYES IN 1 MONTH OF LIFE. • DUE TO MATERNAL INFECTION ACQUIRED AT TIME OF BIRTH • CHLAMYDIA OCULOGENETALIS, STREPTOCOCCUS PNEUMONIAE • D/D-CONGENITAL DACRYOCYSTITIS, CONGENITAL GLAUCOMA

TIMO OF ONSET DIFFERENTIA L DIAGNOSIS CLINICAL PRESENTATIO N TREATMENT WITHIN FIRST 48 HOURS NEISSERIA go norrhoeae Purulent/mucopu rulent discharge with inflammed and chemosed conjunctiva. Marked lid edema Corneal ulceration with perforation Local cleaning of eyes Ceftriaxone im Gentamicin drops 0. 3% Bacitracin eye ointment CHEMICALINSTILLATION OF CREDES SOLN(SILVER NITRATE 1%) CONGESTED EYE WITH WATREY DISCHARGE EYE WASH ERYTHROMYCIN OINTMENT WATCH

TIME OF ONSET DIFFERENTI AL DIAGNOSIS CLINICAL PRESENTATI ON TREATMENT 48 -72 HOURS OTHER BACTERIA RED EYE MUCOPURULE NT DISCHARGE LID EDEME CORNEAL ULCER RARE NEOMYCINBACITRACIN EYE OINTMENT GENTAMICIN OR TOBRAMYCIN DROPS 5 -7 DAYS HERPES SIMPLEX(HSV II) WATERY DICSHARGE PREAURICULA R LYHMPH NODE CORNEAL LESIONS ACYCLOVIR 3% OINTMENT 5/DAYS VIDARABINE EYE DROPS 3% SYSTEMIC ACYLOVIR > 1 WEEK CHYLAMYDIA TRACHOMATIS (D-K) VENEREAL INFECTION LID EDEMATOUS CONJUNCTIVA SUPERFICIAL KERATITIS WITH ERYTHROMYCI N OR CHLOROTERTR ACYCLINE OINTMENT ORAL

OPHTHALMIA NEONATORUM • CONJUNCTIVAL SMEARS FOR GRAM AND GIEMSA STAINS. • CHLAMYDIAL IMMUNOFLUORESCENT ANTIBODY TEST. • PROPHYLACTIC TREATMENT- CLEAN BABY LIDS. APPLICATION OF 1% TETRACYCLINE OR TETRACYCLINE OINTMENT. • COMPLICATIONS- CORNEAL OPACITY, ANTERIOR STAPHYLOMA, COMPLICATED CATARACT, PANOPHTHALMITIS, AMBLYOPIA, NYSTAGMUS

TRACHOMA • TYPE OF ENDEMIC CHRONIC CONJUNCTIVITIS • MAJOR CAUSE OF BLINDNESS. • WHO- 150 MILLION PEOPLE ARE AFFECTED , 6 MILLION PEOPLE ARE BLIND • DISEASE OF PEOPLE LIVING IN UNHYGIENIC CONDITIONS. • HIGHEST PREVALENCE IN AGES 2 -7 YEARS • TRANSMITED BY TOWELS, FINGERS, FLIES • CONTAGIOUS KEARTOCONJUNCTIVITIS • HIGHLY PREVALENT IN NORTH AFRICA, MIDDLEAEST AND SOUTH EAST ASIA.

TRACHOMA • Low contagiousness • Endemic when there are favourable factors like • 1) in endemic Areas seen in infancy with eye to eye transmission. • 2) sporadic cases spreads by genital contact • Environmental factors • 1) overcrowding • 2) abundant fly population • 3)insaniatry condition • 4)low personal hygiene • Secondary bacterial and viral infection which leads to spread of disease.

