CORNEA.pptxneet ug #nta ncert khurana og

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1. DISEASES OF CORNEA Dr.B.DharmaRaju Professor of Ophthalmology NRIIMS

2. DIMENSIONS Avg horizontal dm….11.75mm Avg vertical dm…11mm Avg dm post surface..11.5mm Thickness (centre)…0.52mm Thickness(peripheral)..0.67mm Radius of curvature ( Ant.surface)..7.8mm Radius of curvature(post.surface)..6.5mm Refractive power(Ant.surface)..+48D Refractive power(Post surface)..-5D Refracrive Index..1.376

3. HISTOLOGY Cornea consists of 6 distinct layers Epithelium Bowman’s membrane Substantia propria ( stroma ) Dua’s layer Descemet’s membrane Endothelium

4. EPITHELIUM

5. Limbal epithelium The basal epithelial cells of limbal area constitute limbal stem cells which amplify, proliferate and differentiate into corneal epithelium.

6. PALISADES OF VOGT

7. LAYERS OF CORNEAL EPITHELIUM

8. CORNEAL STROMA

9. DESCEMETS MEMBRANE

10. CORNEAL ENDOTHELIUM

11. Blood supply Cornea is avascular Small loops derived from anterior ciliary vessels invades its periphery Nerve supply Supplied by anterior ciliary nerves, branches of ophthalmic division of 5 th N - Stromal , - Subepithelial - Intraepithelial .

12. APPLIED PHYSIOLOGY 2 primary functions Acts as major refracting medium Protect the intraocular contents Other functions Absorption of topically applied drugs Wound repair after AS surgery or trauma

13. CORNEAL TRANSPARENCY Peculiar arrangement of corneal lamellae Avascularity Relative state of dehydration Swelling pressure of stroma

14. SOURCES OF NUTRIENTS Oxygen - derived from atmosphere & aqueous Glucose - derived from aqueous humour & little from tear film Amino acids - from aqueous humour

15. BIOCHEMICAL COMPOSITION SUBSTANCES PERCENT WATER 78 COLLAGEN 15 OTHER PROTEINS 5 KERATAN SULPHATE 0.7 CHONDROITIN SULPHATE 0.3 SALTS 1

16. METABOLISM Cornea requires energy for normal metabolic activity as well as for maintaining transparency and dehydration Energy is generated by the break down of glucose in the form of ATP Most actively metabolizing layers are Epithelium & Endothelium METABOLIC PATHWAYS 1. Glycolytic pathway…glucose converted into pyruvic acid 2. HMP shunt…converts hexoses into pentoses 3. Sorbitol pathway… glucose produce sorbitol & fructose

17. CONGENITAL ANOMALIES MEGALOCORNEA Horizontal dm 13mm or greater after the age of 2 years Salient features Systemic associations Cornea is usually clear Marfan ’ syndrome Normal thickness Apert’s syndrome Normal vision Ehler’s-Danlos syndrome Not progressive Down’s syndrome Systemic associations: Marfan’s syndrome Apert’s syndrome Ehlers – Danlos syndrome Down syndrome

18. DIFFERENTIAL DIAGNOSIS Buphthalmos IOP raised Eyeball is enlarged as a whole Associated with central or peripheral clouding and Descemet’s tears ( Haab’s striae ) Keratoglobus Thinning & excessive protrusion of cornea Diameter is usually normal

19. MICROCORNEA Horizontal dm is less than 10mm since birth May occur as an isolated anomaly or ass. with * Nanophthalmos (Normal small eyeball) * Microphthalmos (Abnormal small eyeball)

20. CORNEA PLANA Rare anomaly Bilateral condition Cornea is comparatively flat since birth May be associated with microcornea Usually results in marked astigmatism

21. INFLAMMATIONS OF CORNEA (KERATITIS) Classification Tophographic classification Ulcerative keratitis Non-ulcerative keratitis Etiological classification Infective Allergic Trophic Ass.with D. of skin & MM Ass.with syst. D Traumatic Idiopathic

22. Ulcerative keratitis (Corneal ulcer) Depending on location Depending upon depth Central c. ulcer Superficial c. ulcer Peripheral c. ulcer Deep c. ulcer Depending on purulence U lcer with imp.perforation Purulent c. ulcer Perforated c. ulcer Non-purulent c. ulcer Depending upon slough formation Depending on ass.of Non-sloughing c.ulcer hypopyon S loughing c.ulcer Simple c. ulcer Hypopyon c. ulcer

23. Etiological classification Infective keratitis Bacterial Viral Fungal Chlamydial Protozoal Spirochaetal Allergic Keratitis Phlyectenular Keratitis Vernal Keratitis Atopic Keratitis Trophic Keratitis Exposure Keratitis Neurotrophic Keratopathy Keratomalacia Atheromatous ulcer l

24. Keratitis ass.with disease of skin & mucous membrane Keratitis ass. With systemic , collagen vascular diseases Traumatic keratitis Idiopathic keratitis * Mooren’s corneal ulcer * Sup.limbic keratoconj . *SPK of Thygeson

25. ULCERATIVE KERATITIS Corneal ulcer may be defined as discontinuation of normal corneal epithelial surface associated with necrosis of surrounding tissue INFECTIVE KERATITIS Bacterial Viral Fungal Chlamydial Protozoal Spirochaetal

26. BACTERIAL CORNEAL ULCER Cornea prone to get infections Etiology * Damage to corneal epithelium * Infection of the eroded cornea

27. Source of infection Exogenous infection Conjunctival sac Lacrimal sac( dacryocystitis ) Infected F.B Infected vegetative material Water-born infections Air-born infections From ocular tissue … due to anatomical continuity - Diseases of conjunctiva….spread to epithelium - Diseases of sclera…….spread to stroma - Diseases of uvea …….spread to endothelium Endogenous infection Rare

28. Causative organisms Common bacteria associated with Corneal ulcer Staph.aureus Pseudomonas pyocyanea Streptococcus pneumoniae E.coli Proteus Klabsiella N.Gonorrhoea N.meningitidis C.Diphtheriae

29. CLINICAL PICTURE Symptoms Pain & FB sensation Watering Photophobia Blurred vision Redness of eyes Discharge from eye

30. Signs Swelling of lids Blepharospasm Conjunctiva is chemosed Conjunctival hyperemia Ciliary congestion Corneal stromal oedema Established bacterial ulcer is characterised by * Yellowish-white area of ulcer ……oval or irregular * Margins swollen and over hanging * Floor of ulcer covered by necrotic material * Stromal oedema

31. Complications of corneal ulcer Toxic iridocyclitis Secondary glaucoma Descemetocele Perforation of corneal ulcer- Corneal scarring

32. Sequelae of corneal perforation Prolapse of iris Anterior capsular cataract Corneal fistula Endophthalmitis or uveitis Intraocular haemorrhage Subluxation or anterior dislocation of lens

33. MANAGEMENT OF CORNEAL ULCER

34. CLINICAL EVALUATION Thorough history taking To elicit mode of onset Duration of disease Severity of symptoms General physical examination For built Nourishment Anaemia Immuno compromising disease

35. OCULAR EXAMINATION Diffuse light examination * For gross lesions of lids,conjunctiva and cornea Regurgitation test & syringing test to r/o lacrimal sac infection Biomicroscopic examination after staining with 2% flourescein dye or strip. * Ulcer stains as brilliant green,looks opaque green with blue filter * Note site,size,shape,depth,margin,floor&vascularization * Presence of KPs * Depth & contents of AC * Colour & pattern of iris * Condition of crystalline lens

36. FLOURESCIEN STAINING

37. Laboratory investigations Routine laboratory investigations * Hb % * TLC,DLC,ESR * Blood sugar * Complete urine & stool examination Microbiological investigations * Scraping of base and margins of corneal ulcer used for Gram&Geimsa stain for identification of infecting organism 10& KOH wet preparation for identification of fungal hyphae Calcofluor white for fungal filaments Culture on blood agar medium for aerobic organisms Culture on Sabouraud’s dextrose agar medium for fungi

38. TREATMENT Treatment of uncomplicated corneal ulcer Treatment of non-healing ulcer Treatment of impending perforation Treatment of perforated corneal ulcer

39. Treatment of uncomplicated corneal ulcer Specific treatment for the cause Non-specific supportive therapy Physical & general therapy

40. SPECIFIC TREATMENT Topical antibiotics. Initial therapy Subsequent therapy Initial therapy: with combination therapy to cover both gram negative and gram positive organisms * Fortified Cefazoline 5% E/D i.e.50mg/ml freshly prepared by adding sterile water to 500mg powder * Fortified Tobramycin 1.3% ,i.e 13.6mg/ml prepared by adding 2 ml of tobramycin injection in 5ml of 0.3% drops (or) * Freshly prepared fortified vancomycin 5% ,i.e 50mg/ml prepared adding sterile water to 500mg vancomycin powder to form 10ml sol. * Fluoroquinolones eye drops( 0.3% Ciprofloxacin or 0.3% Ofloxacin or 0.3%Gatifloxacin or 0.5% Moxifloxacin

41. TREATMENT - contd - Frequency of instillation - Every 5 minutes for 30 minutes - Every 15 minutes for 2 hours -1 hourly round the clock for first 48 hours -2 hourly during day & 4 hourly at night till healing ensures -4-6 hourly till healing occurs -Once response is obtained, fortified drops can be substituted by commercially available eye drops Subsequent therapy -No need to change initial antibiotics, if the response is good -If the response is poor, change the antibiotics immediately as per culture and sensitivity report Systemic antibiotics -Usually not required -In fulminating cases Cephalosporin & an Aminoglycoside or oral ciprofloxacin 750mg BD may be given

