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Chemical injury clinical manifestations


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Chemical injury clinical manifestations

  1. 1. Chemical injury to eye Presenter : Dr. Chethana Moderator :Dr. Shiva prasad
  2. 2.  Chemical injuries are potentially devastating ocular surface injuries that can result in permanent visual impairment. DEFINATION Principles and practices of ophthalmology: Albert and Jakobiee ‘s
  3. 3. INCIDENCE  Chemical burns constitute between 11% and 18% of all ocular trauma  80% -industrial and/or occupational exposure-young adults ,accidental>homicidal  Male > female  Acid > alkali*  Lime burn(chunna) very common in India *Cite this article: Vathulya M, Tiwari VK (2017) Epidemiological Profile of Chemical Burns from the Largest Burn Centre in India. JSM Burns Trauma 2(1): 1013.
  4. 4. ETIOLOGY- ALKALI  Ammonia - Fertilizers, Refrigerants, cleaning agents , combines with water to form NH4OH,rapid penetration  Lye(NaOH)- Drain cleaners  Potassium hydroxide- Caustic potash  Magnesium Hydoxide – Sparklers  Lime-(Ca(OH)2)- Plaster, whitewash ,cement  AMMONIA,LYE - MOST SERIOUS BURNS
  5. 5. ETIOLOGY-ACID  Sulfuric acid- Industrial cleaners, explosives, dyes, inverter Battery, car batteries, combines with H2O, produce thermal injury  Nitric oxide- fertilisers , rocket propellants, nylon products  Sulfurous acid-Bleach, Refigerants, preservatives  Hydrofluoric acids-Glass polishing – exception  Acetic acids-Vinegars
  6. 6. Mechanism  PH changes  Ulceration and proteolysis  Collagen synthesis defects
  7. 7. BIO CHEMICAL CHANGES-Alkali  Lipophilic and penetrate more rapidly than acids.  Rise in pH  Reacts with cellular lipids- Saponification - cell destruction.  The hydroxyl ion hydrolyzes intracellular glycosaminoglycans and denatures collagen.  2-3 weeks later-stromal ulceration –proleolytic enzymes by PMNL and epithelial cells
  8. 8.  Alkali damage CB aqueous Proline hydroxylysine Lysine synthesis of GAG’s (stroma) ascorbate
  9. 9.  Alkali substances can pass into the anterior chamber rapidly (approximately 5-15 min) exposing the iris, ciliary body, lens, and trabecular network to further damage. Irreversible damage occurs at a pH value above 11.5
  10. 10. Severe chemical injury with early corneal neovascularisation
  11. 11. Alkali burn. Note the severe conjunctival reaction and stromal opacification blurring iris details inferiorly
  12. 12. BIO CHEMICAL CHANGES - Acid burns  Acid burns cause protein coagulation in the corneal epithelium, which limits further penetration.  Thus, these burns usually are nonprogressive and superficial.  Reacts with collagen shrinkage with IOP  Ciliary body damage with decreased aqueous acsorbate levels
  13. 13. Key Features: Pathophysiology  The severity of a chemical injury is related to the surface area of contact and the degree of penetration.  Limbal stem cells are the cells most qualified to restore functional competence of the corneal epithelial surface after injury.  Corneal repair by keratocytes consists of both synthesis and degradation of stromal collagen.  Persistent inflammation may delay reepithelialization and shift the net balance of corneal repair toward progressive stromal ulceration.
  14. 14.  The three major principles guiding evaluation and management of chemical injury are based on addressing each of the three main pathophysiologic mechanisms contributing to the final outcome: (1) regeneration of ocular surface epithelium and its state of differentiation, (2) stromal matrix remodeling, including repair and degradation, and (3) inflammation
  15. 15. PATHOPHYSILOGY  LEUCOCYTIC WAVE CHEMICAL BURN pH rise PED  12-24hrs(PMN+MONONUCLEAR LEUCOCYTES) KERATOCYTE DAMAGE Extensive LSC damage  PHAGOCYTIC DEG. STROMAL THINNING  TYPE I COLLAGENES mmp-8  Plasminogen activities STERILE CORNEAL ULCER  7 days inflam.cells Vit C Vit A Na hyalurnote Heparin Tetracyclin,collagenase inhibitor,oral antioxidents steroids steroids prostaglandins
  16. 16. Immediate phase  Clinical features depend on  The extent of ocular surface involvement,  The depth of penetration, and  The relative toxicity and concentration  The depth of ocular surface penetration, and possible limbal stem-cell damage, can be evaluated indirectly by assessment of vascular ischemia and necrosis of limbal and bulbar conjunctiva.
