etiology, pathology and pathogenesis of corneal ulcer

48
ETIOLOGY, PATHOGENESIS & PATHOLOGY OF CORNEAL ULCER By Dr . SAMARTH MISHRA

Upload: dr-samarth-mishra

Post on 21-Apr-2017

1.147 views

Category:

Health & Medicine


3 download

TRANSCRIPT

ETIOLOGY, PATHOGENESIS &

ETIOLOGY,PATHOGENESIS & PATHOLOGY OF CORNEAL ULCER By Dr . SAMARTH MISHRA

1

. WHAT IS CORNEAL ULCER???

Corneal ulcer may be defined as discontinuation in normal epithelial surface of cornea a/w necrosis of the surrounding corneal tissue.

Pathologically it is charecterised by oedema & cellular infiltration.

TOPOGRAPHICAL (MORPHOLOGICAL) CLASSIFICATION:

CORNEAL ULCER (ULCERATIVE KERATITIS):DEPENDING ON LOCATION : a)central corneal ulcer b) peripheral corneal ulcer

DEPENDING ON PURULENCE a)purulent corneal ulcer or suppurative corneal ulcer (most bacterial & fungal Corneal ulcer ) b)non-purulent corneal ulcers( viral, chlamydial & allergic Corneal ulcer)

DEPENDING UPON ASSOCIATION WITH HYPOPYON: a simple Corneal ulcer (without hypopyon) b) hypopyon corneal ulcer

.DEPENDING UPON DEPTH OF ULCER: a)superficial Corneal ulcer b)deep Corneal ulcer c)corneal ulcer with impending perforation d)perforated corneal ulcer

DEPENDING UPON SLOUGH FORMATION : a)non-sloughing corneal ulcer b)sloughing corneal ulcer

BACTERIAL CORNEAL ULCER:(causative organisms)Staphylococcus aureus

Pseudomonas pyocyanea

Streptococcus pneumoniae

E.coli

Proteus

Klebsiella

N.gonorrhoeaN.meningitidis (can invade intact corneal epithelium)C.diphtheriae

Pathogenesis and pathology of corneal ulcer: 4 stages: infiltration,active ulceration,regression,cicatrization.

STAGE OF INFILTRATION

STAGE OF ACTIVE ULCERATION

STAGE OF REGRESSION

STAGE OF CICATRIZATION

.Damaged epitheliuminvasion by offending agents

Terminal course depends on virulence of agent,host defence mechanism and treatment received.Course of ulcer maybe: a)become localized and heal b)penetrate deep l/t perforation. c)spread fast as sloughing corneal ulcer.

A]PATHOLOGY OF LOC ALIZED CORNEAL ULCER:1. Stage of infiltration: PMN/lymphocytes into epithelium from peripheral circulation.Necrosis may occur.

. 2.Stage of active ulceration: results from sloughing of epithelium and bowmens memb. & necrosisUlcer wall project s(swelling of lamellae by imbibition of fluid & packing by leucocytes).ulcer floor shows grey infiltration & sloughing.Hyperemia of circumcorneal vessels.purulent exudates.vascular congestion of iris & ciliary body.

Iritis d/t absorption of toxins from ulcer.

Exudation into anterior chamber from vessels of iris & cilary body may lead to formation of HYPOPYON(sterile,fluid)

Ulcer progress laterallydiffuse superficial ulceration.Ulcer progress deep descemetocele/perforation.

.3.Stage of regression: host defense mechanism (humoral /cellular & appropriate t/t )Line of demarcation devp.( leucocytes neutralize & phagocytose the offending org. ,debris)Ulcer begins to heal & epithelium starts growing over the edges.

4.stage of cicatrization:Healing continues.Fibrous tissue laid down( corneal fibroblasts & endothelial cells)Stroma thickens & pushes the epithelial surface anteriorly.

inolves epithelium only no scarring bowmans memb.scar forms( nebula)

Macula & leucoma results after >1/3rd of corneal stroma.

.B] PATHOLOGY OF PERFORATED CORNEAL ULCER:ulceration deepens reaches descemets memb.descemetocele. straining,coughing etc l/t perforation.After perforationaquaous leaks,IOP falls,iris-lens diaphragm moves forward.Small perforation,opposite to irispluggs & cicatrization proceeds.Commonest end resultadherent leucoma.

C] PATHOLOGY OF SLOUGHING CORNEAL ULCER:d/t highly virulent agent/low resistance.Whole cornea sloughs,iris becomes inflammedexudates block pupil.

Exudates organize to form PSEUDOCORNEA.

This pseudocornea is weak & thin, so bulges forward along with plastered iris tissue ectatic cicatrixANTERIOR STAPHYLOMA.

Perforated corneal ulcer

SPECIFIC BACTERIAL CORNEAL ULCERS(charecteristics):STAPH AUREUS: rapidly progressive. moderate ant. Chamber reactn with endothelial plaques/hypopyon. round, oval,yellowish-white with dense infiltration & distinct border. stromal microabscess with an ill defined border may develop.

