Ocular trauma

OPHTHALMOLOGY PRESENTATION

1. Ocular Trauma Dr . Sidesh Hendavitharana (Senior registrar in ophthalmology )

2. Ocular trauma is an emergency and requires immediate medical or surgical intervention Classification Direct , 1.Mechanical injuries Extraocular FB Blunt injury(contusion) Penetrating and perforating injury Perforating injury with retained FB

3. 2.Chemical injuries Acid burns Alkali burns

4. . 3.Injuries due to physical agent Thermal injury Electric injury Radiation injury Ultraviolet radiations Infrared radiations Ionizing radiational injuries Indirect ocular trauma

5. Foreign bodies Corneal foreign body is foreign material on or in the cornea, usually metal, glass, or organic material.

6. Corneal foreign bodies: Symptoms Foreign body sensation, Tearing, History of trauma ,photophobia , pain , red eye Signs Corneal foreign body with or without rust ring, edema of the lids, conjunctiva, and cornea, foreign body can cause infection and/or tissue necrosis.

7. Corneal foreign bodies cont. Workup 1.History 2.Document visual acuity. One or two drops of topical anesthetic may be necessary to control pain. 3.Slit-lamp Examination: If there is no evidence of perforation, evert the eyelids and inspect for foreign bodies. 4.Dilate the eye and examine the vitreous and retina 5.Consider a B-scan US, CT of the orbit.

8. Corneal foreign bodies cont. Treatment 1.Apply topical anesthetic, remove the foreign body with a spud or forceps at a slit lamp. If multiple superficial foreign bodies, its easier to remove with irrigation. 2.Remove the rust ring. This may require an ophthalmic drill. 3.Measure the size of the resultant corneal epithelial defect. 4.Treat as for corneal abrasion.

9. Blunt injury to eye Blunt injury to eye caused by blunt objects Modes of injury Direct blow by blunt object Accidental blunt trauma

10. Mechanism 1.Direct impact Produces maximum damage at point of blow. 2.Compression wave force( contrecoup damage) Force of impact transmitted through fluid contents in all directions and strikes angle of ant.chamber,pushes iris-lens diaphragm posteriorly and also strikes choroid and retina. 3.Reflected compression wave force Compression wave reflects towards posterior pole to cause foveal damage.

11. . 4.Rebound compression wave force Compression wave rebounds back anteriorly damaging retina and choroid by forward pull and lens-iris diaphragm by forward thrust. 5.Indirect force Indirect force from bony walls and elastic contents of orbit when globe suddenly strikes against these structures.

12. Modes of damage Mechanical tearing of tissues Damage to tissue cells disruption of their physiological activity. Vascular damage ischemia,oedema,h’age Tropic changes(due to nerve supply disturbances.) Delayed complications like 2ry glaucoma,late rossete cataract,RD . irrit irrit

13. Lesions Extraocular lesion(injury to eye lids,conjunctiva , lacrimal apparatus,optic nerve and orbit. Closed globe injury(injury to intraocular structures including cornea and sclera.) Globe rupture

14. Effects a.Eyelids Ecchymosis Black eye(hematoma in loose subcutaneous tissue) Aberasion , laceration and avulsion Traumatic ptosis Emphysema(due to escape of air from paranasal sinuses.

15. . b.Lacrimal apparatus Dislocation of lacrimal gland Laceration of lacrimal passage c.Conjunctiva Subconjunctival h’age , chemosis , laceration d.Cornea 1.Simple abrasion Very painful Detected by 2%fluorescein staining Treatment Antibiotic oinment with pad and bandage for 24hrs.

16. . 2.Recurrent corneal erosions Follow simple aberasion caused due to fingernail trauma Feature Recurrent attacks of acute pain and lacrimation on opening eye in morning(due to abnormally loose attachment of epithelium to underlying bowman’s membrane Treatment Antibiotic oinment with pad and bandage for 48hrs Debridement of loosely attached epithelium

17. . 3.Partial or complete corneal tears(lamella corneal lacerations) 4.Blood staining of cornea Associated with hyphema and raised intraocular pressure. Features Reddish brown or greenish cornea Simulates dislocation of clear lens into anterior chamber(late stages) Clear very slowly for periphery towards center over 2 yrs 5.Deep corneal opacity Results from corneal stromal edema or folds in descemet’s membrane.