42. NON- SPECIFIC TREATMENT Cycloplegic drugs -1% atropine eye ointment or drops to reduce pain from ciliary spasm & to prevent post.synechiae d/t iridocyclitis . Atropine also increases blood supply to anterior uvea by relieving pressure on anterior ciliary arteries and so brings more antibodies in the aqueous humour -2% homatropine another cycloplegic can be used Systemic analgesic & anti inflammatory drugs - Paracetamol & Ibuprofen to relieve pain & decrease oedema Vitamin A,B-complex and C help in early healing of ulcer

43. PHYSICAL & GENERAL MEASURES Hot fomentation Dark goggles Rest Good diet

44. TREATMENT OF NON- HEALING ULCER Removal of the cause Common causes of non-healing ulcer Local causes * Raised IOP * Concretions * Misdirected cilia * Impacted FB * Dacryocystitis * Inadequate therapy * Wrong diagnosis * Lagophthalmos * Excessive vascularization

45. Systemic causes * Diabetes mellitus * Severe anaemia * Malnutrition * Chronic debilitating diseases * Patients on systemic steroids Mechanical debridement of ulcer To remove necrosed material by scraping of floor of ulcer Cauterisation of ulcer … in non responding cases with pure carbolic acid or 10-20& Trichloracetic acid Bandage soft contact lens Peritomy

46. TREATMENT OF IMPENDING PERFORATION No strain: Avoid sneezing,coughing & straining during stool Pressure bandage to give external support Lowering of IOP A cetazolamide 250mg QID orally or IV mannitol 20% drip stat or Oral glycerol BD or 0.5% Timolol eye drops BD Paracentesis with slow evacuation of aqueous Tissue adhesive glue - cyanoacrylate Bandage soft contact lens Conjunctival flap – to give support to the weak tissue Amniotic membrane transplantation Penetrating therapeutic keratoplasty in suitable cases

47. TREATMENT OF PERFORATED CORNEAL ULCER If perforation occurs, immediate measures to be taken to restore the integrity of perforated cornea Depending on size of perforation, measures like * Tissue adhesive glues * Conjunctival flap * Bandage soft contact lens * Therapeutic keratoplasty

48. PREVENTION Although not always a preventable disease, certain steps may help reduce the potentially severe consequences of suppurative keratitis . Community awareness of risk factors for suppurative keratitis such as minor trauma and the use of contaminated traditional eye solutions in the eye Early recognition and institution of appropriate therapy by community health workers or ophthalmologists Prompt referral of advanced cases to tertiary eye care centres If individuals have dry eyes or if their eyelids do not close completely, they should use artificial tear drops to keep the eyes lubricated.

49. HYPOPYON CORNEAL ULCER Etiopathogenesis Causative organisms * Pneumococcus * The ulcer is called ulcus serpens Source of infection * Usually chronic dacryocystitis Factors predisposing to development of hypopyon * Virulence of the infecting organism & resistance of tissue * Common in debilitated or alcoholic subjects

50. Mechanism of development of hypopyon C.ulcer associated with iritis Outpouring of leucocytes to the bottom of AC to form hypopyon Hypopyon is sterile Once the ulcer is controlled, hypopyon is absorbed

51. CLINICAL FEATURES Symptoms Pain & FB sensation Watering Photophobia Blurred vision Redness Signs Swelling of lids Blepharospasm Conjunctival chemosis Conjunctival hyperemia

52. Characteristic features of ulcus serpens * Greyish -white or yellowish disc shaped ulcer at the centre * Creep over cornea in serpiginous fashion * One edge shows more infiltration * Other side shows cicatrization * Violent iridocyclitis is common * Hypopyon increases rapidly--- Sec.glaucoma * Ulcer spreads rapidly --- early perforation

53. MANAGEMENT -Similar to bacterial corneal ulcer -Special points to be considered are Secondary glaucoma -should be anticipated -0.5% Timolol maleate eyedrops BID -Oral acetazolamide Source of infection - ie ., chronic dacryocystitis if detected treated by dacryocystectomy .

54. MARGINAL CATARRHAL ULCER Situated near the limbus Seen in old people Etiology Hypersensitivity reaction to staphylococcal toxins In association with chr.staphylococcal Blepharo conjunctivitis Moraxella & haemophilus may also cause such ulcers Clinical features Symptoms * Mild ocular irritation * Pain * Photophobia * Watering

55. Signs * Ulcer is shallow, slightly infiltrated often multiple, * Usually associated with staphylococcal conjunctivitis * Vascularization occurs followed by resolution * Recurrence is very common Treatment Short course of topical steroids along with antibiotics Adequate treatment of associated blepharitis and chronic conjunctivitis to prevent recurrences

56. MYCOTIC CORNEAL ULCER Etiology Causative fungi Filamentous fungi- eg.Aspergillus,Fusarium,Alternaria Cephalosporium,Curvularia & Penicillium Yeasts- eg.Candida and cryptococcus Commonest are Aspergillus , Candida and Fusarium Modes of infection Injury by Vegetative material such as crop leaf, branch of tree, straw, hay or decaying vegetable matter Injury by animal tail Secondary fungal ulcers common in immunosuppressed or in dry eye, herpetic keratitis , bullous keratopathy & in post op.cases of keratoplasty

57. Role of antibiotics and steroids Antibiotics disturb the symbiosis between bacteria and fungi Steroids make the fungi facultative pathogens which are otherwise symbiotic saprophytes, so excessive use of steroids predisposes fungal infections

58. CLINICAL FEATURES Symptoms * Similar to central bacterial corneal ulcer * Generally less marked * Overall course is slow and torpid Signs * Ulcer is dry looking, greyish white with elevated rolled out margins * Pigmented ulcer (brownish) caused by dermatiaceous fungi * Delicate feathery finger-like extensions into the surrounding stroma under the intact epithelium * Sterile immune ring is present where fungal antigen and host antibodies meet

59. Signs: -- contd * Multiple small satellite lesions may be present around the ulcer * Usually a big hypopyon may not be sterile as the fungi can penetrate into AC without perforation * Endothelial plaque seen under the stromal lesion * Perforation is rare, but can occur

60. DIAGNOSIS Typical clinical manifestations associated with history of injury by vegetative material Chronic ulcer worsening inspite of most efficient treatment Laboratory investigations for confirmation,include - Wet KOH, - Calcoflour white - Gram’s and Geimsa stain for fungal hyphae - Culture on sabouraud’s agar Methods of sample collection Corneal scrapings Anteriorchamber paracentesis Corneal biopsy Confocal microscopy Polymerase chain Reaction

61. TREATMENT Specific treatment : includes antifungal drugs Topical antifungal eyedrops for a long period of 6-8 wks Natamycin - 5%, Amphotericin B 0.1-0.3% and Fluconazole - 0.2% (or) Miconazole - 10mg/ml (or) Voriconazole – 10% eyedrops Frequency of instillation, one hrly taper slowly 6 to 8 wks These are effective against Aspergillus and Fusarium Nystatin – 3.5% eye ointment 5 times a day for candida Intra cameral, intracorneal &Intra stromal Voriconazole Systemic antifungal drugs may be required for severe cases Tab.Fluconazole or Ketoconazole for 2-3 wks

62. Non-specific treatment Cycloplegic drugs 1% Atropine eye ointment or drops 2% homatropine another cycloplegic can be used Systemic analgesic & anti inflammatory drugs such as Paracetamol Ibuprofen Vitamin A,B-complex and C help in early healing of ulcer Physical &General measures Therpeutic penetrating keratoplasty

63. VIRAL CORNEAL ULCERS Most of the viruses effect the epithelium of both conjunctiva and cornea so the lesions constitute Viral keratoconjunctivitis

64. HERPEX SIMPLEX KERATITIS Ocular infections with herpes simplex virus(HSV) are extremely common & constitute herpetic keratoconjunctivitis and iritis Etiology It is a DNA virus Natural host is man Basically epitheliotropic , may become neurotropic Two types -HSV type I cause infection above the waist -HSV type II effects below the waist (herpes genitalis )

65. Mode of infection HSV-I infection --acquired by kissing or coming in close contact with a patient suffering from herpes labialis HSV-II infection –Transmitted to eyes of neonates through infected genitalia of the mother

66. Ocular lesions of Herpes simplex Primary herpes Skin lesions Conjunctiva-acute follicular conjunctivitis Cornea Fine epithelial punctate keratitis Coarse epithelial punctate keratitis Dendritic ulcer Recurrent herpes Active epithelial keratitis Punctate epithelial keratitis Dendritic ulcer Geographic ulcer Stromal keratitis Disciform keratitis Diffuse stromal necrotic keratitis Trophic keratitis ( Metaherpetic ) Herpetic iridocyclitis

67. PRIMARY OCULAR HERPES Primary infection involves a non-immune person It typically occurs in children of 6 months - 5 yrs & teenagers CLINICAL FEATURES Systemicfeatures -mild fever malaise & non suppurative lymphadenopathy Skin lesions Vesicular lesions on skin of lids,periorbital region&lid margin Ocular lesions Acute follicular conjunctivitis Ass.with regional lymphadenitis, may be only manifestation Keratitis Cornea is involved in 50% of cases in the form of coarse punctate or diffuse branching epithelial keratitis