  17. 17. Signs & Symptoms  Pain  Redness  Irritation  Tearing  Inability to keep the eye open  Sensation of something in the eye  Swelling of the eyelids  Blurred vision
  18. 18. Hughe’s classification  Mild  Moderately severe  Very Severe depending on amount of corneal edema and conjunctival blanching
  19. 19. Classification of severity of ocular surface Burns by Roper-Hall Grade Prognosis Cornea Epi/Conjun limbus  1 Good Yes No limbal ischaemia   2 Good Yes <1/3 Corneal haze, iris details visible  3 Guarded Yes >1/3 -1/2 Iris details obscured  4 poor Yes >1⁄2 limbal ischaemia Cornea opaque,  iris and pupil obscured Br J Ophthalmol. 2004 October; 88(10): 1353–1355 corneal haze as an important prognostic variable. Rapidly changes
  20. 20. Modification in GRADING  Dua et al, limbal fluroscein staining as a marker of limbal stem cell damage.  Fornices & mucocutaneous junction of the conjunctiva are important for conjunctival regeneration  Limbal involvement prefered over limbal ischemia(Transient)
  21. 21. New classification of ocular surface burns. DUA et al  Grade Prognosis Clinical findings Conj.invol.  I Very good 0 clock hours 0%  II Good <3 clock hours. <30%  III Good >3–6 clock hours. >30–50%  IV Guard >6–9 clock hours >50–75%  V poor >9–<12 clock hours >75–<100%  VI Very poor Total limbus 100% 
  22. 22. Estimation of conjunctival injury. For example, 1/6th+1/6th = 1/3rd. BULBAR2/3 & TARSAL 1/3
  23. 23. DIAGRAM
  24. 24. PROGNOSIS-poor  ALKALI  pH > 11  More then 2quadrent ischemia  Corneal anesthesia  ACID  pH < 2.5  Corneal anesthesia  Ischemia  Severe iritis  Lens opacification
  25. 25. Mc. CULLEY CLINICAL COURSE OF CHEMICAL INJURY  Immediate phase  Acute up to 1 week  Early Repair 1-3weeks  Late repair >3wks  (Balance between collagen synthesis & collagen degradation)
  26. 26. Acute stage  Mild burns – epi defect with limbal vessels sparing  Severe burns- epi damage with limbal ischemia  pH will reduce aqueous glucose and ascorbate , which further aggravates ischemia  Inflammation is active / Bimodal rise in iop  Haling and re-epithelisation starts
  27. 27.  Grade I injuries - heal  Grade II injuries - There is slow but progressive reepithelialization , although the sector of limbal stem- cell loss may show little or no reepithelialization.  Grade III and IV injuries - show no reepithelialization. there is little or no collagenolytic activity during this phase. IOP rise, infiltration of the peripheral cornea with polymorphonuclear leukocytes and other inflammatory cells begins.
  28. 28. Early repair- 7 to 21days  Grade 1or 2 burns,  Epithelium regeneration  Corneal neovascularisation  Clearing of stroma  Synthesis of GAG’s  Laying down of new collagen  Peaks at 14th day  Grade 3 0r 4  Epi reg may not start and progress  Stomal haze reduces  ulceration by proteolytic enzymes/collagenase activity  3rd week
  29. 29. Late repair -> 3 weeks  Grade 1 to 2 –heal with good prognosis  Grade 3 to 4 –complications,scarring,xerophthalmia, symblepharon, ankyloblepharon, glaucoma, uveitis, cataract, lagophthalmos, cicatrial entropion or ectropion, trichiasis, dry eye etc,  Conjunctva – goblet cells – keratinisation  Cornea – if breakdown of collagen is more –thinning descmetacoele and perforeation
  30. 30.  If synthesis is more than breakdown – corneal opacity  Which in turn influenced by corneal vascularisation  Nutrients and inhibitors of collagenase are brought to the cornea leading to ulceration  If limbal epi cells are intact – smooth and rapid re- epithelisation , otherwise conjunctivalisation  Lids and adnexa – affect the tear film
  31. 31. (a) Type I healing pattern: normal epithelial recovery. After a grade I injury with no limbal stem-cell loss, complete reepithelialization with a normal corneal phenotype is complete within 1 week. (b) Type II healing pattern: delayed differentiation. After a grade II injury with limbal stem-cell loss from the 7– to 9–o'clock position, there is delayed reepithelialization through the late repair phase, with development of superficial vascular pannus and impaired corneal epithelial differentiation in the affected quadrant. (c) Type III healing pattern: fibrovascular pannus. After a grade III injury with complete limbal stem-cell loss, progressive corneal epithelialization with conjunctivally derived epithelium over a 4–month period results in fibrovascular pannus covering the entire cornea. (d) Type IV healing pattern: sterile corneal ulceration. After a grade IV injury with complete limbal stem-cell loss, as well as loss of conjunctival epithelium and vascularity in the entire nasal quadrant, there is no corneal reepithelialization. Sterile corneal ulceration of the nasal and inferior corneal stroma begins 3 months after injury∼ .
  32. 32. Sequelae  Limbal stem cell deficiency  Conjunctivalisation  Corneal vascularisation  Pesrsistant Epithelial Defects  Inflammed ocular surface  Symblepharon  Dry eye  Lid deformities  Loss of corneal clarity
  33. 33. THANK YOU
  34. 34. References  AAO cornea and external disease  Ophthalmology yanoff and duker  Clinical ophthalmology –kanski 6th edition