TRACHOMA • AETIOLOGY • Caused by a large sized atypical intracellular bacterium • Psittacosis-lymphogranuloma-trachoma group. Chlamydia trachomatis. 14 serotypes ranging from a-k. • Organism isolated from trachoma and inclusion conjunctivitis is same knowm as TRIC agent

TRACHOMA • • • SYMPTOMS MILD CASES ARE USUALLY ASYPMTOMATIC IRRITATION PHOTOPHOBIA WATERING DECREASED VISION IN LATE STAGES

TRACHOMA • PATHOLOGY • CHLAMYDIA TRACHOMATIS( A, B , C)Seen as colonies with HALBERSTAEDTERPROWAZEK inclusion bodies in epithelial cells. • Rapidly divide within the epithelial cell to from elementary bodies. • These swell to form intracellular extranuclear initial bodies. Rapidly divide into small multiple elementary bodies which burst out of the cell to reinfect fresh cells.

TRACHOMA • HISTOLOGY • LYMPHOCYTIC INFILTRATION OF THE ADENOID LAYER FORMING LARGE FOLLICLES. • COMPOSED OF LARGE MULTINUCLEATED CELLS –LEBER CELLS WHICH ENGULF THE CYTOPLASMIC AND NUCLEAR DEBRIS. • FOLLICLES TEND TO NECROSE. • FIBROBLASTS GROW TO FORM SCAR • HYALINE DEGENERATION OCCURS IN LATE STAGES WITH FIBROUS TISSUE BANDS.

Trachoma • Insidious onset with incubation period of 5 -15 days. • 1) symptomless disease with spontaneous regression in patients with good personal hygiene. • 2) subacute condition • 3) acute condition

symptoms • • Foreign body sensation Watering Itching Photophobia Redness Decrease in vision Cicatricial complications – trichiasis and entropion.

TRACHOMA-SIGNS • CONJUNCTIVA • 1) CONGESTION- USUALLY DIFFUSE SEEN MORE IN UPPER TARSUS. RED VELVETY WITH UNIFORM JELLY LIKE THICKENING. • 2) PAPILLARY ENLARGEMENT • 3)FOLLICLES DEVELOPMENT- 5 MM IN SIZE USUALLY IN FORNICES FORMING A ROW IN UPPER TARSUS. • SEEN ON THE CARUNCLE, PLICA, LACRIMAL PASSAGES. RARE IN BULBAR CONJUNCTIVA. • MAY INVADE THE TARSUS PLATE. • MAY CICATRISE EARLY LAEDING TO STELLATE SHAPED SCARS.

TRACHOMA SIGNS • Follicles are bigger in size and variable consistency. • Fine linear scar may be seen in the sulcus subtarsalis- Arlts ‘ line. • White thick dense scarring of upper tarsal conjunctiva leading to trichiasis and entropion.

Trachoma • Infection with serotypes A, B, Ba and C of Chlamydia trachomatis • Fly is major vector in infection-reinfection cycle Progression Acute follicular conjunctivis Pannus formation Conjunctival Herbert pits scarring (Arlt line) Trichiasis Cicatricial entropion Treatment - systemic azithromycin

TRACHOMA SIGNS • CORNEA • 1) SUPERFICIAL KERATITIS –NUMEROUS EPITHELIAL EROSIONS IN UPPER PART OF THE CORNEA SEEN AFTER FLUORESCEIN STAIN. • 2) PANNUS- LYMPHOID INFLITARTION WITH VASCULARIZARTION OF THE SUPERIOR PART OF THE CORNEA. • UPPER CORNEAL MARGIN BECOMES HAZY WITH SUPERFICIAL VASCULARISATION. • HERBERTS PITS AT THE LIMBUS- FOLLICLE LIKE INFILTRATION. • INTIALLY INVOLVE THE BOWMANNS MEMBRANE LATER ON INVOLVING THE SUBSTANSIA PROPRIA. • INVOLVE THE WHOLE CORNEA.

TRACHOMA SIGNS • Divided into • 1) PROGRESSIVE PANNUS • Parallel vessels directed vertical downwards with little anastomosis. Form a vertical line with a zone of infiltration and haze ahead of it. • 2) REGRESSIVE PANNUS • Infiltration extends beyond the zone of infiltration. • Resolution of pannus leaves an opacity. • CORNEAL ULCERS- chronic shallow with little infiltration at advancing edge of the pannus.