68. RECURRENT OCULAR HERPES The virus which lies dormant in trigeminal ganglion, Periodically reactivates and cause recurrent infection Predisposing factors Fever such as malaria and flu Exposure to UV rays General ill health Emotional or physical exhaustion Mild trauma Menstrual stress Following administration of topical or systemic steroids & Immunosuppressive agents

69. EPITHELIAL KERATITIS Punctate epithelial keratitis Initial epithelial lesion of recurrent herpes Resemble those seen in primary herpes Dendritic ulcer Typical lesion of recurrent EK Irregular,zigzag linear branching shape Branches are generally knobbed at the ends Floor of the ulcer stains with fluorescein & virus laden cells at the margin take up rose bengal Marked diminution of corneal sensations Geographical ulcer Branches of dendritic ulcer may enlarge & coalesce to form a large epithelial ulcer with a ‘geographical’ or ‘amoeboid’ configuration Developed as a complication of concomitant use of steroids

70. SPECIFIC TREATMENT Antiviral drugs are the first choice Always start with one drug first and see the response Usually after 4 days the lesion starts healing which is completed by 10 days After healing, taper the drug and withdraw in 5 days Change the drug or do mechanical debridement if there is no response after 7 days Commonly used anti viral drugs are Acycloguanosine (Acyclovir) 3% eye ointment 5 times a day14-21 days until ulcer heals, then 3 times a day for 5 days * It is least toxic and most commonly used * It penetrates intact epithelium and stroma Ganciclovir—0.15% gel 5 times a day until ulcer heals and then 3 times a day for 5 days, more toxic

71. Triflurothymidine 1% drops 2 hourly until ulcer heals and then 4 times a day for 5 days Adenine arabinoside ( Vidarabine ) 3% Ointment 5 times a day until ulcer heals and then 3 times a day for 5 days Mechanical debridement Helpful in resistant cases, non-compliance & allergic to AV drugs Systemic antiviral drugs for a period of 10 to 21 days Acyclovir 400 mgTID or Famcyclovir 250 mg TID or Valacyclovir 500 mg BID N0N-SPECIFIC SUPPORTIVE THERAPY Same as for other bacterial corneal ulcer

72. STROMAL KERATITIS Disciform keratitis Pathogenesis -Due to delayed hypersensitivity reaction to HSV antigen -Primarily, there occurs endothelitis -Endothelial damage results in disciform corneal stromal oedema due to imbibition of aqueous humour Symptoms Photophobia Mild to moderate ocular discomfort Decreased vision

73. Treatment Diluted steroid eye drops instilled 4-5 times a day with antiviral cover — acyclovir 3% twice a day Steroids should tapered over a period of several weeks Signs Focal disc-shaped patch of stromal oedema without necrosis usually with an intact epithelium Folds in descemet’s membrane Keratic precipitates Ring of stromal infiltrate ( Wessley immune ring) Corneal sensations are diminished IOP may be raised In severe cases anterior uveitis may be marked

74. Necrotising interstitial keratitis ( Stromal necrotic keratitis ) It is a type of interstitial keratitis caused by active viral invasion and tissue destruction Symptoms Pain, Photophobia Redness Signs Corneal lesions - - include necrotic,blotchy,cheesy white infiltrates under the epithelial ulcer Mild iritis and KPs (herpetic kerato-uveitis ) Stromal vascularization Treatment Systemic antiviral drugs for 10 to 21days in rec.cases & uveitis Keratoplasty deferred till the eye is quiet

75. Metaherpetic keratitis It is not an active viral disease but is mechanical healing problem due to persistent defect in the basement membrane of corneal epithelium Clinical features Indolent linear or ovoid epithelial defect Margin of the ulcer is grey & thickened due to heaped up epithelium Treatment Promote healing by Use of lubricants Bandage soft contact lens Lid closure ( tarsorrhaphy )

76. HERPES ZOSTER OPHTHALMICUS It is an acute infection of gasserian ganglion of 5 th N by varicella zoster virus It constitutes approximately 10% of all case of herpes zoster It occurs more commonly in immuno compromised individuals Etiology Varicella zoster virus is a DNA virus, produce acidophilic intra nuclear inclusion bodies Neurotropic in nature

77. Pathogenesis * The infection is contracted in childhood, manifest as chickenpox and child develops immunity * It remains dormant in the sensory ganglion of trigeminal N * In elderly people with depressed immunity the virus reactivates, replicates & travels down along branches of ophthalmic division of 5 th N

78. CLINICAL FEATURES Frontal nerve is more frequently affect than lacrimal and nasociliary nerves About 50% cases get ocular complications Hutchinson’s rule implies that ocular involvement is frequent if the side or tip of nose presents vesicles Lesions are strictly limited to one side of the midline of head.

79. CLINICAL PHASES

80. Acute phase lesions -- General features Cutaneous lesions Ocular lesions General features Onset of illness is sudden with fever,malaise and severe neuralgic pain along the course of the affected nerve Cutaneous lesions Appear after 3-4 days of onset of disease Skin of lids &other affected areas become red & oedematous , followed by vesicles In due course of time vesicles converted into pustules which subsequently burst to become crusting ulcers When crusts are shed permanent pitted scars are left Active eruptive phase lasts for about 3 weeks

81. Ocular lesions Conjunctivitis Most common Mucopurulent , with petechial haemorrhage Acute follicular conjunctivitis Necrotizing membranous inflammation Zoster keratitis Occurs in 40% of all patients, in several forms Epithelial keratitis * Fine or coarse punctate epithelial keratitis * Followed by microdendritic epithelial ulcers * Peripheral & stellate ,tapered ends & lack of bulbs

82. Nummular keratitis -Seen in about 1/3 of the cases -Multiple tiny granular deposits -Surrounded by a halo of stromal haze -Nummular scars’ are left behind Disciform keratitis Occurs about 50% of cases, always preceded by NK

83. Episcleritis & scleritis Iridodocyclitis Acute retinal necrosis Anterior segment necrosis Secondary glaucoma Associated neurological complications Motor nerve palsies- - 3 rd , 4 th, 6 th & 7 th Optic neuritis in 1% of cases Encephalitis - - Rare

84. Chronic phase lesions Basically sequelae of acute phase, may persists upto 10 yrs Post herpetic neuralgia *P ersistence of pain, seen in 10% of cases * May persists for years * Anaesthesia dolorosa Lid lesions * Occurs as sequelae of scarring include: Ptosis Trichiasis Entropion Notching

85. Conjunctival lesions I nclude chronic mucus secreting conjunctivitis Corneal lesions Neuroparalytic ulceration d/t gasserian ganglion destruction Exposure keratitis : d/t ass. Facial palsy Mucous plaque keratitis in 5% of cases Scleritis & uveitis M ay persists in chronic form.

86. Relapsing phase lesions May recur even after 10 years of acute phase, * Nummular keratitis * Mucous plaque keratitis * Episcleritis * S cleritis * Secondary glaucoma

87. TREATMENT Aim To prevent devastating ocular complications To promote rapid healing of skin lesions To prevent scarring of nerves & post herpetic neuralgia Systemic therapy for herpes zoster Oral antiviral drugs- decreases pain,curtails vesiculation , stop viral progression and reduce keratitis and iritis -Acyclovir- - 800mg 5 times a day for 10 days (or) - Valaciclovir - - 500mg tds Analgesics: Pain is severe during first 2 weeks, should be treated by analgesics as mephenamic acid & paracetamol

88. Systemic steroids for post herpetic neuralgia, 3 rd N palsy & optic neuritis Cimetidine in a dose of 300mg qid for 2-3 weeks to reduce pain and pruritis in acute zoster Amitriptyline to relieve depression in acute phases Local therapy for skin lesions : Antibiotic-corticosteroids skin ointment or lotions 3 times a day No calamine lotion Local therapy for ocular lesions For zoster keratitis,iridocyclitis & scleritis Topical steroid eyedrops 4 times a day Cycloplegics such as cyclopentolate eyedrops BD (or) atropine eye ointment OD Topical acyclovir 3% eye ointment 5 times a day for 2 wks

89. To prevent secondary infection Topical antibiotics are used For secondary glaucoma 0.5% timolol or 0.5% betaxolol drops,BD Acetazolamide 250mg,QID For mucous plaques T opical mucolytics , eg . Acetyle cysteine 10% three times a day For persistent epithelial defect Lubricating artificial tear drops Bandage soft contact lens Surgical treatment For Neuroparalytic corneal ulcer Lateral tarsorrhaphy , Amniotic membrane transplantation or conjunctival flap, considered for non-healing cases Tissue adhesives Keratolplasty

90. CORNEAL ULCER BACTERIAL FUNGAL VIRAL

91. PROTOZOAL KERATITIS ACANTHAMOEBA KERATITIS Naturally occuring amoeba First diagnosed in 1973 90% of the cases involving contact lens wearers Increasing in incidence Difficulty in diagnosis Unsatisfactory treatment 2 species are responsible A.castellani . A.polyphaga ETIOLOGY Causative organism - - Acanthamoeba (free lying) found in soil,fresh water, well water, sea water, sewage and air * It exists in trophozoite and encysted forms Mode of infection * Direct corneal contact with any material or water contaminated with the organism

92. Situations of contamination Contact lens wearers using home made saline Non-contact lens related Mild trauma with contaminated vegetable matter, salt water diving, wind blown contaminant and hot tub use Opportunistic infection: in patients with herpetic keratitis , Bacterial keratitis , bullous keratopathy & NP keratitis Clinical features Symptoms * FB sensation * Mild pain to severe pain * Watering * Photophobia * Blepharospasm * Blurred vision

