Corneal edema

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<ul><li>1.CORNEAL EDEMA Dr. Kishore Khade</li></ul> <p>2. corneaThickness of the cornea in the centre is 0.52mmWhile at periphery is 0.67mm.Epithelium is 50-90mthickBM 8-14mStroma 0.5mm thick &amp;constitute most of cornea.Dm is 10-12mEndothelium 18-20mwith 2400-3000cells/mm2 3. CORNEA To perform its primary function of refractionof light the cornea must be relatively thin &amp;dehydrated with smooth anterior surface. In normal cornea, optical transparency isdirectly related to the state of hydration ofthe tissue. If cornea swells, it increases its thickness , itssurface becomes irregular both changesdowngrades its optic properties. 4. CORNEAL HYDRATION Cornea is relatively in dehydrated state for itstransperancy. Water content of cornea is 80% which ishighest of any connective tissue in body. If hydration becomes above 80% its centralthickness increases &amp; transperancy reduces. Cornea swells only in the direction of itsthickness therefore, corneal thickness &amp;hydration are linearly related. 5. CORNEAL HYDRATION Hydration is maintained by:-A}Factors draw water in to the cornea:-1)Swelling pressure of stromal matrix ( GAGs).2)Intraocular pressure.B} factors which prevent flow of water into thecornea:-1)Mechanical barriers.2) Na+-K+ active pump of endothelium. 6. stromal barrierpressure Hydration IOPNa-kpump Evaporation 7. {A} Stromal swelling pressure Pressure exerted by corneal stroma mainlyGAGs is stromal pressure (SP). Sp is 60 mmhg, is a keystone of cornealbiophysics. Anionic charges on GAGs molecule expandsthe tissue, draws fluid with equal but negativepressure called imbibation pressure. 8. Contd..... In vivo imbibation pressure is reduced by IOP,so IP= IOP SP IP= 17- 60, IP = -43mmhg. In vitro IP = SP Sp generates interfibrillar tension may bebiophysical mechanism to maintain fibrilsnormal arrangement. Cornea has an swelling pressure, which ismaintained by endothelial metabolic pump 9. {B} Barrier mechanism Both epithelium &amp; endothelium acts as abarrier for excessive flow of water &amp; diffusionof electrolytes into stroma. As compare to endothelium, epithelium offerstwice resistance. Endothelium allows diffusion of small soluteslike NaCl &amp; urea, while epithelium produceshypertonicity of the solution bathing thecornea. 10. Barrier mechanism Endothelial cells are attached to each other bydiscontinuous tight junctions i.e maculaeoccludentes. Endothelial barrier function is mainly calciumdependent. A calcium free solution will reduce the barrierfunction &amp; cause stromal edema. 11. {C} Na - K pump++ Present in endothelium, several fold moreactive than its epithelium counterparts. Activated ATPase mediates active extrusion ofNa from stroma to the aqueous. It causes diffusion gradient for water. Na conc in aqueous is more compare tostroma, which draws water from the stroma. 12. Sodium activity acrossendotheliumstroma Na-K pump Na 134 meq/l Aqueous humour 13. Bicarbonate dependent ATPase has also beenreported in the endothelial cells. Depletion of bicarbonates induces swelling. Carbonic anhydrase enzyme has also beenimplicated in fluid transport, CAE inhibitorsdecreases flow of fluid from stroma toaqueous ( found only in endothelium). 14. Wounded cornea 142.3meq/l AqueousNA humour149.8Meq/l H2O 15. {D} EVAPORATION Evaporation of water from precorneal tearfilmincreases its osmolarity relative to cornea. Hypertonicity of tear film could draw waterfrom cornea. However this water loss is readily replaced byaqueous, it results in only a little cornealdehydration. 16. {E} Intra ocular pressure Most of early writers assume corneal edema isdue to mechanical forcing of aqueous into thecornea. But experimental event found out that toachieve this,effect pressure required is200mmHg. More likely explanation is that thedetermining factor is endothelial damage. 