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Ocular Injuries
Ocular Injuries
Terminologies
American Ocular Trauma Society:
1.Closed-globe injury: The eyewall (sclera
and cornea) does not have a full thickness wound but intraocular damage is present. 1. Contusion. It refers to closed-globe injury resulting from blunt trauma 2. Lamellar laceration. Partial thickness wound of the eyewall caused by a sharp object or blunt trauma. 3. Superficial foreign body.
2. Open-globe injury: a full thickness wound of the sclera or cornea or both. 1. Rupture: A full-thickness wound of eyewall caused by blunt trauma (inside-out injury) 2. Laceration: A full-thickness wound of eyewall caused by a sharp object (outside-in)
Laceration:
1. Penetrating injury: A single laceration of eyewall caused by a sharp object. 2.Perforating injury: Two full thickness lacerations (one entry and one exit) of the eyewall caused by a sharp object or missile. 3. Intraocular FB: A penetrating injury associated with retained intraocular foreign body.
Superficial/Extraocular FB
Most common Site Conjunctiva: sulcus subtarsalis, Forniceal
Cornea: epithelial, stromal Type iron Emery Coal In agriculture husk / insect wings
Symptoms Pain
Watering Inability to tolerate bright light Foreign body sensation
Signs
Conjunctival congestion FB seen Stromal infiltration around if old
Treatment
Removal Pad /patch 24 hrs Antibiotic drops and ointment
Complications
bacterial conjunctivitis Corneal ulcer Pigmentation / opacity
BLUNT TRAUMA
Modes of injury: Direct blow to the eye ball by fist, ball Accidental blunt trauma to eyeball following roadtraffic accidents, agricultural and industrial injuries
Mechanics of blunt trauma to eyeball 1. Direct impact: It produces maximum damage at the point of the blow. 2. Compression wave force: Transmitted through the fluid contents in all the directions Strikes the angle of anterior chamber, pushes the iris lens diaphragm posteriorly, and also strikes the retina and choroid.
3. Reflected compression wave force: Cause foveal damage 4. Rebound compression wave force. After striking the posterior wall rebound back anteriorly. This force damages the retina and choroid by forward thrust from the back 5. Indirect force
Modes of damage
1. Mechanical tearing 2. Cellular injuries disruption of physiological activity 3. Vascular damage ischaemia, oedema, haemorrhage 4. Trophic changes 5. Secondary glaucoma 6. Late rosette cataract 7. Retinal detachment
Closed-globe injury
Cornea 1. Simple abrasions 2. Recurrent corneal erosions 3. Partial corneal tears 4. Deep corneal opacity
Iris, pupil and ciliary body 1. Traumatic miosis 2. Traumatic mydriasis 3. Sphincter tear 4. Radiating tears in the iris stroma 6. Antiflexion of the iris 7. Iridodialysis
8. Traumatic aniridia 9. Angle recession 10. Traumatic iridocyclitis Treatment: Atropine Antibiotics Steroids
Lens 1.Vossius ring. 2.Concussion cataract. Discrete subepithelial opacities Early rosette cataract Late rosette cataract Traumatic zonular Total cataract Early maturation
3. Traumatic absorption of the lens 4. Subluxation of the lens 5. Dislocation of the lens
Vitreous 1. Liquefaction 2. PVD 3. Vitreous haemorrhage Choroid 1. Rupture of the choroid 2. Choroidal haemorrhage 3. Choroidal detachment
Retina 1. Commotio retinae (Berlins oedema) 2. Retinal haemorrhages flame-shaped preretinal (subhyaloid) 3. Retinal tears 5. Retinal detachment 6. Maculopathy and macular hole.