93. SIGNS Initial lesions Limbitis in 94% of cases Radial keratoneuritis Epitheliopathy - Punctate epitheliopathy -Epithelial ridges -Pseudo or true dendrites -Irregular epitheliopathy

94. Advanced cases -Patchy stromal infiltrates -Satellite infiltrates -Central or paracentral ring infiltrates - Hypopyon Severe cases -Ring abscess - Hypopyon and stromal necrosis

95. DIAGNOSIS Clinical diagnosis D ifficult, suspected in nonresponsive cases Laboratory diagnosis C orneal scrapings may be helpful Confocal microscopy Direct visualization of cysts - - diagnostic Potassium hydroxide mount(KOH): reliable in experienced hands for acanthamoeba cysts Calcofluor white stain is a fluorescent brightener which stains the cysts bright apple green Lactophenol cotton blue stained film for cysts Culture in non-nutrient agar ( E.coli enriched) may show trophozoites within 48 hrs, gradually turn into cysts Polymerase chain reaction Corneal biopsy

96. TREATMENT Usually unsatisfactory Non-specific treatment Cycloplegic drugs -1% atropine eye ointment to reduce pain & ciliary spasm -2% homatropine eyedrops can also be used Systemic analgesics & anti-inflammatory drugs such as - Paracetamol and ibuprofen to relieve pain & oedema -Vitamins A, B, and C help in early healing of ulcer Physical & general measures: Hot fomentation: Local application of heat gives comfort Dark goggles to prevent photophobia Rest, good diet and fresh air may have soothing effect

97. Specific treatment Topical Antiamoebic agents Diamidines : Propamidine isethionate 0.1% and Hexamidine 0.1% Biguanides : Polyhexamethylene biguanide (PHMB) - - 0.02% Chlorhexidine - - 0.02% Aminoglycosides : Neomycin and paromycin Imidazoles : Clotrimazole and miconazole Multiple drug therapy needed for long time 3 - 4 months in early epithelial lesions and 6 -12 months for stromal lesions Frequency of instillation Hourly for a week, then taper slowly,

98. Combinations of drugs - Propamidine or hexamidine +PHMB (or) - Chlorhexidine + Neomycin (or) - Paromycin + Clotrimazole or miconazole or itraconazole Oral ketoconazole 200mg BID or Itraconazole 100mg BID, may be added in advanced cases Long term prophylactic therapy with PHMB,BID for a year Penetrating keratoplasty : in non-responsive cases Surgery after full course of maximum medical therapy and a quiescent phase of atleast 6 months “Unfortunately, if not promptly treated, Acanthamoeba keratitis can cause permanent vision loss or require a corneal transplant to recover lost vision”

99. ALLERGIC KERATITIS PHLYCTENULAR KERATITIS It is an allergic response of cornea to endogenous allergens Corneal involvement may occur secondarily from extension of conjunctival phlycten or rarely as a primary disease Etiology Delayed hypersensitivity response to endogenous microbial proteins Causative allergens * Tuberculous proteins- - commonest * Staphylococcal proteins * Other allergens like Moraxella and certain parasites

100. Predisposing factors * Age: 3-15 yrs * Sex: More in girls * Undernourishment: More common in undernourished * Living conditions: Overcrowded & unhygienic * Season: More in spring & summer It may present as 2 forms Ulcerative phlyctenular keratitis Diffuse infiltrative keratitis

101. Ulcerative phlyctenular keratitis Sacrofulous ulcer: is a shallow marginal ulcer d/t limbal phlycten Fascicular ulcer: parallel leash of blood vessels leaves a band-shaped superficial opacity after healing Miliary ulcer: Multiple small ulcers are scattered over cornea SACROFULOUS ULCER FASCICULAR ULCER MILIARY ULCER

102. Diffuse infiltrative phlyctenular keratitis Superficial or deep May appear in the form of central infiltration of cornea with rich vascularization from periphery around limbus Clinical course * u sually self limiting * Phlycten disappears in 8 – 10 days * Recurrences are common Treatment Local therapy * Topical corticosteroids ( dexamethasone or betamethasone ) eye drops or ointment, produce dramatic effect * Antibiotic drops & ointment in secondary infections * Atropine 1% eye ointment OD Specific therapy to exclude TB, septic focus & parasitic infestation General measures: high protein diet & vitamins A C & D

103. VERNAL KERATITIS Corneal involvement in VKC may be primary or secondary to extension of limbal lesions It includes 5 types Punctate epithelial keratitis * Involving upper cornea * Associated with palpebral form * S tain with Rose bengal & flourescein Ulcerative vernal keratitis (Shield ulceration) * Shallow transverse ulcer in upper part * Ulceration due to epithelial macroerosions * May be complicated by bacterial keratitis

104. Vernal corneal plaques Due to coating of bare areas of epithelial macroerosions with a layer of altered exudates Subepithelial scarring In the form of ring scar Pseudogerontoxon characterised by cupid’s bow outline Vernal corneal plaques Pseudogerontoxon

105. TREATMENT Punctate epithelial keratitis Flourometholonemedrysone,dexamethasone betamethasone eyedrops to be instilled 4 hourly 1 st 2 days followed by 3-4 times a day for 2 weeks Large vernal plaque Requires surgical excision by superficial keratectomy Severe shield ulcer * Debridement * Superficial keratectomy * Excimer laser therapeutic keratectomy * Amniotic membrane transplantation

106. ATOPIC KERATITIS Adult equivalent of VKC Usually associated with atopic dermatitis Seen young atopic adults Incidence more in males Symptoms Itching eyes Photophobia Blurred vision Signs Lid margins inflammed Cornea shows punctate epithelial keratitis more severe in lower half Corneal vascularization,thinning and plaques TREATMENT Treat facia leczema & lid margin disease

107. TROPHIC CORNEAL ULCERS Develop due to disturbance in metabolic activity of epithelial cells Types Neurotrophic keratopathy Exposure keratopathy

108. NEUROTROPHIC KERATOPATHY It occurs due to decreased corneal sensation owing to damage of sensory nerve supply of the cornea ETIOLOGY Congenital A. Familial dysautonomia (Riley-Day syndrome) B. Congenital insensitivity to pain C. Anhidrotic ectodermal dysplasia

109. Acquired Following alchohol -block or electrocoagulation of Gasserian ganglion or section of the sensory root of trigeminal nerve for trigeminal neuralgia A neoplasm pressing on Gasserian ganglion Gasserian ganglion destruction due to acute infection in herpes zoster ophthalmicus Acute infection of Gasserian ganglion by herpes simplex Syphilitic ( luetic ) neuropathy Involvement of corneal nerves in leprosy Injury to Gasserian ganglion

110. PATHOGENESIS Exact pathogenesis is not clear, but disturbances in the corneal sensations occur due to damage to sensory nerves As a consequence metabolic activity of corneal epithelium is disturbed, leading to accumulation of metabolites Which in turn cause oedema and exfoliation followed by ulceration CLINICAL FEATURES Symptoms * Red eye * Swollen eyelids * Defective vision * No pain, No watering

111. Signs Ciliary congestion Corneal signs * Sensations are decreased * Sheen is lost (dull sheen) * Punctate epithelial erosions involving inter- palpebral area * Frank epithelial defects d/t exfoliation of corneal epithelium * Corneal ulcer formation , which is typically horizontally oval located in the lower ½, with grey heaped-up epithelial borders

112. TREATMENT Conventional treatment Should be started immediately * Antibiotics * Cycloplegics * Lubricating eyedrops * Patching Special treatment * Topical nerve growth factors, eg:Murine ..200micrg/ml * Autologous serum drops Amniotic membrane transplantation in large non-healing ulcers Lateral tarsorrhaphy - To promote healing & prevent relapses should be kept at least 1 year, along with artificial tears

113. EXPOSURE KERATOPATHY When eyes are covered insufficiently by the lids and there is loss of protective mechanism of blinking, the condition of exposure keratopathy ( lagophthalmos ) develops ETIOLOGY Extreme proptosis - - inadequate closure of eyelids Bell’s palsy or any other cause of facial palsy Ectropion of severe degree Symblepharon Deep coma Physiological lagophthalmos , during sleep

114. PATHOGENESIS Due to exposure the corneal epithelium is dries up Followed by dessication After epithelium is cast off, invasion by infective organisms may occur

115. PROPTOSIS BELL’S PALSY ECTROPION SYMBLEPHARON COMA

116. CLINICAL FEATURES Symptoms Ocular irritation Burning F.B sensation Redness Signs Dryness of cornea Punctate epithelial defects Corneal ulceration

117. TREATMENT Prophylaxis To prevent exposure keratitis * Artificial tears to be instilled frequently * Instillation of ointment & closure of lids by a tape or bandage during sleep * Soft bandage contact lens with frequent instillation of artificial tears in moderate exposure * Treatment of cause of exposure eg . Proptosis Treatment of corneal ulcer A s in any corneal ulcer Tarsorrhaphy , if not possible to treat the cause

118. PERIPHERAL ULCERATIVE KERATOPATHY Characterized by peripheral corneal thinning, infiltrates & ulceration Some of the PUK PUK ass. with CT disorders Mooren’s ulcer Rosacea keratitis Marginal keratitis Terrien marginal degeneration Pellucid marginal degeneration Phlyctenular keratitis Dellen