18. . e.Sclera Partial thickness scleral wounds(lamella scleral lacerations) Rupture of eyeball(commonly at limbus or behind insertion of recti) f.Anterior chamber 1.Hyphema Due to injury to iris or cilliary body vessels 2.Exudates Following traumatic uveitis

19. . g.Iris,pupil and cilliary body 1.Traumatic miosis Due to irritation of ciliary nerves Associated with spasm of accomodation . 2.Traumatic mydriasis ( iridoplegia ) permenant and associated with traumatic cycloplegia . 3.Rupture of pupillary margin 4.Radiating tear in iris stroma (sometimes reaching upto cilliay body) 5.Iridodialysis(detachment of iris from its root at ciliary body) Produces D shaped pupil and black biconvex area at periphery.

20. . 6.Antiflexion of iris (rotation of detached portion of iris such that posterior part faces anteriorly) 7.Traumatic aniridia (sinking of completely torn iris to bottom of anterior chamber 8.Angle recession(tear longitudinal and circular muscle fibers of ciliary body) Deepening of anterior chamber and widening of ciliary body Complicated by glaucoma Major source of bleeding 9.Inflammatory changes(traumatic iridocyclitis , post traumatic iris atropy , and pigmentory changes

21. . h.Lens 1.Vossius ring -circular ring of stippled brown amophous pigment granules on anterior capsule Due to striking of contracted margin against crystalline lens Always smaller than pupilary size. 2.Concussion cataract Due to inbibition of aqueous and direct mechanical effect of injury on lens fibers

22. . Shape, Discrete subepithelial opacities Early rossete cataract(punctate)feathery lines of opacities along star shaped suture lines in posterior cortex seen after 1-2yrs Traumatic zonular cataract Diffuse(total) concusion cataract Early maturation of senile cataract Traumatic dislocation of lens(in young children) Subluxation of lens Due to partial tear of zonules Lens slight displaced but still present in pupilary area. May be vertical(upward or downward)or lateral(nasal or temporal) Dislocation of lens Due to complete rupture of zonules May be intraocular dislocation into either anterior or posterior chamber or extraocular dislocation in subconjunctival space or outside the eye ball. Tear in lens capsule with absorption of lens matter Total lens opacification

23. . i.Vitreous Liquefaction and appearance of clouds of fine pigmentary opacities(most common) Detachment of vitreous either anterior or posterior Vitreous h’age Vitreous herniation in anterior chamber(with subluxation or dislocation of lens) j.Choroid 1.Rupture of choroid Lateral and concentric to optic disc May be multiple or single Appear whitish crescent with fine pigmentation at margin and retinal vessels passing over it. 2.Choroidal h’age-subretinal 3.Choroidal detachment 4.Traumatic choroiditis -appear as pigmentary patches and dislocation

24. . k.Retina 1.Commotio retinae(berlin’s edema) Milky white cloudiness at posterior pole with cherry red spot in foveal region May disappear or followed by pigmentory changes 2.Retinal h’age Multiple flame shaped and preretinal subhyaloid D shaped h’age . 3.Retinal tears-common in myopic eyes and eyes with senile degeneration 4.Traumatic proliferative retinopathy(retinitis proliferans )-2ry to vitreous h’age forming tractional bands 5.Retinal detachment-follows retinal tears or vitreotractional bands 6.Concussion changes at macula Traumatic macula edema pigmentory degeneration Macular cyst rupture lamella or full thickness macular hole.

25. . l.Intraocular pressure changes Traumatic glaucoma(due to intense vasodilatation of ciliary vessels,damage to trabecular meshwork and other factors like hyphema,lens damage) T raumatic hypotony (due to damage of ciliary body) m.Refractive changes Myopia(due to ciliary spasm or rupture of zonules or anterior displacement of lens) Hypermetropia and loss of accomodation (due to damage of ciliary body) n.Optic nerve Injury associated with fracture of base of skull Manifest as traumatic papillitis,laceration of optic nerve,optic nerve sheath h’age , and avulsion of optic nerve

26. . o.Orbital injury Associated with fractures of orbital walls esp.blowout # Orbital h’age sudden proptosis Ethmoidal sinus rupture Orbital emphysema p.Globe rupture(full thickness wound of eye ball) Indirect rupture due to compresion force(more common) Impact momentory increase in IOP inside out injuryof eye ball at weakest part esp.vicinity of canal of schlemm concentric to limbus (mostly superonasal limbus ) Associated with prolapse of uveal tissue,vitreous loss,IO h’age and dislocation of lens Ultimately IOP decreases