TRACHOMA SEQUELAE • CORNEA- TOTALLY OPAQUE WITH TATAL VASCULARISATION. CORNEAL ULCERS WITH BACTERIAL SUPPURATION. • CONJUNCTIVA-WHITE CONJUNCTIVAL SCAR SEEN AT JUNCTION OF LOWER 1/3 AND UPPER 2/3 OF THE TARSUS- ARLT LINE. • DRY EYE • LIDS • 1) PTOSIS- DUE TO DENSE INFILTRATION. • 2) ENTROPION- INTURNING OF THE EYELID DUE TO SACR TISSUE • 3) TRICHIASIS- INTURNING OF THE EYELASHES. • 4) TYLOSIS- THICKENING OF THE TARSAL PLATE

TRACHOMA- DIAGNOSIS • CLINICAL – • 1)FOLLICLES IN PALPEBRAL CONJUNCTIVA • 2)SUPERFICIAL EPITHELIAL KERATITIS EARLY • 3)PANNUS IN SUPERIOR PARTOFL • 4)LIMBAL FOLLICLES / HERBERTS PITS • 5)STELLATE CONJUNCTIVAL SCARING • CULTURE- MICRO IMMUNOFLUORESCENCE • Mc. COY CELL CULTURES

WHO CLASSIFICATION FISTO TRACHOMATOUS FOLLICLE ACTIVE S DISEASE NEEDS TREATMENT 5 OR MORE FOLLICLES PALPEBRAL BLOOD VESSELS SEEN CLEARLY. PROPER TREATMENT LEAD TO NO SCARING TRACHOMA INTENSE SEVERE DISEASE URGENT TREATMENT NUMEROUS FOLLICLES AND PAPILLAE SEROIUS COMPLICATIO N TRACHOMATOUS SCARRING OLD INACTIVE INFECTION TARSAL CICATRIZATIO

WHO CLASSIFICATION TRACHOMATO US TRICHIASIS NEEDS CORRECTIVE SURGERY TRACHOMATO US TRICHIASIS TRACHOMATOU S OPACITIES VISUAL LOSS CORNEAL OPACITIES COVERING PART OF PUPILLARY AREA

Complication and sequelae • • 1) corneal ulceration 2) iritis 3) trachomotous ptosis 4)triachiasis 5) entropion 6)xerosis and symblepharon 7) corneal scar

Differntial diagnosis • 1) acute follicular conjunctivitis- inclusion conjunctivitis, , Adenoviral, Herpectic conjunctivitis • 2) chronic conjunctivitis • 3) miotic drugs

TREATMENT • SAFE-SURGERY, ANTIBIOTICS, FACE WASHING, ENVIRONMENT. • ANTIBIOTIC – REDUCE SEVERITY OF INFLAMMATION, DECREASE TRANSMISSION. • ORAL TREATMENT- TETRACYCLINE, ERYTHROMYCIN, RIFAMPICIN, SULPHONAMIDES • 1) TETRACYCLINE/ ERYTHROMYCIN- 250 -500 MGM QID FOR 3 -6 WEEKS • 2)DOXYCYCLINE – 100 MGM BD • 3)CLARITHROMYCIN- 250 -500 MGM BD • TETRACYCLINE /ERYTHROMYCINEYE OINTMENT BD- 6 WEEKS • SURGICAL CORRECTION OF PTOSIS OR ENTROPION • EPILATION OF TRICHIATIC EYELASHES.

Trachoma control • • Personal hygiene Environmental sanitation Clean towel Stop kajal

OPHTHALMIA NODOSA • IRRITATION CUSED BY CATERPILLAR HAIR • SMALL SEMITRANSLUCENT REDDISH OR YELLOWISH GREY NODULES ARE SEEN IN THE CONJUNCTIVA, CORNEA, IRIS • FOREIGN BODY SENSATION WITH WATERING • EXCISION OF NODULES WITH REMOVAL OF HAIR. • LOCAL ANALGESICS WITH STEROID DROPS TO DECREASE THE INFLAMMATION

ALLERGIC CONJUNCTIVITIS • TYPE OF IMMUNOPATHOLOGICAL REACTIONS • 1) TYPE 1(ACUTE ANAPHYLACTIC) • Mediated by Ig. E. severe lid chemosis with generalized urticaria. Vernal conjunctivitis. • 2)TYPE 2 (COMPLEMENT DEPENDANT) • Antibody antigen reaction which results in cell death due to activation of lytic complement or macrophages.

