Chemical burns

1. CHEMICAL BURNS PRESENTER -DR RAHUL MODERATOR -DR SANGIT

2. OCULAR BURNS Ocular burns constitute true ocular emergencies Both thermal and chemical burns represent potentially blinding ocular injuries

3. Thermal burns result from accidents associated with -firework explosions - steam - boiling water -molten metal (commonly aluminium)

4. Chemical burns Chemical burns may be caused by either alkaline or acidic agents Alkali more frequently used in household cleaning agents and many building materials So Alkali injuries occurs more frequently than acid injuries

5. Causes Common sources of alkali are as follows: Cleaning products ( eg .ammonia) most serious injury Fertilizers ( eg , ammonia) Cement, plaster, ( eg , lime) most common injury Fireworks ( eg , magnesium hydroxide)

6. Pathophysiology Alkaline agents have both hydrophilic and lipophilic properties which allow them to rapidly penetrate cell membranes and enter the anterior chamber Alkali damage results from interaction of the hydroxyl ions

7. Pathophysiology It causes saponification of cell membranes and cell death along with disruption of the extracellular matrix Cations react with carboxyl group of stromal collagen And Glycosaminoglycans (GAGS) Hydration of Gagas result in loss of clarity of stroma

8. Increased IOP:

9. Pathophysiology Penetration into AC may be almost immediately after ammonia Within 3-5 min after sodium hydroxide injury

10. Penetration into AC

11. Acid injury Common sources of acids are as follows: Battery acid ( eg , sulfuric acid) Bleach ( eg , sulfurous acid) Glass polish ( eg , hydrofluoric; )

12. Pathophysiology Acids tend to cause less damage than alkalis corneal proteins bind acid and act as a chemical buffer. coagulated tissue acts as a barrier to further penetration of acid. Acid binds to collagen and causes fibril shrinkage which can cause symblepharon formation

13. Classification There is no ideal classification or grading system for ocular alkali burns The principal weakness of grading system is that injuries to the cornea are not uniformly associated with injuries to the surrounding tissues

14. Classification of severity of ocular surface burns by Roper-Hall Grade prognosis cornea limbus 1 good Corneal epithelial damage No limbal ischaemia 2 good Corneal haze, iris details seen <1/3 limbal ischaemia 3 guarded Total epithelial loss,stromal haze,iris details obscured 1/3-1/2 limbal ischaemia 4 poor Cornea opaque,iris and pupil obscured >1/2 limbal ischaemia

15. Grade Prognosis Clinical findings Conjunctival involvement Analogue scale 1 Very good 0 clock hours of limbal involvement 0% 0/0% 2 good <3 clock hours of limbal involvement <30% 0.1-3/1-29.9% 3 good >3-6 clock hours of limbal involvement >30-50% 3.1-6/31-50% 4 Good to guarded >6-9 clock hours of limbal involvement >50-75% 6.1-9/51-75% 5 Guarded to poor > 9-<12 clock hours of limbal involvement >75-<100% 9.1-11.9/75.1-99.9% 6 Very poor Total limbus (12 clock )involved Total conjunctiva 12/100%

16. Clinical stages The clinical course can be divided into three distinct stages I )Acute stage (immediate to 1 week) II) Early repair stage (1-3week) III) Late repair stage and sequel ( 3 weeks and longer )

17. I )Acute stage (immediate to 1 week) In mild burns the corneal and conjunctival epithelium have defects with sparing of limbal blood vessels in severe burns the epithelium is destroyed and there is immediate limbal ischaemia due to damage to blood vessels.

18. intraocular pressure Rise in intraocular pressure in a bimodal manner An initial peak is due to compression of the globe as a result of hydration and longitudinal shortening of collagen fibrils. The second peak due to impedence of aqueous humor outflow

19. II Early repair stage (1-3week): This stage is characterized by replacement of destroyed cells and extracellular matrix. In grade I and II chemical burns - regeneration of epithelium - neovascularization of cornea -clearing of stroma -beginning of synthesis of collagen glycosaminoglycans

20. In grade III and IV regeneration of epithelium may not start and progress stroma remains hazy endothelium replaced by a retrocorneal membrane.

21. Cont.. In this stage, corneal ulceration tends to occur. Stromal ulceration is due to action of digestive enzymes such as collagenase,metalloprotinase released from regenerating corneal epithelium and polymorphonuclear leukocytes.

22. III Late repair stage and sequele ( 3 weeks and longer ) This stage is characterized by completion of healing with a good prognosis (grade I and II ) complication in those with a guarded visual prognosis (grade III and IV) Complications are primary and secondary

23. Complications Primary complications Conjunctival inflammation Corneal abrasions Corneal haze and edema Acute rise in IOP Corneal melting and perforations

24. Secondary complications Secondary glaucoma Secondary cataract Conjunctival scarring Corneal thinning and perforation Complete ocular surface disruption with corneal scarring and vascularization Corneal ulceration (sterile or infectious) Complete globe atrophy (phthisis bulbi ): 

25. Clinical case 4 yr boy presented to LEI with h/o plaster falling into eyes while playing at construction site Eye wash given

26. History Most often, the patient gives a history of a liquid or a gas being splashed or sprayed into the eyes or of particles falling into the eyes. we have to ask the patient regarding the specific nature of the chemical and the mechanism of injury ( eg , simple splash vs high-velocity blast).