17. EDEMA Word edema is derived from greek wordodma 1400bc , means "swelling. Formerly known as dropsy or hydropsy whichmeans accumulation of excessive fluid. Etiology of corneal edema: SECONDARY CAUSES PRIMARY CAUSES 18. CORNEAL EDEMA 19. [I] Mechanical trauma1) Blunt non penetrating injury causes edemaby injury to endothelium, mostly it isreversible.2) Perforating injuries cause direct damage tothe cornea, intra ocular FB in AC can causeedema mainly in inferior periphery where FBmainly settles.3) Forceps delivery cause pressure on globe,may cause edema due to DM tear. 20. DESCEMETs TEAR 21. Mechanical trauma4) Noxious chemicals mainly alkalies whichpenetrates cornea cause endotheliumdamage.5)Intraocular sx can cause acute endothelial lossmost notably in superior &amp; central cornea.6) BROWN McLEAN syndrome: peripheraledema with brown black discolouration ofunderlying endothelium seen in ICCE,ECCE,CCPE, pars plana vitrectomy. 22. Brown Mclean Syndrome 23. Mechanical trauma7)Cold induced reversible corneal edema has beenreported in trigeminal nerve dysfunction.8) Certain systemic medications like amantadine &amp;cefaclor can cause edema.9) Lasers used for iridotomy can cause focal cornealedema.10) High altitude corneal decompensation has beenreported causing hypoxia induced cornealedema. 24. [ II ] GLAUCOMA Acute rise in IOP which exceeds swellingpressure of stroma causes epithelial edema. Hypoxic Endothelial decompensation occursdue to diminished aqueous flow. When corneal endothelium is compromised,edema occurs even @ lower level of IOP. Chronic elevation of IOP permanentlydamages the endothelium. Irreversible corneal edema may occur. 25. GLAUCOMA 26. GLAUCOMA Penetrating keratoplasty is the only treatmentof choice in irreversible corneal edema, butIOP must be first controlled. In hypotony, AC is shallow or flat. Mechanicaltrauma by cornea iris or iris corneal touchleads to edema. Normal human volunteers experiment study can be explained by hypotony induced edema,(corneal edema occurs in tightly patched eye). 27. [ III ] Contact lenses Most common cause of corneal edema isprolonged use of contact lens. It is mainly due to insufficient supply ofoxygen to epithelium. Edema presents as microcystic epithelialedema near the center of resting position ofthe lens. It is best seen with scattered illumination ofslit lamp referred as Sattlers veil. 28. Contd.... If allowed to continue, itll cause stromaledema, descemets membrane folds. Edema easily clears if contact lens is removed. Even altering the fit of contact lens is alsosuccessful in reducing edema if it providessufficient oxygen to the epithelium. The response &amp; recovery from edema isindependent of age. 29. [IV] ICE syndrome Iridocorneal endothelial syndrome is basicallyspectrum of disorders that includesA) Progressive iris atrophy.B) Chandlers syndrome. C) Iris nevus syndrome ( Cogan Reese) 30. Chandler syndrome Corneal endothelial abnormalities (hammeredsilver). Presents with blurred vision &amp; haloes due tocorneal edema Corectopia may be mild to moderate Glaucoma may be less severe &amp; but atpresentation IOP may be normal. Chandler syndrome have more severe edema. 31. Cogan Resse syndromeCharacterised by diffuse naevus Which coversiris or iris nodule.Iris atrophy may beabsent in50% of patients,but corectopia &amp;GlaucomaMay be severe. 32. Iris atrophyEssential iris atrophycharacterised by distortionOf pupil, peripheral anterior synechie &amp; iris atrophyWith full thickness holes.Glaucoma commonly present in the involved eye.Unilateral occurs in 4th &amp; 5thDecades of life in caucasians 33. [V] Essential corneal edema Idiopathic , episodic &amp; often cyclic may beunilateral. Presents with typical features of corneal edemalike fb sensation,diminished vision &amp; haloeswhich persists for months then disappears. Recurrent erosions on cornea may be noted. It may progress to the formation of bullae withciliary injection &amp; urgent symptoms of pain &amp;photophobia. 