ALLERGIC CONJUNCTIVITIS • TYPE 3 HYPERSENSITIVITY(IMMUNE COMPLEX) • COMBINATION OF ANTIBODY AND ANTIGEN IN TISSUE FLUID OR PLASMA ACTIVATES COMPLEMENT SYSTEM. LEADS TO INFLAMMATION, NECROSIS, THROMBOSIS. • TYPE 4(CELL MEDIATED)-THYMUS DEPENDANT LYMPHOCYTES • TYPE 5(STIMULATING)- LATS IMMUNOGLOBULIN CONTACTS WITH SPECIFIC SITE ON THYROID.

ALLERGIC CONJUNCTIVITIS • ASSUME 3 FORMS • 1)ACUTE /SUBACUTE CATARRHAL CONJUNCTIVITIS • 2) VERNAL CATARRH-EXOGENOUS ALLERGENS. Giant papillary conjunctivitis is a variety. • 3)PHLYCTENULAR CONJUNCTIVITISreaction to ENDOGENS

Allergic conjunctivitis • • Symptoms 1) Eyelid swelling 2) itching 3) minimal redness which may be sectoral 4) watering 5) recurrent attacks 6) systemic associations like fever, URTI, urticaria, asthma

ALLERGIC CONJUNCTIVITIS • Lid edema • Face may be involved with eryisepalatous reaction • Follicular reaction in conjunctiva • Chemosis

ALLERGIC CONJUNCTIVITIS • CAUSES • Exogenous cause- Hay fever • -contact with animals, pollen , flowers • - local applications of drugs like brimonidine, atropine, cosmetics • Endogenous cause- bacterial protein staphylococcal infection of upper respiratory tract

ACUTE ALLERGIC CONJUNCTIVITIS • • TREATMENT 1)REMOVAL OF THE ALLERGEN 2)DESENSITIZATION WITH INJECTIONS 3)ANTI HISTAMINICS OR MAST CELL STABILISER DRUGS- sodium cromoglycate, olopatadine, ketotifen • 4)SHORT TERM CORTICOSTREOID DRUGS • 5)Systemic antihistaminics – cetrizine / levocetrizine • 6) systemic steroids

Vernal conjunctivitis • Also called as seasonal allergic conjunctivitis, vernal keratoconjunctivitis. • Recurrent bilateral conjunctivitis • Onset of hot weather • Seen in young people usually boys • Sporadic , seen in all class of patients • Family history of atopy • Type 1 hypersensitivity due to reaction to pollen and atmospheric exogens mediated by Ig. E • Some patients have symptoms throughout the yearperennial allergic conjunctivitis. •

Vernal conjunctivitis • • Symptoms 1) burning 2) itching 3) photophobia 4) lacrimation 5) white ropy discharge 6) children have a self limited course and can grow out of it in 5 -10 years. • 7) adults show severe disease with indefinate recurrences.

Vernal conjunctivitis • SIGNS • 1)PALPEBRAL FORM • 2) LIMBAL OR BULBAR FORM

Vernal conjunctivitis- PALPEBRAL FORM • Easy to diagnose • seen in upper palpebral conjunctiva • Hypertrophy of the conjunctiva which is mapped out into flat topped polygonal raised areas like cobblestones • These are bluish white in colour and rarely seen in lower palpebral conjunctiva. • Nodules are hard consisting of dense fibrous tissue covered by thickened epithelium. • Fornix is usually not involved • Recurrence in hot weather.