NON-AUREUS STAPH. :cause oppertunistic infectn. >85% of eyelid cultures from normal population are +ve for non-aureus staph. m/c isolated org. from bacterial keratitis. severe ulcers with dense infiltration may occur if untreated

.STREP. PNEUMONIAE/ PNEUMOCOCCUS: after corneal trauma,dacryocystitis etc acute,purulent,rapidly progressive with a deep stromal abscess. ant. Chamber reactn is severe with marked hypopyon. hypopyon corneal ulcer by pneumococcus. corneal ulcer with hypopyonhypopyon d/t any other cause. charecteristic feature of hypopyon corneal ulcer caused by pneumococcus is called ULCER SERPENS.

NOCARDIA ASTEROIDES: gram +ve,acid fast bacillus with branching filaments. produces indolent ulcers after minor trauma particularly in exposure to contaminated soil. nocardia can survive in neutrophils & macrophages a/w production of superoxide dismutase.

.Pseudomonas: m/c gram ve org isolated from severe keratitis. a/w soft contact lens.

rapid progression,dense sromal infiltration.

marked suppuration,liquefactive necrosis & descemetocele formation or corneal perforation are charecteristic.

Neisseria: invade intact epithelium. l/t rapid perforation.

B.cereus: chr. By distinct stromal ring infiltrate remote from the site of injury.

rapid progression to stromal abscess.

corneal perforation.

FUNGAL/MYCOTIC CORNEAL ULCER: Incidence has increased d/t injudicious use of antibiotics & steroids.Antibiotics: Disturb the symbiosis b/w bacteria & fungi.Steroids: make fungi facultative pathogens(actually symbiotic saprophytes).

ETIOLOGY: Filamentous fungi: Aspergillus(m/c), Fusarium, Alternaria, Cephalosporium, Curvularia, Penicillium YEASTS: Candida albicans, Cryptococcus

MODE OF INFECTION: A)Injury by vegetative material. E.g: leaf,thorn,crop etc. (field workers affected ) B)Injury by animal tail

.

C) Secondary fungal ulcers: immunocompromised pts.

CHARECTERISTIC FEATURES: a)dry looking,greyish white,rolled out margin b)feathery finger like extension (in stroma underlying intact epithelium).

c)sterile immune ring( of wesseley) i.e a yellow line of demarcation seen d/t fungal Ag- host Ab reaction.

d) multiple,small,sattellite lesion seen.

e)non-sterile ,thick ,immobile,big hypopyon seen d/t fungal hyphae invasion in contrast to bacterial hypopyon( sterile, mobile).

f)symptoms milder than the clinical signs.

fungal ulcer with deep stromal infiltration and sattellite lesions.

close up view of stromal infiltrations

Stromal infiltrations and sattellite lesions.

VIRAL CORNEAL ULCER affect conjunctiva & cornea,so typical lesionkeratoconjunctivitis.Etiological agents: HSV,HZV,Adenovirus etc

CLASSIFICATION OF HSV KERATITIS : 1)Infectious epithelial keratitis: a) cornea vesicles b) dendritic ulcer c) geographical ulcer d) marginal ulcer 2) neurotrophic keratopathy/ trophic ulcer/ metaherpetic ulcer/indolent ulcer

3) stromal keratitis: a)necrotizing stromal keratitis b)immune stromal keratitis

. 4) endothelitis: a)disciform b)diffuse c)linear

The m/c recognized clinical manifestation of infectious epithelial keratitis are dendritic & geographic ulcer.

small vesicles in epithelium (punctate epithelial keratopathy)

vesicles coalesce

dendritic ulcer

geographic ulcer

.In immunocompromised arrested @ the vesicle stage.

vesicles may coalesce to form a raised dendritic lesion (displaces fluorescin(-ve stain))

This raised lesion, which is clinically the precursor of dendritic ulcer in immunocompetent host, may not progress to a dendritic ulcer in the immunocompromised host & therefore may not be recognized as infectious epithelial keratitis.

So, all pts with HSV corneal vesicles

should be recognized as having infectious keratitis & treated promptly.

Hsv two types. Hsv 1 (above waist), hsv 2 (below waist)

Hsv are epitheliotrophic,but may become neurotrophic.

DENDRITIC ULCER: dendron=tree(greek)Typical lesion of recurrent epithelial keratitis.Irregular,branching,linear lesions with terminal bulbs & swollen epithelial borders which contain live virus.TRUE ULCER, as it extends through basement membrane.Stains +ve for fluorescin along the length of lesion

.swollen borders actually raised (stain ve with fluorescin).

Rose bengal stain which stains devitalised cells ,is typically taken up by swollen epithelial cells at ulcer border.

After ulcer healsabnormal appearing epithelium (for several weeks) HSV DENDRITIC EPITHELIOPATHY( dendritic in shape but not ulcerated, represents ulcer healing epithelium)

D/D : a) varicella zoster pseudodendrites b) recently healed epithelial defects

Diff. from HSV because,these are raised rather than ulcerated & do not stain fluorescin.