119. PUK ass.with C.T. disorders ETIOLOGY Rhematoid arthritis Systemic lupus erythematosus (SLE) Polyarteritis nodosa Wegener’s granulomatosis Clinical features Unilateral/bilateral peripheral acute corneal ulceration with rapid progression, usually in one sector, at the limbus Peripheral corneal guttering or thinning, involve entire periphery Peripheral corneal melting result in descemetocele or perforation Corneal ulceration may be the first manifestation of systemic disease & ass. with systemic features

120. TREATMENT Topical medication * Antibiotics * Cycloplegics * Frequent instillation of lubricating drops Steroids with caution Systemic medication * Immunosuppressants,,,corticosteroids methotrexate & Cyclophosphamide etc) Doxycycline Oral vitamin C Surgical measures * Excision of adjacent inflamed conjunctiva * Bandage contact lens or conjunctival flap for imp. Perforation * Application of cynoacrylate tissue adhesive or peripheral tectonic keratoplasty for actual perforation

121. MOOREN’S ULCER It is a severe inflammatory peripheral ulcerative keratitis also known as chronic serpiginous or rodent ulcer Etiology Exact etiology is not known Most probably it is an autoimmune disease Clinical picture Benign or limited form- usually unilateral, slowly progressive Virulent type or progressive form- is bilateral rapidly progressive with high incidence of scleral involvement Symptoms Severe pain Photophobia Lacrimation Defective vision

122. Signs It is a superficial ulcer, starts at corneal margin as patches of grey infiltrates, which coalesce to form a shallow furrow Peripheral ulcer is associated characteristic whitish overhanging edge. At the end stage, the cornea is thinned & conjunctivised The ulcer rarely perforates & sclera remains uninvolved

123. TREATMENT Highly unsatisfactory Topical corticosteroids instilled every 2-3 hours Immunosuppressive therapy such as cyclosporin with systemic steroids may be useful in virulent type Soft contact lenses to relieve pain Lamellar or full thickness corneal grafts

124. ROSACEA KERATITIS Corneal ulceration is seen in 10% of cases of acne rosacea which is primarily a disease of sebaceous glands of skin Clinical features Typically occurs in elderly women in the form of facial eruption as butterfly configuration, involving malar & nasal area Ocular lesions include Chronic blepharoconjunctivitis & keratitis Rosacea keratitis occurs as yellowish white marginal infiltrates and small ulcers and almost always become vascularised

125. TREATMENT Local treatment Responds to topical steroids, but recurrences are common Systemic treatment Systemic tetracycline 250mg QID X 3 wks TDS X 3 wks, BID X 3 wks & OD X 3 months

126. DELLEN It is a shallow, saucer shaped excavation or thinning seen at the periphery of the cornea Usually at the temporal side Caused by localized dehydration of corneal stroma Etiology Strabismus surgery Cataract surgery Swelling of limbus as in episcleritis Rigid contact lens wearers Suture granuloma Limbal tumours Senility Filtering bleb

127. Symptoms Usually asymptomayic Irritation FB sensation Signs Corneal thinning usually at the limbus Adjacent focal conjunctivitis Corneal elevation Minimal to moderate hyperemia Fluorescein pooling in the area Treatment Lubricating or antibiotic ointment, every 2-4 hrs Artificial eye drops 4-8 times a day Patching

128. NON-ULCERATIVE KERATITIS Non-ulcerative superficial keratitis Non-ulcerative deep keratitis Non-ulcerative SK Diffuse superficial --Acute --Chronic SPK DK Suppurative Non-suppurative

129. Diffuse superficial keratitis Acute diffuse superficial keratitis Etiology Mostly infective,,staphylococcal & gonococcal Clinical features Faint diffuse epithelial oedema Grey farinaceous appearance interspersed with clear cornea Epithelial erosions at places If uncontrolled, converts into ulcerative keratitis Treatment Antibiotic eye drops Tobramycin or Gentamycin 2-4 hrly Chronic diffuse superficial keratitis Seen in Rosacea , Phlyctenulosis associated with pannus

130. Superficial punctate keratitis Multiple spotty lesions in superficial layers of cornea ETIOLOGY Viral infections , chief cause eg.HZ,.Adenovirus & EKC Chlamydial infection, eg:Trachoma,incl.conj. Toxic lesions, eg: staphyylococcus Trophic lesions , eg: Exposure keratitis & NPK Allergic lesions, eg:VKC Irritative lesions, eg drugs as Idoxuridine Disorders of skin & MM, eg Acne rosacea & pemphigoid Dry eye syndrome eg:K.sicca Idiopathic,eg:Thygeson’s SPK Photo-ophthalmitis

131. SPK

132. TREATMENT Topical steroids have marked suppressive effect Artificial tears Specific treatment of cause

134. PHOTO-OPHTHALMIA

136. SUPERIOR LIMBIC KERATOCONJUNCTIVITIS Inflammation of superior limbic,bulbar & tarsal conjunctiva associated with punctate keratitis of superior part of cornea Etiology Exact etiology is not known Seen in patients with hyperthyroidism More common in females Clinical features Clinical course is chronic with remissions and exacerbations Symptoms Bilateral ocular irritation Mild photophobia Redness in superior bulbar conjunctiva

137. Signs Congestion of superior limbic,bulbar & tarsal conjunctiva Punctate keratitis , stains with fluorescein & rose bengal Corneal filaments seen in the involved area Treatment Topical artificial tears Low dose topical corticosteroids Faint diathermy of superior bulbar conjunctiva Recession or resection of a 3-4 mm wide perilimbal strip of conjunctiva from 10.30 to 1.30 O’clock position Therapeutic soft contact lens for a longer period in keratitis

138. THYGESON’S SUPERFICIAL PUNCTATE KERATITIS It is a type of chronic,recurrent bilateral SPK Etiology Exact etiology is not known A viral origin has been suggested An allergic or dyskeratotic nature is also suggested Clinical features Age & sex: may involve all ages, no sex predilection Laterality: usually bilateral Course: chronic disease with remissions and exacerbations Symptoms May be asymptomatic, usually associated with FB sensation Photophobia Lacrimation

139. Signs Conjunctiva is uninflammed Corneal lesions * Coarse punctate epithelial lesions (snow flake) * Circular, oval or stellate in shape * Slightly elevated * Situated in central part of cornea ( pupillary area) * Each lesion is a cluster of heterogenous granular grey dots Treatment The disease is self-limiting, permanently disappear in 5-6 yrs Respond quickly to topical steroids Therapeutic soft contact lenses in steroid resistant cases

140. FILAMENTARY KERATITIS It is a type of SPK with formation of corneal epithelial filament PATHOGENESIS Corneal filaments which essentially consists of a tag of elongated epithelium are formed due to aberrant epithelial healing Any focal epithelial erosion may produce filamentary keratopathy ETIOLOGY Keratoconjunctivitis sicca (KCS) Superior limbic keratoconjunctivitis Epitheliopathy due to radiation keratitis Following epithelial erosions as in herpes s.keratitis,Thygeson’s SPK, recurrent corneal erosion syndrome, trachoma Prolonged patching of eye eg ; cataract surgery Diabetes ectodermal dysplasia and psoriasis Idiopathic

141. Clinical features Symptoms Mod.pain,irritation Lacrimation FB sensation Signs Filaments- Fine tags of elongated epithelium which are firmly attached at the base, interwined with mucus and degenerated cells SPK- of varying degree with corneal filaments Treatment Management of filaments include mechanical debridement & patching for 24 hrs & lubricating drops Therapeutic contact lenses in recurrent cases Treatment of underlying cause to prevent recurrence

142. DEEP KERATITIS Inflammation of corneal stroma with or without involvement of posterior layers constitutes deep keratitis May be non- suppurative or suppurative Non- suppurative deep keratitis * Interstitial keratitis * Disciform keratitis * Keratitis profunda * Sclerosing keratitis Suppurative deep keratitis * Central corneal abscess * Posterior corneal abscess

143. INTEERSTITIAL KERATITIS Inflammation of the corneal stroma without primary involvement of epithelium or endothelium Causes * Congenital syphilis * Tuberculosis * Cogan’s syndrome * Acquired syphilis * Trypanosomiasis * Malaria * Leprosy * Sarcoidosis

144. Syphilitic interstitial keratitis - Associated more frequently with congenital syphilis - Bilateral in inherited syphilis, unilateral in acquired syphilis - In cong.syphilis , manifestations develop between 5-15 yrs Pathogenesis The disease is a manifestation of local antigen-antibody reaction Trepa . pallidum invades the cornea and sensitizes it during period of its general diffusion throughout the body in foetal stage Later a small-scale fresh invasion by Trepanema or toxins excite inflammation in sensitized cornea The inflammation is triggered by an injury or an operation on eye

145. Clinical features Hutchinson’s triad- IK, Hutchinson’s teeth & deafness Clinical picture divided into 3 stages 1. Initial progressive stage 2. Florid stage 3. Stage of regression Initial progressive stage Begins with oedema of endothelium and deeper stroma , secondary to ant.uveitis as evidenced by presence of KPs There is associated pain,lacrimation photophobia,blepharospasm and circumcorneal injection followed by diffuse corneal haze giving ground-glass appearance, stage lasts for 2 weeks

146. Florid stage Eye remains acutely inflamed Deep vascularization of cornea consisting of radial bundle brush like vessels develops As these vessels are covered by hazy cornea, they look dull reddish pink called as “Salmon patch” appearance Moderate degree of superficial vascularization These vessels arising from terminal arches of conjunctival vessels, run a short distance over the cornea These vessels & conjunctiva heap at the limbus This stage lasts for 2 months