Vernal conjunctivitis • Histologically • Hypertrophic papillae • Eosinophillic leucoytes are seen with infiltration by plasma cells, macrophages, lymphocytes and basophils. • D/D- TRACHOMA

Vernal conjunctivitis • BULBAR FORM • Opacification of limbus with nodules or gelatinous thickening. • HORNER TRANTAS DOTS-white dots consisting of eosinophils and epithelial debris seen at limbus.

VERNAL CONJUNCTIVITIS • • • COURSE AND COMPLICATIONS SELF LIMITED TO RECURRENT ATTACKS 1) SUPERFICIAL PUNCTATE KERATITIS 2)DEVELOPMENT OF SEVERE DRY EYE 3)CORNEAL ULCER- SHIELDS ULCER 4)CONJUNCTIVAL THICKENING AND DISCOLORATION

Progression of vernal keratopathy Punctate epitheliopathy Plaque formation (shield ulcer) Epithelial macroerosions Subepithelial scarring

VERNAL CONJUNCTIVITIS • • TREATMENT SYMPTOMATIC TREATMENT 1)ACUTE IRITATION COLD COMPRESSES ANTI HISTAMINICS TOPICAL STEROIDS DROPS 4 -6 HOURLY 2) MAINTAINENCE LOW DOSE STEROIDS- SHORT TIME WITH SUPERVISION • MAST CELL STABILISER- DISODIUM CROMOGLYCATE 2%-4% QID –BD • OLOPATADINE-BD • SUBTARSAL INJECTION OF STEROIDS AND CRYO OF NODULES

Vernal conjunctivitis • Complications- chronic steroid use, secondary bacterial or fungal infection. • Acetyl cysteine is used as 10 -20% drops to control excess mucus. • Cold compresses an dark glasses act as adjuvant measures to alleviate discomfort. • Avoid rubbing of eye as this will lead to mast cell degranulation with histamine release. • Cryotherapy of papillary nodules.

GIANT PAPILLARY CONJUNCTIVITIS • Involves the superior tarsal conjunctiva • Cause-soft contact lens, protruding sutures, ocular prosthesis • Type 1 and 4 hypersensitivity reaction. • Symptoms- itching, watering, foreign body sensation, blurring of vision • Signs-upper conjunctival congestion with large polygonal papillae 1 -2 mm in size. • Macropapoillae are 0. 3 -1 mm in size.

GIANT PAPILLARY CONJUNCTIVITIS • Remove the cause- discontinue the contact lens, remove the suture and prosthesis • Local drops • Mast cell stabiliser- cromonyl sodium, olopatadine • Anti histaminics • Artificial tears • Decongestants • Steroid drops • Subtarsal injection of steroid depot preparation.

PHLYCTENULAR CONJUNCTIVITIS • • Allergic reaction caused by endogenous bacterial proteins mostly tubercular. • May be due to mild long standing infection like infection of adenoid or tonsils. • Seen in areas with bad hygiene and prevalence of tuberculosis. Disease involving the limbal and bulbar conjunctiva. • Rare in palpebral conjunctiva. • Congested vessels seen surrounding the limbus • PHLYCTEN- Small round grey- yellow nodules seen in bulbar conjunctiva around the limbus.

PHLYCTENULAR CONJUNCTIVITIS • Symptoms- discomfort and irritation reflex lacrimation with itching. • Redness localised. • Foreign body sensation • Corneal involvement may lead to photophobia. • Visual impairment. • In case of superadded infection there may be mucopurulent discharge with intensely congested eye. • .

PHLYCTENULAR CONJUNCTIVITIS • Signs • One or more small round grey or yellow nodules which are slightly raised are seen on bulbar conjunctiva and at the limbus. • Local vessels localised to phlyctens. • Rare on palpebral aspect. • Are small blebs may have a vesicular stage 1 mm in size. • Epithelium is necrotic with ulcer formation later. • May form a yellow ulcer with staphylococcal infiltration. • If deep infiltration there is opacity.

PHLYCTENULAR CONJUNCTIVITIS • • • TREATMENT Steroids as drops or ointment Anti histaminic- local and systemic Tear supplements Corneal ulcer- antibiotics and cycloplegics Dark shades.

