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CGI, HYPHAEMIA & CHEMICAL INJURIES OF THE EYE Ayesha S Abdullah 29.11.2013 1.

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Presentation on theme: "CGI, HYPHAEMIA & CHEMICAL INJURIES OF THE EYE Ayesha S Abdullah 29.11.2013 1."— Presentation transcript:

1 CGI, HYPHAEMIA & CHEMICAL INJURIES OF THE EYE Ayesha S Abdullah

2 Learning outcomes By the end of this lecture the students would be able to 1.Correlate the effects of CGI on various parts of the eye with the mechanism of close globe trauma 2.Identify the complications of CGI 3.Diagnose hyphaema and describe the principles of management and complications of hyphaemia 4.Correlate the pathophysiology of chemical injury (with acids and alkali) to the clinical presentation & complications of chemical injuries of the eye 5. Describe the first aid measures and specific management of a case with chemical injury 6.Identify the complications of chemical injury 2

3 3  A 20 year old man while fighting another young man had sustained trauma to the right orbit 2 days back. He had minimal enophthalmos and restricted upward movement of the right eye with double vision in up-gaze only. The CT scan shows fracture of the floor of the orbit. The most appropriate line of management is a)Surgical repair of the fracture through conjunctival incision via the inferior fornix b)Surgical repair of the fracture with a plastic plate c)Surgical repair via Caldwell Luc approach d)Surgical repair via skin incision over the inferior orbital rim e)Wait for 02 weeks and provide symptomatic treatment

4 Effects of close globe injury (CGI)  Mechanism  AP compression  Expansion in the equatorial plan  Transient & excessive increase in IOP  Impact is primarily absorbed by ?? Lens –Iris diaphragm & vitreous  The damage can happen in any tissue  commonly has long-term effects/ sequelae 4

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7 Close Globe Injuries  Subconjunctival Haemorrhage  Corneal abrasion  Acute corneal oedema  Traumatic iritis  Traumatic Mydriasis / Miosis  Hyphaema  Iridodialysis  Cyclodialysis / Angle recession  Ciliary shock 7

8 Close Globe Injuries  Subluxation and dislocation of lens  Cataract  Posterior vitreous detachemet  Vitreous haemorrhage  Choroidal rupture  Commotio retinae  Retinal Breaks Dialysis Equatorial tears Macular holes  Optic nerve avulsion 8

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14 Hyphaema  Source of bleeding?  Iris /ciliary body / both  Immediate threat –  Secondary haemorrhage  Can happen up to a week, mostly first 24 hrs  The haemorrahge is larger than the original bleed  Most common problem is raised intraocular pressure 14

15  Most hyphaemas resolve without complications but complications can happen with long standing cases  The complications are, secondary glaucoma, optic nerve damage and corneal staining  The greater the extent of hypahema greater the chances of complications i.e blood filling more than half of the AC Hyphaema 15

16 Treatment of Hyphaema  Small (less than 1/3 rd of the AC) can be managed at home  Larger hyphaema requires hospitalization for closer monitoring to avoid secondary bleed and complications  For lowering the IOP; beta blockers, Alpha agonist, CA inhibitors  For associated traumatic uveitis; topical steroids  Immobilization of the iris in the dilated position to avoid secondary haemorrhage; mydriatics 16

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18 Hyphaema 18

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20 Chemical Injuries of the Eye  About 2/3 rd of the chemical injuries happen at workplace the rest at home  Almost any chemical can cause ocular irritation  Serious damage however happen with acids and alkalis  Alkali injuries are more common because they are used more frequently  Bilateral chemical exposure could be extremely damaging resulting in blindness and disfigurement 20

21 Sources  Common sources of alkali are  Cleaning products (eg, ammonia)  Fertilizers (eg, ammonia)  Drain cleaners (e.g, lye)  Cement, plaster, mortar (e.g, lime)  Airbag (automobile) rupture (e.g, sodium hydroxide)  Fireworks (eg, magnesium hydroxide)  Potash (eg, potassium hydroxide)  Commonest alkalis causing chemical injury are ammonia, sodium hydroxide & lime 21

22 Sources  Common sources of acids are  Battery acid (eg, sulfuric acid)  Bleach (eg, sulfurous acid)  Glass polish (eg, hydrofluoric; behaves like an alkali)  Vinegar (eg, acetic acid)  Chromic acid (brown discoloration of conjunctiva)  Nitric acid (yellow discoloration of conjunctiva)  Hydrochloric acid  Commonest acids are sulphuric, sulphurous, hydrofluoric, acetic, chromic and hydrochloric acid. 22

