Ocular trauma

Black Eye

Ocular traumas are one of the common presentations in the ophthalmologic emergency. This lecture note presents the outline of types of ocular trauma, complications and how to manage them.

TYPES OF OCULAR TRAUMA

  • Mechanical
  • Chemical
  • Thermal
  • Electrical
  • Radiational

MECHANICAL INJURIES

  • Contusional / blunt trauma
  • Perforating / peneterating
  • Perforating eye injury (PEI) with intra ocular foreign body
  • Retained extraocular foreign body
  1. Extraocular foreign body

Common sites

  • Sulcus subtarsalis
  • Fornices or bulbar
  • Conjunctiva
  • Corneal epithelium
  • Stroma

Types

  • Iron
  • Coal
  • Dust
  • Glass
  • Insect

Symptom

  • Pain
  • Redness
  • Watering
  • Photophobia
  • Discomfort

Examination

  • Double eversion of upper eyelid

Complication

  • Ulcer
  • Pigmentation
  • Opacity

Treatment

  • Removal

Prophylaxis

  • Use of protective glasses
  1. Contusion injuries
  • Varies from corneal abrasion to an extensive rupture of globe.

Cause

  • Direct blow ( fist , stone )
  • Accidents — fall on roadside , injury by agricultural & industrial instrument

Mechanism

  • Direct impact on the globe
  • Compression wave force (contre — coup damage): maximum damage produced at a point distant from the actual place of impact.
  • Reflected compression wave force: causes foveal damage
  • Rebound compression wave force: pull on retina , choroid & lens — iris diaphragm
  • Indirect force –bony orbit and elastic tissue

Modes of damage

  • Mechanical tearing
  • Damage to tissue cell
  • Vascular damage
  • Trophic changes
  • Delayed complications
  • Glaucoma
  • Retinal detachment
  • Cataract

TRAUMATIC LESIONS

Lids

  • Ecchymosis
  • Ptosis

Orbit

  • Blow out fracture — enophthalmos / hypotropia
  • Hemorrhage
  • Emphysema( Ethmoid sinus)

Lacrimal apparatus

  • Laceration of lacrimal passages

Cornea

  • Sub-conjunctival hemorrhage
  • Foreign body

Sclera — rupture

  • Direct
  • Indirect — 3mm away from limbus

Anterior chamber

  • Traumatic hyphema
  • Traumatic uveitis
  • Collapse of AC

Iris / pupil / ciliary body

  • Traumatic miosis
  • Traumatic mydriasis
  • Ruptures of pupillary margins
  • Iridodialysis
  • Aniridia
  • Cyclodialysis
  • Iris atrophy

Lens

  • Vossius ring
  • Rosette cataract
  • Traumatic absorption of lens (children )
  • Subluxation / dislocation of lens (tear of zonules)

Vitreous

  • Vitreous hemorrhage
  • Detachment of vitreous
  • Vitreous loss

Choroid

  • Rupture of choroid
  • Choroidal hemorrhage
  • Choroidal detachment
  • Choroiditis

Intra ocular pressure

  • Glaucoma
  • Hypotony

Retina

  • Commotio retinae (Berlin’s edema )
  • Cherry red spot ( foveal region )
  • Retinal haemorrhage
  • Retinal tear
  • Proliferative retinopathy
  • Retinal detachment
  • Macular edema
  • Pigmentary degeneration
  • Macular hole

Optic nerve

  • Papillitis
  • Avulsion
  • Optic nerve sheath hemorrhage

Refraction

  • Myopia
  • Ciliary spasm
  • Rupture of zonules
  • Anterior shift of lens
  • Hypermetropia
  • Damage to ciliary body

PERFORATING EYE INJURY (PEI) WITH RETAINED INTRAOCULAR FOREIGN BODY (IOFB)

Common foreign body:

  • Iron
  • Steel (90% )
  • Glass,stone, pellets,
  • Lead,copper, plastic ,wood

PEI ( Modes of damage )

Mechanical damage

  • Size, velocity & type of FB.
  • FB greater than 2mm (extensive damage)

Introduction of infection

  • Endophthalmitis
  • Panophthalmitis

Reaction of foreign body

  • Siderosis bulbi
  • Chalcosis
  • Iridocyclitis
  • Sympathetic ophthalmia

SYMPATHETIC OPHTHALMIA

  • Rare, bilateral, granulomatous panuveitis.
  • Occurs after penetrating ocular trauma.
  • Usually associated with uveal tissue prolapse following intraocular surgery.
  • Traumatized eye : exciting eye
  • Fellow eye : sympathizing eye
  • 65% cases develop — sym. Opht bet. 2 weeks — 3 months after initial injury & 90% of all injuries within the 1st year.