PHLYCTENULAR KERATITIS • Phlytcens can occur within corneal margin also. • Involving superficial layers of cornea as it a conjunctival lessons. • Corneal phlyctens is a grey nodule forms a yellow ulcer if epithelium break down. • Marked pain and photophobia. • They may absorb without destruction of superficial layers of stroma leaves no opacity. • Secondary infection with staphylococcus leading to superficial ulcer. • Treatment same as conjunctival except add atropine with antibiotics once corneal ulcer forms.

Endogenous or immune system • Activation of immune and immunologically mediated inflammation due to allergic and drug reaction , autoimmune reaction involving mucous membrane. • Disease causing reaction in eyes • 1) ERYTHEMA MULTIFORME • 2) STEVENS- JOHNSONS • Mucous membranes like conjunctiva, mouth, nose urethra and vulva. • Skin eruptions with systemic involvement • Type 2 hypersensitivity due to immunological reaction to drugs- sulphonamides, NSAIDS, antibiotics , antimalarials, anti epileptics. • Systemic infections- Mycoplasma pneumoniae, herpes simplex virus and fungus. •

• STEVENS- JOHNSON • Serious disease sometimes fatal characterized by skin rash, erythematous lesions followed by bullae and epidermal necrosis, fever, malaise and ulcer of mucous membranes. • Involves eyelid and conjunctiva with ulcers. • Severe dry eye, symblepharon , lid deformity( cicatricial entropion), corneal vascularization and scarring.

Treatment • Supportive therapy with lubricant. • Antibiotic therapy in bacterial infection. • Glass roding – lysis of adhesions forming between the bulbar and palpebral conjunctiva by passing a glass rod coated with antibiotics ointment. • Cicatricial complication treatment with surgery. • Dry eye traeted with amniotic membranes.

DEGENERATIVE CHANGES • 1) CONCRETIONS • • • (LITHIASIS) MINUTE HARD YELLOW SPOTS IN PALPEBRAL CONJUNCTIVA. ACCUMULATION OF EPITHELIAL CELLS AND MUCUS IN HENLES GLANDS DO NOT CALCIFY. COMMON IN ELDERLY ARE ASYMPTOMATIC IF THEY PROJECT THEN MAY CAUSE FOREIGN BODY SENSATION REMOVED WITH 26 GAUGE NEEDLES IF SYMPTOMATIC

PINGUECULA • Yellowish , triangular deposits on conjunctiva near limbus in palpebral aperture. • Found in elderly patients who are exposed to strong sunlight dust, wind. • Apex of triangle is away from the cornea and it affects the nasal side first. • Hyaline infiltration and elastotic degeneration of submucosal tissue. • Normal asymptomatic. • If inflamed then treat with local antiinflammatory and steroid drops.

Pterygium • Definition- degenerative condition of the subconjunctival tissue that proliferates as vascularized granulation tissue to invade the cornea destroying the superficial layer of stroma and Bowmann membrane the whole being covered by conjunctival epithelium. • Can be • 1) Primary • 2) Recurrent- after excision of primary pterygium

Pterygium • • Comprises of 1) Head- apex with avascular cap 2)Neck- over limbus 3) Body – over sclera Occurs 1) Nasal 2) rarely temporal 3) double pterygium- nasal and temporal

Pterygium • Numerous deposits seen anterior to apex. • Fold at superior and inferior border. • Deposition of iron Stockers line is seen in corneal epithelium in front of the apex.

PTERYGIUM • SYMPTOMS • 1) NOTICES A SWELLING OR MASS IN THE EYE • 2) REDNESS/ FOREIGN BODY SENSATION • 3) DIMINISHED VISION WHEN IT CROSSES PUPILLARY MARGIN AND ASTIGAMTISM. • 3) RARELY DIPLOPIA – DUE TO LIMITATION OF OCUALAR MOVEMENTS.