27. Physical examination A thorough physical examination should be deferred until the affected eye is irrigated copiously The pH of the ocular surface is neutralized. Topical anesthetic drops may be used to aid in patient comfort and cooperation.

28. Cont.. After irrigation, a thorough eye examination is performed special attention given to - clarity and integrity of the cornea -degree of limbal ischemia - IOP.

29. Physical manifestations Decreased visual acuity: It can be decreased because of -corneal epithelial defects, -haze, -increased lacrimation or discomfort.

30. Particles in the conjunctival fornices - This finding is more common with particulate injuries, such as plaster. - If not removed the residual particles can serve as a reservoir for continued chemical release and injury. -These particles must be removed before ocular surface healing can begin

31. Perilimbal ischemia : -The degree of limbal ischemia (blanching)is the most significant prognostic indicator for future corneal healing -The limbal stem cells are responsible for repopulating the corneal epithelium. -The greater the extent of blanching, the worse the prognosis.

32. Cont.. But, the presence of intact perilimbal stem cells does not guarantee normal epithelial healing. The extent of blanching should be documented in terms of clock hours involved

33. Corneal epithelial defect It can range from mild diffuse punctate epithelial keratitis (PEK) to a complete epithelial defect. A complete epithelial defect may not take up fluorescein dye rapidly , so, it may be missed.

34. Cont.. If an epithelial defect is suspected but not found on the initial evaluation, the eye should be reexamined after several minutes. The size of the defect should be recorded so as to document response to treatment on subsequent visits

35. Stromal haze : Haze can range from a clear cornea (grade 0) to a complete opacification (grade 5) with no view into the anterior chamber. Corneal perforation : A very rare finding at presentation it is more likely to occur after the initial presentation (from days to weeks) in severely injured eyes that have poor healing capacity.

36. A. c inflammatory reaction This can vary from trace cell and flare to a vigorous fibrinoid anterior chamber reaction. Generally, this finding is more common with alkaline injuries because of the greater depth of penetration

37. Adnexal damage/scarring : Similar to chemical injuries on other skin areas, it can lead to severe exposure problems eyelid scarring prevents proper closure, exposing an already damaged ocular surface

38. Medical Care Regardless of the underlying chemical involved, common goals of management include (1)removing the offending agent, (2) promoting ocular surface healing (3) controlling inflammation, (4) preventing infection, (5) controlling IOP.

39. Immediate therapy Immediate copious irrigation remains the single most important therapy for treating chemical injuries. Ideally, the eye should be irrigated with a sterile balanced buffered solution, such as normal saline solution or Ringer's lactate solution. However, immediate irrigation with even plain tap water is preferred without waiting for the ideal fluid.

40. The irrigation solution must contact the ocular surface. This is best achieved with a special irrigating tubing ( eg , Morgan lens) or a lid speculum. Irrigation should be continued until the pH of the ocular surface is neutralized, usually requiring 1-2 liters of fluid.

41. artificial tear supplements play an important role in healing. Ascorbate plays a fundamental role in collagen remodeling , leading to an improvement in corneal healing. Placement of a therapeutic bandage contact lens helpful in some patients.

42. Control inflammation Inflammatory mediators released from the ocular surface at the time of injury cause tissue necrosis This inflammatory response not only inhibits reepithelialization but also increases the risk of corneal ulceration and perforation. Controlling inflammation with topical steroids can help break this inflammatory cycle. .

43. Citrate both promotes corneal wound healing and inhibits PMNs via calcium chelation . Acetylcysteine (10% or 20%) can inhibit collagenase to reduce corneal ulceration

44. Prevent infection When the corneal epithelium is absent, the eye is susceptible to infection. Prophylactic topical antibiotics are warranted during the initial treatment stages.

45. Control IOP The use of aqueous suppressants is advocated to reduce IOP secondary to chemical injuries both as an initial therapy and during the later recovery phase, if IOP is high (>30 mm Hg) Carbonic anhydrase inhibitors Topical beta-blockers

46. Control pain Severe chemical burns can be extremely painful. Ciliary spasm can be managed with the use of cycloplegic agents however, oral pain medication may be necessary initially to control pain Cycloplegic mydriatics

47. Surgical therapy A)Promote Reepithelialization B)Support repair and minimize ulceration C)Late rehabilitation

48. A)Promote Reepithelialization 1) Conjunctival / tenons advancement ( tenoplasty ) 2) Limbal stem cell transplantation 3) Conjunctival transplantaion 4) keratoepithelioplasty

49. B)Support repair and minimize ulceration 1) Tenoplasty 2) Limbal stem cell transplantation 3)Large diameter therapeutic pk 4)Tissue adhesive

50. C)Late rehabilitation 1)Late stem cell transplantation 2) Conjunctival transplantation 3)Mucosal membrane grafts 4)PK

51. Prevention Education and training regarding the prevention of chemical exposures in the workplace can help prevent chemical injuries to the eye. Persons who may be exposed to chemicals in the workplace are advised to wear safety goggles.

52. Patient Education If the injury resulted from a preventable accident, proper safety instruction should be provided. If a patient is left functionally monocular from an injury, the patient should be instructed in the use of safety eyewear ( eg , polycarbonate lens)