23 Pathophysiology  Severity depends upon  The nature/ properties & concentration of the chemical  Area of the affected surface  Length of exposure  Associated damage e.g. thermal /electrical/ explosive 23

24 Pathophysiology  Alakli burns are more damaging than acid burns because it penetrates deeper 1  Necrosis and shedding of the corneal and conjunctival epithelium  Damage to the limbal vasculature  Limbal ischemia  Persistent corneal epithelial defects  Conjunctivaliztion & vascularization of the cornea  Corneal ulceration and perforation  Conjunctival and adnexal scarring 24

25 Corneal healing  Loss of epithelium  Migration of cell derived from the limbal stem cells  Phagocytosis of the necrosed collagen by the keratocytes and new collagen is laid down 25

26 Clinical presentation  History  Ascertain the nature of the chemical and mode of injury  Complaints are  Pain (often extreme)  Foreign body sensation  Blurred vision  Excessive tearing  Photophobia  Red eye(s) 26

27  Physical examination  A thorough physical examination should be deferred until the affected eye is irrigated copiously, and the pH of the ocular surface is neutralized.  After irrigation, a thorough eye examination is performed focusing on  clarity and integrity of the cornea  degree of limbal ischemia  Anterior chamber reaction  Signs of deeper penetration of the chemical  IOP. 27

28 Signs  Conjunctival inflammation  Particles in the conjunctival fornices  Perilimbal ischemia (LI-blanching) The most significant prognostic indicator for corneal healing.  Greater the extent of blanching, the worse the prognosis  LI is documented as number of clock hours 28

29 Signs  Corneal epithelial defect: Corneal epithelial damage can range from mild diffuse punctate epithelial keratitis (PEK) to a complete epithelial defect.  Stromal haze: Haze can range from a clear cornea (grade 0- 5) to a complete opacification  Corneal perforation  Anterior chamber inflammatory reaction: more common with alkali injury  Increased IOP  Adnexal damage/scarring 29

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37 Principles of management  Treat Systemic injury  Ocular involvement  removing the offending agent  controlling inflammation  promoting ocular surface healing  preventing infection  controlling IOP 37

38 First Aid Remove the chemical (irrigation)  Immediate copious irrigation remains the single most important therapy for treating chemical injuries  Immediate irrigation with even plain tap water is preferred without waiting for the ideal fluid  The irrigation solution must contact the ocular surface. Irrigation should be continued until the pH of the ocular surface is neutralized, usually requiring 1-2 liters of fluid 38

39 Promote ocular surface (epithelial) healing  Artificial tears  Bandage contact lens  Ascorbate plays a fundamental role in collagen remodeling, leading to an improvement in corneal healing.  Amniotic membrane transplant  topical Sodium Ascorabte 10% given 2 hourly and 1-2 g of vitamin C given orally ( not recommended in renal disease) 39

40 Control inflammation  Inflammatory mediators  Controlling inflammation with topical steroids can help break this inflammatory cycle  Citrate both promotes corneal wound healing and inhibits PMNs via calcium chelation. 40

41 Prevent infection  When the corneal epithelium is absent, the eye is susceptible to infection.  Prophylactic topical antibiotics during the initial treatment stages Control IOP Oral acetazolamide 41

42 Control pain  Severe chemical burns can be extremely painful.  Oral NSAIDS  Ciliary spasm can be managed with the use of cycloplegic agents 42

43 Surgical Care  Early  Debridement  Temporary amniotic membrane  Limbal stem cell transplant  Lysis of conjunctival symblepharon  Late  Surgery for conjunctival adhesions  Keratoplasty  Cataract extraction  Keratoprosthesis  Glaucoma surgery 43

44 Follow up  In patients with severe chemical injuries, short hospitalization in an ophthalmic care unit to closely monitor  In general, the prognosis of ocular chemical injuries is directly correlated with the severity of insult to the eye and adnexal structures.  Roper-Hall grading system 44

45 Complications  Primary complications include the following  Conjunctival inflammation  Corneal abrasions  Corneal haze and edema  Acute rise in IOP  Corneal melting and perforations 45

46 Complications  Secondary complications include the following:  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)  Blindness 46

47 Management summary  Immediate, prolonged irrigation  Followed by referral to ophthalmologist for aggressive early management  Close long-term monitoring  Essential to promote ocular surface healing and to provide the best opportunity for visual rehabilitation 47

48 Home work  How can we grade the severity of chemical injury of the eye?  Not more than 4 lines  By Thursday next week before the Friday class  Both homeworks 48


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