PTERYGIUM- EPIDEMIOLOGY AND RISK FACTORS • Common in warm and dry climates • Peri equatorial belt 37 degree north and south of equator. • Common age of onset is 20 -30 years. • Risk factors • 1) Environmental –risk of exposure to UV light • Absorbed by cornea and conjunctiva promotes cellular damage and proliferation. • 2) Genetic-p 53 oncogene marker for pterygium. • 3) Chronic irritation and inflammation at the limbus or periphery cause limbal deficiency. • Dust, low humidity, microtrauma, dry eye.

Pterygium- Pathogenesis • Chronic degeneration based on histological examination. Elastotic degeneration characterized by abnormal subepithelial tissue containing altered collagen fibers. • LIMBAL DEFICIENCY-Stem cell death • • -conjunctival ingrowth • -vascularization/chronic inflammation • -destruction of basement membranes and fibrous ingrowth. .

Pterygium • Based on slit lamp examination Tan be divided into • 1)Atrophic-episcleral vessels underlying body of pterygium are unobscured and clearly distinguished. • 2) Intermediate- episcleral vessels are indistinctly seen or obscured. • 3)Fleshy- thick pterygium in with underlying episcleral vessels are totally obscured by the mass.

Types of pterygium

PTERYGIUM • • TREATMENT BEST LEFT ALONE INDICATIONS FOR TREATMENT 1)PROGRESSING TOWARD PUPILARY AREA 2)EXCESSIVE ASTIGMATISM 3)RESTRICTED OCULAR MOVEMENT 4) COSMETIC LEAVES A SCAR UNLESS THERE IS A LAMELLAR CORNEAL GRAFT

Pterygium treatment • Main four groups • 1) Bare sclera excision • 2)Excision with conjunctival closure /transposition • 3)Excision with antimitotic membrane adjunctive therapy • 4)Ocular surface transportation technique. • • • Anesthesia used 1) Subconjunctival or topical anesthesia 2) Long procedure- local anesthesia 3) General anesthesia – if uncooperative patient or recurrent pterygium.

PTERYGIUM • BARE SCLERA METHOD • Excising head and body of pterygium back to nasal canthus laying the area of bare sclera to reepithelialize • High recurrence rates- 24 - 89% • Complications include • 1) aggressive recurrence exceeding the primary disease. • 2)symblepharon, ocular motility restriction, • 3) Scleral necrosis with infective scleritis •

PTERYGIUM -TREATMENT • 2) EXCISION WITH CONJUNCTIVAL CLOSURE / TRANSPOSITION • After bare sclera excision the conjunctiva is closed over the excised area with sutures • Not of much benefit.

Pterygium treatment • EXCISION WITH ADJUNCTIVE MEDICAL THERAPY • 1) BETA IRRADIATION • Strontium -90 has been tried in single or multiple applications. • MOA- maximal effects on immature or rapidly growing tissues. Prevents recurrence by reducing fibroblasts proliferation and causing end arteritis. • Adverse effects – scleral necrosis, endophthalmitis, corneal perforation, cataract formation, secondary glaucoma. • Potential serious complications hence role is limited. • Recurrence rates= 10%

PTERYGIUM • EXCISION WITH ADJUNCTIVE MEDICAL THERAPY • 2) MITOMYCIN C- antibiotic- anticancer drug • Inhibits RNA, DNA, protein synthesis. Long term effect on cell proliferation. • Localized inhibition of Tennon fibroblasts thus reducing scarring and recurrence. • Indications in ocular surgery • 1) adjunctive in pterygium surgery • 2)glaucoma surgery • 3)reduce corneal scaring after PRK • 4)treat conjunctival intraepithelial neoplasia.

Pterygium • Used in 2 ways • 1)Post operative use of topical Mitomycin C as eyedrops. 0. 02% concentration administered 4 times for 1 -2 weeks. • Severe complication similar to B radiation. • 2) Intraoperative application of surgical sponges soaked in Mitomycin solution. • 0. 01%-0. 04% for 3 -4 minutes. • Recurrence 3 -43%. • Complications – early punctate keratitis, chemosis, delayed conjunctival wound healing, corneal and scleral melting.