34. Essential corneal edema Pupils may be semidilated &amp; sluggishlyreacting to light. If secondary infection does not set up attackpasses of &amp; the condition eventually cleansup. Some of these cases may be earlypresentation of dystrophic changes like Fuchsdystrophy. 35. [VI] Metabolic disorders Some vague concepts suggested by cornealedema occuring in some metabolic conditionslike myxedema. It has also seen in hypercholesterolemia. In malaria mainly in patients taking mepacrinefor its treatment, in this condition edema islimited to basal layer of epithelium &amp;superficial layer of stroma. 36. PRIMARY CAUSESA) Primary endothelial dystrophies: dystrophies involving endothelium &amp; descemets membrane causes symmetrical marked stromal edema which is gradually progressive over a period of years.B) Primary endothelial dystrophy which develop later in life are fuchs dystrophy. 37. Primary Endothelial Dystrophy Congenital hereditary endothelial dystrophy:characterised by diffuse edema at birth orsoon thereafter, without significant anteriorsegment abnormalities. Posterior polymorphous dystrophy: B/Lvesicular or linear lesions at the level ofdescemets membrane &amp; endothelium ispresent, it presents with congenital cornealedema. 38. FUCHs dytrophyAD pattern of inheritance,Earliest changes are limitedTo posterior cornea &amp;presents with central B/Lasymmetrical cornealGuttata.In fuchs dystrophyendothelial cells transforminto fibroblastLike cells capable ofsecreting collagen fibrils.Contribute to BM thickening. 39. FUCHs dytrophy Progressive endothelial decompensation leadsto stromal &amp; epithelial edema. Fluid in the stroma permeates the epiteliallayer causes microcystic epithelial edema. Individual epithelial cells burst, intercellularedema occurs &amp; typical blisters or bullaeformed. These changes are confined to centre ofcornea initially. 40. Bullous keratopathyIt represents the terminalstage of severe orProlonged epithelialedema.In the affected area the epithelium is steamyIrregular &amp; on its surface one or more large bullaeAppears, raised in theform of blebs. 41. Bullous keratopathy After 2-3 days the bullae rupture only toreappear, the cycle associated with considerableirritation &amp; pain. Treatment is extremely difficult; retrobulbarinjection of alcohol, removal of endothelium byscraping, cauterisation of cornea by tinctureiodine, trichloro-acetic acid. Bandage contact lens to relieve pain. Lamellar grafting, if measures of therapy fails &amp; ifrecurrence persists treatment is enucleation. 42. Manifestations of edema Depends upon cause &amp; degree of thecondition. Mild discomfort in conditions like fuchsdystrophy. Severe neuralgic pain is seen in bullouskeratopathy. Colour haloes. Severe visual loss. 43. Visual acuity Small amount of epithelial edema can result insubstantial reduction in visual acuity. Although 70% stromal edema is compatiblewith normal visual acuity. Decreased acuity is more severe in earlymorning. IOP, iritis glaucoma &amp; optic nerve changesmay contribute to reduced acuity. 44. Pain &amp; discomfort As edema increases epithelium is detachedfrom basement membrane to form bullae. This rupture of bullae causes severe pain,photophobia, epiphora &amp; narrowing ofpalpebral fissure. Photophobia is due to light scattering in theedematous cornea. Coloured haloes. 45. Coloured haloes 46. Evaluation of corneal morphologySlit lamp examination.Specular biomicroscopy.Pachymetry.Optical coherence tomography.Scheimpflug camera.Orbscan. 47. Slit lamp examinationSlit lamp examination revealscornea guttata, stromaldensity,Descemets membrane folds.Bullae are easily observed byslitlamp. In case of chronicCorneal edemaneovascularization,pannus formation or dystrophiesare visible. In case of stromaledema thickness exceeds 0.6mm. 48. Specular biomicroscopyMeasures cell density.Normally endothelialcell count is 3000 --2000 cells/mm2.Cell count less</p>