Pathogenesis:

  • Uveal pigment acts as an antigen.
  • Retinal S — antigen.

Pathology

  • Granulomatous uveitis.
  • Nodular aggregation of lymphocytes,plasma cells , epitheloid cells ,giant cells scattered in uveal tract.
  • Dalen — Fuch’s nodules.
  • Perivascular cellular infiltration.

Clinical features

  • Anterior segment
  • Chronic granulomatous anterior uveitis.
  • Iris nodules
  • Mutton fat KPs.
  • Posterior segment
  • Multifocal choroiditis
  • Optic disc swelling

Treatment

  • Meticulous repair.
  • Steroids
  • Atropine
  • Enucleation
  • Uveitis — corticosteroids

Complications

  • Cataract
  • Glaucoma
  • Phthisis bulbi

CHEMICAL INJURY (most important ocular injury )

Modes of injury:

  • Domestic ( ammonia , detergents , cosmetics , tea )
  • Agricultural ( fertilizers , insecticides ,toxins )
  • Chemical laboratory accidents :acids , alkalis
  • Deliberate chemical attack
  • Chemical warfare
  • Self-inflicted

Types

  • Alkali induced injury
  • Acid induced injury

ALKALI INDUCED INJURY

Alkali injury is the worst one!

Mechanism

  • Dissociates & saponifies fatty acids of the cell membrane & hence destroy the structure of the cell membrane of the tissue.
  • Alkali’s combine with lipids of the cells to form stable compounds — produce a condition of softening & gelatinization.
  • Deep penetrations of alkali are into the tissue.

Clinical features

  1. Stage of ischemic necrosis
  2. Stage of reparation
  3. Stage of complications

1. Stage of ischemic necrosis

  • Conjunctiva ( edema ,congestion, necrosis )
  • Cornea ( sloughing of epithelium , edema , opalescence of stroma )
  • Iris — iritis

2. Stage of reparation

  • Conjunctiva & corneal epithelium regenerate
  • Corneal vascularization & inflammation of iris subsides .

3. Stage of complications

  • Symblepheron
  • Recurrent corneal ulcer
  • Complicated cataract
  • Secondary glaucoma

ACIDS INDUCED INJURY (H2SO4, HCL, HNO3)

Mechanism

  • Coagulation of all proteins — which acts as a barrier for further penetration of acids into the tissues.

Clinical features

  • Conjunctiva — necrosis & sloughing — symblepheron — fibrosis.
  • Cornea — severe cases — corneal sloughing — staphyloma formation.

Treatment

  • Immediate & thorough wash with available clean water or saline .
  • Mechanical removal of contaminant
  • Removal of contaminated & necrotic tissue
  • Application of corticosteroids , atropine ,antibiotics , tear supplements .

Classification (modified roper — hall)

  • Grades the chemical injury of eyes based on status of cornea and conjunctiva
  • Gives the prognosis

Grade I

  • Cornea: epithelial damage
  • Conjunctiva: chemosis, no ischemia
  • Prognosis: excellent

Grade II

  • Cornea: hazy but iris details visible
  • Conjunctiva: congestion/chemosis; Ischemia: affects less than 1/3rd of limbal conjunctiva
  • Prognosis: good

Grade III

  • Cornea: total epithelial loss, stromal haze, iris details not visible.
  • Conjunctiva: ischemia affecting 1/3rd -1/2 of limbal conjunctiva
  • Prognosis: doubtful

Grade IV

  • Cornea: opaque ,no view of iris & pupil
  • Conjunctiva: ischemia & necrosis more than ½ of limbal conjunctiva
  • Prognosis: poor

Treatment of complications

  • Glaucoma: antiglaucoma medications
  • Corneal opacity: keratoplasty
  • Symblepheron:
  • Rings
  • Grafting
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