Pterygium • 3)Subconjunctival injection • MMC preoperatively directly into pterygium tissue. • Before 1 month of pterygium excision. • 0. 1 ml of 0. 15 mg/ml MMC in balanced salt solution injected directly in the pterygium.

Pterygium treatment • OCULAR SURFACE TRANSPLANTATION TECHNIQUES • 1)Conjunctival autograft transplantation • 2)Amniotic membrane transplantation

Pterygium treatment • Gold standard in pterygium surgery • 1) pterygium excision • 2) measure the size of bare sclera- vertical and horizontal • 3) Free conjunctival autograft from superior conjunctiva oversized by 1 mm compared to the bare scleral area. • 4)removing all underlying fibrovascular and Tennon tissue • 5) avoiding buttonholing of graft • 6)achieving stable tension free graft by use of anchoring sutures(8 -0 vicryl) with episcleral bites or tissue glue

Pterygium treatment • Complications- graft edema, retraction, necrosis, granuloma. • Modifications • 1) conjunctival rotational autograft – conjunctiva over the graft is used • 2) cultivated conjunctival transplantation – ex vivo • 3) Amniotic membrane- anti scaring, anti angiogenic and anti inflammatory. • Preservation of superior conjunctiva. ALLOGRAFT

Pterygium treatment • Role of fibrin glue/ sutureless ptreygium excision • Biological and biodegradable. Used under the graft/ amniotic membrane. • Reduces operative time • Less postoperative discomfort Expensive surgery

DIFFERENTIAL DIAGNOSIS PTERYGIUM PSEUDOPTERYGIU M POSITION INTER PALPEBRAL AREA FROM THE FORNICES CAUSE DEGENERATIVE SECONARY TO CORNEAL ULCER OR POST STEVEN JOHNSON PROBE TEST NEGATIVE POSITIVE

NODULE AT LIMBUS • 1) DEGENERATIONS- Pincuegula, Pterygium • 2) ALLERGIC-PHLYCTENS • 3) INFLAMMATION- EPISCLERITIS, SCLERITIS • 4)POST OPERATIVE- SUTURES, TRABECULECTOMY BLEB • 5) FOREIGN BODY, GRANULOMA • 6) CONJUNCTIVAL CYSTS • 7) SUBCONJUNCTIVAL CYSTICERCUS AND HYDATID CYST • 8) VITAMIN A DEFECIENCY- BITOT SPOTS

NODULE AT LIMBUS • CONJUNCTIVAL TUMOURS • BENIGN-LIMBAL DERMOID, NEAVUS, PAPILLOMATA • PREMALIGNANT- INTRAEPITHELIAL EPITHELIOMA / CARCINOMA IN SITU • MALIGNANT- SQUAMOUS CELL CARCINOMA, BASAL CELL CARCINOMA, LYMPHOMA, KAPOSI SARCOMA, MALIGNANT MELANOMA

DRY EYE • TEAR FILM INSTABILITY • 1)DEFICIENCY OF TEARS –SJOGRENS SYNDROME • 2)DEFECIENCY OF CONJUNCTIVAL MUCUSSTEVEN JOHNSON , OCULAR PEMPHIGOID , OLD TRACHOMA, • 3) ALTERED CORNEAL SURFACE CHANGESPOST CHEMICAL INJURIES • 4)INSUFFICIENT WETTING – DECREASED BLINK RATE, LID PARALYSIS, FORMATION OF DELLEN

DRY EYE • BURNING, IRRITATION, DISCOMFORT, FOREIGN BODY SENSATION, ITCHING • TEAR FILM BREAKS UP INTO DRY SPOTS BETWEEN BLINKS EXPOSING CORNEA AND CONJUNCTIVA TO EVAPORATION. • TEAR FLUID CONTAINS MUCUS STAINED WITH ALCIAN BLUE AND DRY EPITHELIUM STAINED WITH ROSE BENGAL • TREATMENT- ARTIFICIAL TEAR DROPS, GELS, SLOW REALEASE PELLETS • LIFE STYLE MODIFICATION- DARK GOGGLES, AVOIDING AC • OCCLUSION OF CANALICULUS- COLLAGEN PLUGS