147. . Stage of regression: lasts for 1 to 2 yrs -Acute inflammation resolves with progressive vascular invasion -Clearing of cornea is slow, begins from periphery to centrally -Resolution of lesion leaves some opacities & ghost vessels Diagnosis by clinical profile Positive VDRL or TPI test confirm the diagnosis Treatment Local treatment Topical corticosteroid drops eg;dexamethasone 0.1% drops-2-3hrly Atropine eye ointment 1% 2-3 times a day Dark goggles for photophobia Keratoplasty where dense corneal opacities are left Systemic treatment Penicillin in high doses should be started to prevent further lesions Systemic steroids may be added in refractory case of keratitis

148. TUBERCULOUS INTERSTITIAL KERATITIS Features similar to syphilis except that it is more frequently unilateral and sectorial , involving lower sector of cornea Treatment Systemic antitubercular drugs Topical steroids Cycloplegics

149. COGAN’S SYNDROME A type of non syphilitic interstitial keratitis , comprises Interstitial keratitis Acute tinnitus Vertigo Deafness Seen in middle-aged adults Bilateral Etiology unknown Symptoms Redness of eyes Pain & photophobia Lacrimation Diminution of visual acuity

150. Signs Granular and irregular corneal infiltrate affects posterior part of cornea Limbal oedema Stromal opacity Fine vascular loops extending in to the mid stroma Diagnosis by high resolution MRI & antibodies to inner ear antigens Treatment Topical & systemic corticosteroids for 2-4 weeks, early treatment prevents deafness and blindness

151. CORNEAL DEGENERATIONS It refers to the conditions in which the normal cells undergo some degenerative changes, d/t age or some pathology Classification I Depending on location Axial corneal degenerations Fatty degeneration Hyaline degeneration Amyloidosis Calcific degeneration(Band keratopathy ) Salzmann’s nodular degeneration

152. Peripheral degenerations Arcus senilis Vogt’s white limbal girdle Hassal-Henle bodies Terrien’s marginal degeneration Mooren’s ulcer Pellucid marginal degeneration Furrow degeneration

153. Depending upon etiology A. Age related degenerations Arcus senilis Vogt’s white limbal gurdle Hassal-Henle bodies Mosaic degeneration B. Pathological degenerations Fatty degeneration Amyloidosis Calcific degenerarion Salzmann’s nodular degeneration Furrow degeneration Spheroidal degeneration Pellucid marginal degeneration Terrien’s marginal degeneration Mooren’s ulcer

154. AGE RELATED CORNEAL DEGENERATIONS ARCUS SENILIS It is an annular lipid infiltration of corneal periphery Age related change Bilateral in 60% , between 40 and 60 years All individuals over the age of 80 Arcus juvenilis , seen in young persons Clinical features The arcus starts in the superior and inferior quadrants then progresses circumferentially to form a ring about 1 mm wide Peripheral border is sharp, central border is diffuse This ring opacity is separated from limbus by a clear zone ( the lucid interval of Vogt) Some times there may be double ring of arcus

155. VOGT’S WHITE LIMBAL GIRDLE It is also an age related change seen frequently in elderly people It appears as bilateral chalky white opacities-- inter palpebral No clear area between opacity & limbus Opacity at the level of Bowman’s membrane

156. HASSAL-HENLE BODIES These are drop-like excrescences of hyaline material projecting into anterior chamber around corneal periphery Arise from Descemet’s membrane Commonest senile change seen in cornea May become larger in pathological conditions called as CORNEA GUTTATA

157. PATHOLOGICAL CORNEAL DEGENERATIONS FATTY DEGENERATIONS (LIPID KERATOPATHY) Characterised by whitish or yellowish deposits The fat deposits mostly consists of cholesterol & fatty acids Initially fat deposits are intracellular Types: primary or secondary Primary lipid keratopathy -Rare -Occurs in a cornea free of vascularization -Serum lipid levels are normal Secondary lipid keratopathy -Occurs in vascularized cornea Treatment: usually unsatisfactory, in some case slow resorption of lipid infiltrate can be induced by argon laser photocoagulation of new blood vessels

158. HYALINE DEGENERATION Characterized by hyaline spherules in superficial stroma Can be primary or secondary Primary hyaline degeneration -Bilateral -Associated with granular dystrophy Secondary hyaline degeneration -Unilateral -Associated with corneal diseases like keratitis etc. -May be complicated by recurrent corneal erosions Treatment Keratoplasty when it causes visual disturbances

159. AMYLOID DEGENERATION Characterized by deposition of amyloid material underneath the epithelium Rare condition Occurs in Primary form ……in healthy cornea Secondary form …….. In diseased cornea

160. CALCIFIC DEGENERATION (BAND SHAPE KERATOPATHY) It is essentially a degenerative change associated with deposition of calcium salts in Bowman’s membrane,superficial part of troma and in deeper layers of epithelium Etiology Ocular diseases — chr.uveitis.phthisis bulbi , chr.glaucoma chr.keratitis and ocular trauma Age related BSK –is common Primary BSK is familial Metabolic conditions – hypercalcimia,hyperphosphataemia hyperuricemia and chr.renal failure

161. Clinical features Typically presents as a band shaped opacity in interpalpebral zone with clear area between band and the limbus Begins at the periphery and gradually progresses towards centre Opacity is beneath the epithelium Surface of the opaque band is stippled due to holes in calcium plaques in nerve canals of Bowman’s membrane In later stages transparent clefts due to cracks or tears in cal.plaques

162. Treatment Chelation : chemical removal of deposited calcium salts with EDTA ( chelating agent) Phototherapeutic keratectomy with excimer laser Keratoplasty performed when BSK is obscuring vision Treatment of underlying cause

163. SALZMANN’S NODULAR DEGENERATION Etiology It occurs in eyes with recurrent attacks of phlyctenular keratitis , rosacea keratitis and trachoma Common in women Usually unilateral Pathogenesis Raised hyaline plaques are deposited between epithelium & BM Associated destruction of BM and adjacent stroma Clinical features 1 to 10 bluish white elevations (nodules) arranged in a circular fashion are seen within the cornea Discomfort due to loss of epithelium from surface of nodules Visual loss occurs when nodules impinge on central zone Treatment: Keratoplasty

164. FURROW DEGENERATION (SENILE MARGINAL DEGENERATION) In this condition thinning occurs at the periphery of cornea leading to formation of a furrow In the presence of arcus senilis , furrow occupies area of lucid interval of vogt Thinning occurs due to fibrillar degeneration of stroma Patient develops defective vision due to induced astigmatism Treatment: usually not necessary

165. SPHEROID DEGENERATION Etiology Typically occurs in men who work out-doors Common in hostile climates Related to UV rays, ageing, & corneal diseases Clinical features Amber coloured spheroidal granules (Small droplets) accumulates at the level of B M and anterior stroma in interpalpebral zone Vision is affected in marked degeneration Treatment: Corneal transplantation in advanced cases

166. PELLUCID MARGINAL DEGENERATION Characterized by corneal thinning involving the periphery of lower cornea It induces astigmatism, which is corrected by scleral type contact lenses

167. TERRIEN’S MARGINAL DEGENERATION It is non-ulcerative thinning of marginal cornea Clinical features Affects males after 40 years Involves superior peripheral cornea Initial lesion is asymptomatic corneal opacification , seperated from limbus by a clear zone The lesion progresses very slowly over many years with thinning and superficial vascularization Dense yellowish white deposits seen at sharp leading edge Irritation & defective vision due to astigmatism Complications Perforation & pseudo pterygia Treatment: Non-specific, patch of corneal graft in severe thinning

168. CORNEAL DYSTROPHIES These are inherited disorders In which the cells have some inborn defects Due to which pathological changes may occur Development of corneal haze in otherwise normal eyes Free from inflammation & vascularization No associated systemic diseases Bilateral Age—1 st or 2 nd decade

169. Classification Epithelial & sub-epithelial dystrophies Epithelial basement membrane dystrophy Epithelial recurrent erosion dystrophy Subepithelial mucinous corneal dystrophy Meesmann corneal dystrophy Lisch epithelial corneal dystrophy Gelatinous drop-like corneal dystrophy Bowman Layer Dystrophies Reis-Bucklers corneal dystrophy-Granular corneal dystrophy Thiel-Behnke corneal dystrophy Grayson- Wilbrandt corneal dystrophy

170. Stromal dystrophies TGFBI corneal dystrophies Lattice corneal dystrophy Classic lattice corneal dystrophy (LCD1) Lattice corneal dystrophy,gelsolintype (LCD2) Granular corneal dystrophy Granular corneal dystrophy type 1(GCD1) Granular corneal dystrophy type 2(GCD2) Granular corneal dystrophy type 3(GCD3) Macular corneal dystrophy Schnyder corneal dystrophy Congenital stromal corneal dystrophy Fleck corneal dystrophy Posterior amorphous corneal dystrophy Central cloudy dystrophy Pre- Descemet corneal dystrophy

171. Descemet membrane & Endothelial Dystrophies Fuch’s endothelial corneal dystrophy Posterior polymorphous corneal dystrophy Congenital hereditary endothelial dystrophy 1 Congenital hereditary endothelial dystrophy 2 X-linked endothelial corneal dystrophy