27. risk factors Gender : 75%-80% of them are in males Age: more in children and young age group Occupation : construction, industry Sports : boxing , racket sports Motor vehicle accidents

28. Hyphema: Blood in the Anterior Chamber Symptoms Pain, Blurred vision, History of blunt trauma Signs Blood in the Anterior Chamber. Gross layering or clot or both, usually visible without a slit lamp. A total (100%) hyphema may be black or red; when black its called “8-ball” or “black ball” hyphema .

29. Clinical classification Microscopic Grade 1(<1/3AC volume) Grade 2(1/3-1/2AC volume) Grade 3(>1/2 AC volume) Grade 4(total)

30. Problem and complication Rebleeding Depending on size of hyphema Grade 1 hyphema (25% will rebleed ) Grade 3 hyphema (75% will rebleed ) Increase IOP Dependent on size and rebleeding Corneal blood staining dependent on size,IOP and rebleeding

31. Indication for surgical treatment Ocular factors Corneal blood staining Total hyphema of IOP of >50mmHg for 5days(to prevent optic nerve damage) hyphema that are initially total and do not resolve below 50%at 6 days with IOP>25mmHg(to prevent corneal blood staining) Hyphema that remain unresolved for 9 days (to prevent PAS)

32. . Patient factors Risk of glaucoma damage( elderly,glaucoma pts , vascular diseases) Risk of corneal blood staining and amblyopia ( clildren ) Management Medical Conservative Bed rest , head elevation Topical steroids and cycloplegic agents Topical glaucoma medications Avoids aspirin

33. Types of surgical management AC paracentsis and wash out clot expression and limbal delivary Automated hyphectemy

34. Penetrating and perforating injury Three times more common in males than females. Common causes are assault, domestic and occupatioanal accidents and sports. Extent of damage is determined by kinetic energy caused by flying FBs. Risk factors include delay in primary repair, ruptured lens capsule and a dirty wound

35. corneal Technique of primary repair depend on the extent of the wound and associated complications such as iris incarceration , flat anterior chamber and damage to intraocular contents. Small shelving wounds with formed AC , May not requir suturing as they often heal spontaneously or with the aid of a soft BCL. Medium sized wounds , Usually require suturing ,esp. the ant.chamber is shallow or flat. With lens damage, Suture the wound and remove the lens by phacoemulsification or with vitreous cutter +/_ IOL.

36. Intraocular FB IOFB may traumatize mechanically,introduce infection or exert other toxic effects on the intraocular structures Initial management Accurate history -vital to determine the origin of the FB Examination, Special attention to possible sites of entry or exit. Logical deduction of the probable location of a FB. Gonioscopy and funduscopy must be performed.

37. . CT with axial ,coronal cuts is used to detect and localize a metallic intraocular FB MRI is contraindicated in the context of a metallic IOFB. Technique of removal Magnetic removal of ferrous Fbs involves the creation of a sclerotomy adjecent to the FB. Scleral bucking may be performed to reduce the risk of retinal detachment if this is judged to be high. Forcep removal is used for non-magnetic FBs and magnetic FBs that can not safely removed with a magnet. Prophylaxis against infection .

38. siderosis Steel –commonest FB projected into the eye A ferrous IOFB undergoes dissociation resulting in the deposition of iron in the intraocular epithelial structures notably the lens epithelium,iris and cilliary body epithelium and sensory retina Exerts toxic effect on cellular enzyme systems with resultant cell death. Signs, Anterior capsular cataract consisting of radial iron deposits on the anterior lens capsules and reddish brown staining of the iris( heterochromia iridis ) Complications include 2ry glaucoma due to trabecular damage,pigmentory retinopathy followed by atropy of retina and RPE. ERG show progressive attenuation of the b-wave over time.

39. chalcosis The ocular reaction to IOFB with a high CU content involves a violent endophthalmitis like picture,often progreesion to phthisis bulbi . Cu deposited intraocularly resulting in a picture similar to that of wilsons disease. K-F ring,anterior sun flower cataract developed Retinal deposition results in golden plaques visible in ophthalmoscopy.

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