Other Traumatic glaucoma Traumatic hypotony Myopia following ciliary spasm Hypermetropia and loss of accommodation
Sequence of events:
Injury Displacement of orbital contents backwards Raised intraorbital pressure Fracture of orbital wall
Clinical Features:
Lid edema Lid emphysema Epistaxis Anesthesia in area supplied by infraorbital nerve Subconjunctival hemorrhage Ptosis Enophthalmos Restriction of ocular movements
Management
Investigations:
Surgical intervention
Enophthalmos > 3 mm Large herniation of tissue into maxillary antrum Diplopia Floor repair with or without implant (10-14 days after injury)
Effects of penetrating/perforating injury 1. Mechanical effects of the trauma 2. Infection 3. Post-traumatic iridocyclitis 4. Sympathetic ophthalmitis
Mechanical effects Conjunctiva: Subconjunctival hemorrhage Cornea: Uncomplicated corneal wounds Complicated corneal wounds Sclera: with corneal damage Lens: cataract Severely damaged eye
body Foreign bodies: Iron and steel chips(90%) Particles of glass Stones Plastic Wood
Size and Velocity of foreign body Corneo-scleral tear Hyphema Cataract Vitreous hemorrhage Choroidal hemorrhage Retinal hemorrhage and detachment
1. 2. 3. 4. 5. 6. 7.
Anterior Chamber Iris Posterior chamber Lens Vitreous cavity Retina/choroid/sclera Orbital cavity
Inert: glass, plastic, gold, silver Local: alluminium and lead Suppurative: copper, zinc Specific: Siderosis, chalcosis
Siderosis bulbi Degenerative changes produced by an retained iron foreign body After 2 months of injury
Mechanism: Electrolytic dissociation Disseminated throughout the eye Combine with the intracellular proteins Degenerative changes Epithelial structures most affected
Clinical manifestations 1. Capsule of the lens 2. Iris: stained greenish reddish brown 3. Retina: Pigmentary degeneration 4. Trabecular meshwork: Secondary open angle glaucoma
Chalcosis The alloy of copper Mechanism: Dissociated electrolytically Deposited under the membranous structures of the eye Clinical manifestations: 1. Kayser-Fleischer ring 2. Sunflower cataracts
Reaction of organic foreign bodies Wood and other vegetative materials Produce a proliferative reaction The formation of giant cells Caterpillar hair ophthalmia nodosum
Management
Examination: diffuse light , slit lamp, Indirect
ophthalmoscopy, gonioscopy
Localisation with imaging modalities:
Older: Plain x-ray X-ray with limbal ring Newer: USG CT Scan
Removal:
Depends on the location of lodgement In the anterior chamber:
Direct incision over corneal periphery. Magnetic: with the help of electromagnet Non-magnetic: with forceps
In the lens:
Magnetic : extraocular magnet pars plana route Nonmagnetic: 3 port Pars Plana Vitrectomy (PPV) forceps removal
Chemical Injuries
Commonly seen Chemicals:
Types: Alkali burns Lime, caustic soda, ammonia Acid burns Hydrochloric acid, sulphuric acid
Alkali Burns
Mechanism:
Saponify fatty acids in cell membrane lipid reaction: softening of the tissues dehydrate cells by hygroscopic action
Stages:
Stage of ischemic necrosis Tissue edema and necrosis Stage of reparation Regeneration of epithelium and vascularisation Stage of complications Complicated Cataract, Symblepharon, Glaucoma
Acid Burns
Less serious
Coagulation of tissue protein Which prevents deeper penetration of the acids into the tissues Sharply demarcated lesions seen
I.
Epithelial damage only Chemosis No ischaemia Good II. Hazy but iris details visible Congestion, Chemosis, Ischaemia affecting less than 1/3rd of limbal conjunctiva Good
III. Total epithelial loss, stromal haze and iris details not visible Ischaemia affecting 1/3rd to 1/2 of limbal conjunctiva Guarded IV. Opaque, no view of the iris and pupil Ischaemia and necrosis more than 1/2 of limbal conjunctiva Poor
Treatment
Thorough wash with clean water/ saline Chemical neutralization not preferred Removal of chemical particles by forceps
e.g., Lime Remove slough and necrosed tissues Antibiotics eyedrops Artificial tears Corticosteroids Cycloplegia Prevention and treatment of Complications