172. EPITHELIAL & SUBEPITHELIAL DYSTROPHIES Epithelial basement membrane dystrophy Also known as map-dot-fingerprint dystrophy (or) Cogan microcystic epithelial dystrophy (or) anterior basement membrane dystrophy No inheritence Genetic locus and gene are 5q31 & TGFBI Onset & course- Present in adult life,rarely seen in children Symptoms: Asymptomatic or recurrent erosions with Pain Lacrimation Blurred vision Irregular astigmatism Irritation & discomfort

173. Signs Maps Irregular islands of thickened,gray,hazy epithelium with scalloped,circumscribed borders Affects central or paracentral cornea Isolated or combined with other signs Dots( cogan ) Irregular round,oval or comma shaped Non- staining,putty gray opacities Clustered like an archipelago Seen in central cornea Typically combined with other signs especially with maps

174. Fingerprint lines Parallel,curvilinear lines Usually paracentral Best seen in retro illumination May be isolated or combined with maps Bleb pattern ( Bron ) A subepithelial pattern like pebbled glass seen by retro-illumination Isolated or combined with other signs

175. Epithelial recurrent erosion dystrophy Autosomal dominant Onset & course: usually occurs in 1 st decade of life.. 4-6 yrs Signs Corneal erosions are seen during attack, recurrent erosions appear typically at 4-6 yrs of age decline at the age of 50yr Subepithelial haze or blebs seen between the attacks Central subepithelial corneal opacities appear as early as 7yrs vary from subepithelial fibrosis to keloid like nodules Symptoms Redness,photophobia,epiphora and ocular pain Treatment Corneal grafts at the mean age of 45 years

176. Subepithelial mucinous corneal dystrophy Inheritance: Autosomal dominant Onset: Ist decade of life Course: Progressive loss of vision in adolescence Signs Bilateral sub-epithelial opacities Corneal haze Symptoms Painful episodes of recurrent corneal erosions

177. Meesmann corneal dystrophy ( or) Juvenile hereditary epithelial dystrophy Inheritance: Autosomal dominant Onset: Occurs in early childhood Course: Slowly progressive Variant: Stocker-Holt dystrophy Genetic loci: 12q13(KRT3) & 17q12(KRT12) for SH variant Genes involved: KeratinK3(KRT3) KeratinK12(KRT12) for SH variant Symptoms Typically asymptomatic or may have Mild visual reduction Glare Light sensitivity Painful epithelial erosions Scarring

178. Signs Multiple tiny epithelial vesicles inter- palpebral area Whorled and wedge-shaped epithelial patterns Corneal thinning In Stocker-Holt variant entire cornea shows fine, grayish punctuate epithelial opacities

179. Lisch epithelial corneal dystrophy (or) Band-shaped or microcystic dystrophy Onset Occurs in childhood Course Slowly progressive Inheritance X-chromosomal dominant Signs D/I-- Localized gray opacities-whorl like, radial, flame shaped, band shaped & club shaped I/D—Multiple densely crowded clear cysts Symptoms Asymptomatic Blurring of vision if pupillary area is involved

180. Gelatinous drop-like corneal dystrophy (or) Subepithelial amylodosis Onset:Occurs in first decade Course: Progressive Genetic locus: 1p32 Gene: Tumour associated calcium signal transducer 2 Inheritance: Autosomal recessive Signs Subepithelial lesions or small multiple nodules Superficial vascularization Stromal opacification Symptoms Decreased vision Photophobia Redness Irritation & watering

181. BOWMAN LAYER DYSTROPHIES Reis-Bucklers corneal dystrophy Onset: Occurs in childhood Course: Slowly progressive Genetic locus: 5q 31 Gene: TGFBI Inheritance: Autosomal dominant Signs Confluent,irregular & coarse geographic-like opacities Develop at the level of BM & stroma Opacities may extend to limbus Symptoms Vision is impaired from childhood Ocular discomfort Pain

182. Thiel-Behnke corneal dystrophy Onset: Occurs in childhood Course: Slowly progressive Genetic locus: 5q 31 Gene: TGFBI Inheritance: Autosomal dominant Signs Symmetrical subepithelial reticular( honeycomb) opacities Peripheral cornea typically uninvolved Progress to deep stromal layers Symptoms Ocular discomfort Pain Gradual visual impairment

183. Grayson- Wilbrandt corneal dystrophy Onset:Occurs in 1 st & 2 nd decade Course: Progressive Inheritance: Autosomal dominant Signs Diffuse mottling to diffuse gray white opacities Extend anteriorly into epithelium Cornea between deposits is clear Refractile bodies seen in corneal stroma Symptoms Decreased to normal visual acuity Ocular discomfort Pain

184. STROMAL CORNEAL DYSTROPHIES TGBFI Corneal dystrophies Lattice corneal dystrophy Classic lattice corneal dystrophy (LCD1) Lattice corneal dystrophy, gelsolin type (LCD2) Granular corneal dystrophy Granular corneal dystrophy, type 1 (classic) Granular corneal dystrophy type 2 (granular-lattice) Granular corneal dystrophy type 3

185. Classical lattice corneal dystrophy Appears at the age of 2 yrs Progressive, recurrence common Progressive clouding of central cornea at 20yrs Symptoms Pain Ocular discomfort Signs Branching spider-like amyloid deposits forming irregular lattice work in the central stroma

186. Lattice corneal dystrophy,Gelsolin Type Familial amyloidosis of Finnish Autosomal dominant Onset—4 th decade Slowly progressive Signs Lattice lines more peripheral Less numerous than type 1 Central cornea spared Symtoms Dry eye symptoms Vision normal until 6 th decade

187. Granular corneal dystrophy Type 1 Seen as early as 2 yrs Autosomal dominant Signs Milky granular hyaline deposits Intervening stroma is clear Opacities do not extend to limbus Vortex pattern of brownish granules in BM Symptoms Glare Photophobia Recurrent erosions Ocular discomfort Decreased vision

188. Granular corneal dystrophy Type 2 Seen as early as 3 yrs Progressive Signs Superficial stromal tiny whitish dots Rings or stellate -shaped snowflake stromal opacities Lattice lines, deeper Superficial, transluscent flattened bread-crumb opacities, final stage Symptoms Vision decreased Pain Ocular discomfort

189. Macular corneal dystrophy Occurs in childhood Autosomal recessive Signs Diffuse stromal haze Macules Posterior peripheral white lesions Corneal sensations reduced Symptoms Recurrent corneal erosions Visual impairment 10 & 30yrs

190. Schnyder corneal dystrophy Patients may have hyper- lipoproteinemia Autosomal dominant Appears in infancy or at birth Slowly progressive & Asymptomatic Signs Round ring shaped central Stromal Opacities d/t needle like cholesterol crystals Corneal sensations decreased Symptoms Vision is decreased Glare

191. Congenital stromal corneal dystrophy Occurs congenitally Non-progressive Autosomal dominant Signs Diffuse,bilateral,corneal clouding with flake-like Stromal opacities Symptoms Moderate to severe visual loss

192. Posterior amorphous corneal dystrophy Congenital appears as early as 16 wks Autosomal dominant Non-progressive Signs Diffuse gray white sheet like opacities Involves posterior layers of stroma Symptoms Asymptomatic Vision decreased mildly

193. Fuch’s endothelial corneal dystrophy Slowly progressive Bilateral More in females Occur in 5 th & 7 th decade Endo epithelial dystrophy Clinical features 4 stages Stage of cornea guttata -beaten metal appearance Oedematous stage-early stromal oedema Stage of bullous keratopathy-bullae Stage of scarring

194. TREATMENT Hypertonic saline 5% sodium chloride in oedema Warm air blown on the eyes IOP lowering drugs 0.5% Timolol eye drops Bandage soft contact lens in Bullous keratopathy Penetrating keratoplasty if vision is reduced markedly

195. Posterior polymorphous corneal dystrophy Occurs in early childhood Very slowly progressive Symptoms Often asymptomatic Signs Deep corneal lesions of various shapes Rail road tracks appearance lesions Varying gray tissue at DM

196. C. DEGENERATION C. DYSTROPHY Onset Old age 1 st or 2 nd decade Family H/O Uncommon Common Laterality Unilateral Bilateral Location Peripheral Central Symmetry Asymmetric Symmetric Vascularization Common Not common Etiology Inflammatory Hereditary Progression Slow or rapid Slow

197. ECTATIC CONDITIONS OF CORNEA KERATOCONUS KERATOGLOBUS KERATOCONUS POSTERIOR

198. KERATOCONUS (CONICAL CORNEA) Ectatic condition of cornea Non inflammatory Bilateral (85%) Usually starts at puberty Progresses slowly Etiopathogenesis Not clear, various theories proposed - Developmental condition - Degenerative condition - Hereditary dystrophy - Endocrine anomaly

199. Pathological changes Defective synthesis of mucopolysacch aride & collagen Ectasia & thinning Symptoms Defective vision Glare & haloes Streaking of light Uniocular diplopia or polyopia Signs Window reflex distorted Placido disc Ex..shows irregularity of circles Keratometry shows mal-alignment of mires Photokeratoscopy shows distortion of circles

200. PLACIDO’S DISC` KERATOMETRY PHOTOKERATOSCOPY DISTORTION OF IMAGES

201. Signs … contd Fleischer’s ring at base of cone Folds in descemet’s membrane & BM Vogt lines( very fine, vertical,deep stromal striae ) Scissor reflex on retinoscopy Ophthalmoscopy show annular dark shadow(oil droplet) Munson’s sign.. Localised bulging of l. lid in down gaze

