CGI, HYPHAEMIA & Chemical injuries OF THE EYE

1. CGI, HYPHAEMIA & Chemical injuries OF THE EYE Ayesha S Abdullah 29.11.2013

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

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 • Surgical repair of the fracture through conjunctival incision via the inferior fornix • Surgical repair of the fracture with a plastic plate • Surgical repair via Caldwell Luc approach • Surgical repair via skin incision over the inferior orbital rim • 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

7. Close Globe Injuries • SubconjunctivalHaemorrhage • Corneal abrasion • Acute corneal oedema • Traumatic iritis • Traumatic Mydriasis / Miosis • Hyphaema • Iridodialysis • Cyclodialysis / Angle recession • Ciliary shock

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

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

15. Hyphaema • 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

16. Treatment of Hyphaema • Small (less than 1/3rd 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

18. Hyphaema

20. Chemical Injuries of the Eye • About 2/3rd 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

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

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.

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

24. Pathophysiology • Alakli burns are more damaging than acid burns because it penetrates deeper1 • 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

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

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)

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 limbalischemia • Anterior chamber reaction • Signs of deeper penetration of the chemical • IOP.

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

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 • Adnexaldamage/scarring

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

38. First AidRemove 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

39. Promote ocular surface (epithelial) healing • Artificial tears • Bandage contact lens • Ascorbateplays 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)

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.

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

42. Control pain • Severe chemical burns can be extremely painful. • Oral NSAIDS • Ciliaryspasm can be managed with the use of cycloplegicagents

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

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

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

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

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

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