Geographic ulcer:

When dendritic ulcer is no longer linear.

A widened dendritic ulcer.

TRUE ULCER

Has swollen border that contains live virus.

The scalloped or geographic borders are imp. to recognise to diff this lesion from healing abrasions & neurotrophic keratopathy, which tend to have smooth border.

.EPIDEMIOLOGIC STUDY :

wlhemus et al : geographical ulcer 22% of all cases of infectious epithelial keratitis. a/w with use of topical steroids.

Liesegang: geographical ulcer 4% of inf ep keratis cases. not a/w topical steroids use.

Marginal ulcer:

Another manifestation of hsv inf epi. keratitis.

Proximity to limbus a/w unique features.

Infiltrated quickly by WBCs from nearby blood vessels.

Typical presentation: anterior stromal infiltrate underlying the ulcer & adjacent limbal injection.

Patient more symptomatic d/t intense inflammation.

D/D : staphylococcal marginal(catarrhal) disease.

.

HSV marginal ulcer staph. Marginal infiltrateEtiology: active HSV immunologic response to staph AgEpithelial always absent(if present,late) defectNeovascn often neverProgression centrally circumferentiallyBlepharitis unrelated usuallyLocation any meridian typically @2,4,8,10 oclock position

Sequelae:

4 recognized sequelae:

Complete resolution.

dentritic epitheliopathy

stromal scarring, ghost figures or footprints of HSV.

subsequent stromal inflammation (in 25%)

Neurotrophic keratopathy/trophic ulcer:who have had infec.epi.keratitis at risk.

Arises from impaired corneal innervation in combination with decreased tear secretion.

Oval,smooth border ( in contrast to geograph. ulcer)Stroma at ulcer bed develops typically a grayish white opacification.

Complications: stromal scarring,neovascularisation,necrosis,perforation,secondary bacterial infection.

Irregularity of corneal surface lack of normal corneal lusture punctate epithelial erosion persistent epithelial defect stromal ulceration.

HERPES ZOSTER OPHTHALMICUS:

d/t reactivation of latent virus.

A)MICRODENDRITIC EPITHELIAL ULCER: peripheral & stellate rather than dendritic in shape.in contrast to HSV dendritis,these have tapered ends which lacks bulbs.

B)NEUROPARALYTIC ULCER: occur as a sequelae of acute infection & gasserion ganglion destruction.

Moorens ulcer:(chr. Serpiginous ulcer/rodent ulcer/ulcus rodens)Ulcus rodens: term by Mc kenzie:1854Idiopathic corneal ulcer.Severe,inflammatory,painful,peripheral ulcerative keratitis.Diagnosis of exclusion

ETIOLOGY: A) idiopathic degenerative condition. B) ischaemic necrosis resulting from vasculitis of limbal vessels. C) d/t enzyme collagenase & proteoglyconase produced from conjunctiva. D) autoimmune d/s: Ab against corneal epithelium present in serum. E) a/w HCV,helminthiasis ( molecular mimicry to cross reacting epitopes of cornea, Ag-Ab reactn to helminth @ peripheral cornea provokes inflammation & ulceration)

.

Clinical varieties of moorens ulcer:

A)BENIGN FORM: -unilateral -slow progress -elderly -mild to mod. Symptoms -respond well to t/t

B) VIRULENT FORM: -bilateral -rapidly progressive -younger pt -scleral inolvement(high) -a/w pain -doesnot respond to t/t

.FEATURES: starts @ corneal margin as gray infiltrates. coalesce to form shallow furrow over whole cornea. peripheral central progression ulcer undermines epithelium & superficial stromal lamellae & forms whitish overlying edge base--> becomes vascularisedRARELY perforates,sclera uninvolved.

D/D:Terriens marginal degeneration.(non inflammatory,thinning of corneaepithelium intact)Pellucid marginal degenerationSenile furrow degeneration.Staph. Marginal keratitis.

Non-infectious ulcers:Tiny tears: may also cause ulcers. Can form from direct trauma,scratches,or particles such as sand,glass,metal. Such injury make it easier for bacteria to invade & cause a serious ulcer.DRY EYES :( SICCA) e.g sjogrens syndromeCHEMICAL BURNS: alkali /acidic burnTHERMAL /RADIATION BURNSD/T EXPOSURE KERATITIS: lagophthalmos,lid abnormalities,facial palsy,proptosis,thyroid d/s.ATOPIC: d/t follicles / pappilaVITAMIN A DEFICIENCY: dietary deprivation,secondary d/s that affect fat absorption & storage like celiac d/s and cystic fibrosis. BASEMENT MEMBRANE ABNORMALITIES: microcysts,evidence of map-dot-finger or anterior stromal dystrophiesIMMUNE RELATED D/S:wegeners granulomatosis,RA,other collagen vascular d/s.

Thank you