202. Morphological classification * Nipple cone… <5mm & steep curvature (small) * Oval cone …… 5mm ellipsoid in shape (large) * Globus cone ….>6mm & globe like (very large) Complications * Acute hydrops * sudden development of corneal oedema , associated pain,photophobia & lacrimation

203. Associations Ocular conditions Ectopia lentis Congenital cataract Aniridia Retinitis pigmentosa VKC Systemic conditions Marfan’s syndrome Down’s syndrome Ehler’s Danlos syndrome Osteogenesis imperfecta Mitral valve prolapse

204. TREATMENT Spectacle correction: may improve in early cases only Contact lenses: RGP lenses in early cases INTACS: Intracorneal ring segments in early cases Corneal collagen cross linking with riboflavin (C3R) Keratoplasty: Deep anterior lamellar keratoplasty or penetrating keratoplasty

205. KERATOGLOBUS Characterised by thinning & hemispherical protrusion of the entire cornea Familial,hereditary and congenital Bilateral Non-progressive Autosomal recessive Differential diagnosis Congenital buphthalmos

206. KERATOCONUS POSTERIOR Characterized by conical bulging of posterior surface Extremely rare Non-progressive Ass. with stromal thinning Conical protrusion of posterior corneal curvature Anterior surface normal

207. ABNORMALIIES OF CORNEAL TRANSPARENCY ETIOLOGY Corneal oedema Drying of cornea Depositions on cornea Inflammations of cornea Corneal degenerations Corneal dystrophies Vascularization of cornea Scarring of cornea (corneal opacities)

208. CORNEAL OEDEMA ETIOLOGY Raised intraocular pressure Endothelial damage * Due to injuries * Due to corneal dystrophies * Due to inflammation Epithelial damage * Mechanical injuries * Chemical injuries * Radiational injuries

209. CLINICAL FEATURES SIGNS Stromal haze Epithelial vesicles Bullous keratopathy SYMPTOMS Blurred vision Pain Discomfort Photophobia

210. Treatment Treat the cause Dehydration of cornea * Hypertonic agents eg ; 5% NaCl drops, anhydrous glycerine * Hot forced air from hair dryer Therapeutic contact lenses Penetrating keratoplasty

211. CORNEAL OPACITY ETIOLOGY Congenital opacities Healed corneal wounds Healed corneal ulcers CLINICAL FEATURES Loss of vision when dense opacity covers pupillary area Blurred vision due to astigmatic effect

212. TYPES OF CORNEAL OPACITY Nebular corneal opacity * Faint scar * Involving BM,superficial stroma * Produce more discomfort d/t irregular astigmatism Macular corneal opacity * Semi-dense opacity * Involves ½ of the stroma Leucomatois corneal opacity * Dense white opacity * Involves > ½ of the stroma

213. ADHERENT LEUCOMA * Healing of corneal perforation with incarceration of iris CORNEAL FACET * Corneal surface depressed at the site of healing KERECTASIA * Corneal curvature increased at the site of opacity ANTERIOR STAPHYLOMA * Ectasia of pseudocornea with iris plastered behind

214. TREATMENT Optical iridectomy Phototherapeutic keratectomy Keratoplasty Cosmetic coloured contact lens Tattooing of scar

215. CORNEAL VASCULARIZATION Pathogenesis Not clear, chemical or mechanical factor play a role Release of vaso -formative stimulus Compactness of Stroma loosened d/t mechanical factor TYPES -- Superficial Deep Superficial vascularization Vessels are arranged in arborising pattern Present below the epithelial layer Continuity can be traced with conjunctival vessels

216. ETIOLOGY Trachoma Phlyctenular keratoconjunctivitis Superficial corneal ulcers Rosacea keratitis Pannus Superficial vascularization associated with white cuff of cellular infiltration

217. Deep vascularization Vessels derived from anterior ciliary arteries Lie in the corneal stroma Straight & not anastmosing Continuity can not be traced beyond limbus Arranged as terminal loops,brush,parasol, Umbel network or interstitial arcade Causes Interstitial keratitis Disciform keratitis Deep corneal ulcer Chemical burns Sclerosing keratitis Grafts

218. TREATMENT Usually unsatisfactory Treatment of the cause Corticosteroids have vasoconstrictive & suppressive effect on permeability of capillaries Irradiation is helpful in superficial Peritomy

219. CORNEAL SURGERY Keratoplasty– I s an operation in which the patient’s diseased cornea is replaced by healthy clear cornea Also called as corneal grafting or corneal transplantation TYPES Autokeratoplasty Rotational keratoplasty Contralateral keratoplasty Allografting or Allo-keratoplasty Penetrating keratoplasty Lamellar keratoplasty Deep anterior keratoplasty (DALK) Descemet’s stripping endothelial keratoplasty Small patch graft

220. INDICATIONS Optical: to improve vision * Corneal opacity * Bullous keratopathy * Corneal dystrophies * Advanced keratoconus Therapeutic: to replace inflammed cornea * Not responding to conventional therapy Tectonic: to restore integrity of eye ball * After corneal perforation * Marked corneal thinning Cosmetic: to improve appearance

221. KERATOPLASTY

222. EVALUATION OF DONOR CORNEA Donor eye should be removed as early as possible …6 hrs Biomicroscopic examination of whole globe before storage Donor tissue graded into Excellent,very good, good,fair & poor depending on condition METHODS OF CORNEAL PRESERVATION Short term storage upto 48 hrs, in 4°C in moist chamber Intermediate storage Upto 2 wks McCarey -Kaufman(MK) medium Chondroitin sulphate enriched media Longterm storage Upto 35 days Organ culture method Cryopreservation method at -70ºC

223. Surgical technique of penetrating keratoplasty Excision of donor corneal button Should be cut o.25mm larger than recipient Excision of recipient corneal button - With 7.5-8mm size trephine partial thickness incision made on host cornea -Anterior chamber entered with razor blade knife -Excision is completed by corneo-scleral scissors Suturing of corneal graft into host bed With continuous or interrupted 10-0 nylon sutures

224. KERATOPLASTY

225. KERATOPLASTY

226. Complications Early Flat AC Iris prolapse Infection Secondary glaucoma Epithelial defects Primary graft failure Late Graft rejection Recurrence of disease Astigmatism

227. Graft rejection Refers to immunological response of host to donor cornea It can occur 2 weeks – upto several years Delayed type of hypersensitivity response Risk factors Young age Previous graft failure Corneal vascularization Larger graft size Donor epithelium Massive blood transfusion

228. Clinical presentation of graft rejection Epithelial rejection Characterized by elevated epithelial rejection line stains with flourescein Subepithelial infiltrates known as Kayes dots Stromal rejection sudden onset of stromal haze Endothelial rejection Khodadaust line Diffuse endothelial rejection with lot of KPs

229. REFRACTIVE CORNEAL SURGERY Radial keratotomy Astigmatic keratotomy Photorefractive keratectomy Laser assisted in-situ keratomileusis (LASIK) Thermal laser keratoplasty Conductive keratoplasty Orthokeratoplasty Intracorneal ring (ICR) implants

230. RADIAL KERATOTOMY Deep radial incisions in superficial stroma only, in the periphery, leaving Central 4mm optical zone On healing flatten the central cornea Reduce its refractive rower Gives good correction in low to moderate myopia

231. ASTIGMATIC KERATOTOMY Making transverse cuts in the mid periphery of steep corneal meridian Can be performed for astigmatism PHOTOREFRACTIVE KERATECTOMY Central OZ of ant.stroma is photoablated by using excimer laser To cause flattening of central cornea Good correction in -2 to -6D myopia

233. CONDUCTIVE KERATOPLASTY Non-ablative & non- incisional procedure Cornea is steepened by collagen shrinkage through radiofrequency energy in to the peripheral stroma in a ring pattern Corrects hyperopia upto 3D ORTHOKERATOLOGY Non-surgical reversible method of moulding the cornea by RGP For correction of myopia upto -5D Used in below 18 yrs

234. INTRACORNEAL RING IMPLANTS ICR implants into 2/3 stromal depth at periphery Flattens the cornea by vaulting effect Decreased myopia Reversible

235. PHOTOTHERAPEUTIC KERATECTOMY Ablation of superficial corneal lesion with excimer laser Indications Superficial corneal scars Corneal degenerations Epithelial dystrophies Recurrent corneal erosions Procedure Spot mode: small spot(<1mm) can be ablated Shapping mode: uniform removal of corneal tissue from large zone

236. Contraindications Excessive thin corneas Moderate - severe dry eyes Deep corneal lesions Complications Faint corneal haze (common) Secondary infections Induced hypermetropia Secondary keratectasia

237. KERATOPROSTHESIS Artificial corneal device, in unsuitable for keratoplasty Central optical cylindrical part made of PMMA TYPES Osteo-odonto keratoprosthesis : fixed with the help of patient’s own tooth & alveolar bone Chondro-keratoprosthesis : with patient’s own cartilage Onycho-keratoprosthesis : with patient’s nails Singh & Worst collar-stud keratoprosthesis : S.S sutures

238. KERATOPROSTHESIS

239. Indications Bilateral corneal blindness, not suitable for keratoplasty Steven-Johnson’s syndrome Chemical burns Ocular cicatricial pemphigoid Severe trachoma Failed corneal grafts Complications Extrusion of prosthesis Intractable glaucoma Retroprosthetic membrane formation Uveitis Retinal detatchment