Ocular Injuries

Ocular Injuries

MECHANICAL INJURIES

Extraocular foreign bodies
Common sites: On the conjunctiva, it may be lodged in the sulcus subtarsalis, fornices or bulbar conjunctiva. In the cornea, it is usually embedded in the epithelium, or superficial stroma and rarely into the deep stroma.

Contusional injuries

Partial or complete corneal tears

Blood staining of corneal may occur occasionally from the associated hyphaema and raised intraocular pressure. Cornea becomes reddish- brown or greenish in colour, which clears very slowly from periphery towards centre. Blood staining of cornea simulates dislocation of clear lens in the anterior chamber.

Scleral tears (globe rupture) may occur in two ways: direct rupture, at the site of injury and indirect rupture (because of compression force) at its weakest part, 3 mm away and concentric to the limbus in the neighbourhood of canal of schlemm.

Iridodialysis (detachment of iris from its root at the ciliary body): It results in a D-shaped pupil.

Antiflexion of the iris i.e., rotation of the detached portion of iris in which its posterior surface faces anteriorly.

Retroflexion of the iris i.e., whole of the iris is doubled back into the ciliary region and becomes invisible.

Vossius ‘s ring is a circular ring of brown pigment seen on the anterior capsule. It occurs due to striking of the contracted pupillary margin against the crystalline lens.

Early rosette cataract is most typical form of concussion cataract. It appears as feathery lines of opacities along the star-shaped suture lines; usually in the posterior cortex.

Late rosette-shaped cataract: It develops in the posterior cortex 1 to 2 years after the injury. Its sutural extensions are shorter and more compact than the early rosette cataract.

Ruptures of the choroid: These are concentric to the optic disc and situated temporal to disc and look like a whitish crescent with fine pigmentation at its margins.

Commotio retinae (Berlin’s oedema): It manifests as milky white cloudiness involving the posterior pole with a ‘cherry-red-spot’ in the foveal region.

Chorio-retinitis sclopeteria i.e., chorio-retinal rupture with retinal haemorrhage.

Ocular InjuriesIntraocular foreign bodies

Common foreign bodies

Chips of iron and steel (90%), particles of glass, stone, lead pellets, copper percussion caps, aluminium, plastic and wood.

Reactions of the foreign body

(a) Inorganic foreign body

1. No reaction: inert substances, glass, some plastics, porcelain, gold, silver, platinum, tantalum and stone.

2. Local irritative reaction leading to encapsulation of the foreign body: lead and aluminium particles.

3. Suppurative reaction is excited by pure copper, zinc, nickel and mercury particles.

4. Specific reactions are produced by iron and copper alloys (most toxic) as follows:

Siderosis bulbi: It refers to the degenerative changes produced by an iron foreign body. These usually occur after 6 months to 2 years of the injury. Mechanism. The iron particle undergoes electrolytic dissociation by the curent of rest and its ions are disseminated throughout the eye. These ions combine with the intracellular proteins and produce degenerative changes. In this process, the epithelial structures of the eye are most affected.

Clinical manifestations: I. The anterior epithelium and capsule of the lens are involved first of all. Here, the rusty deposits are arranged radially in a ring. Eventually, the lens becomes cataractous.

2 Iris: It is first stained greenish and later on turns reddish-brown.

3. Retina develops pigmentary degeneration which resembles retinitis pigmentosa.

4. Secondary open-angle type of glaucoma occurs due to degenerative changes in the trabecular mesh- work

Chalcosis: It refers to the specific changes produced by the alloy of copper in the eye.

Mechanism: Copper ions from the alloy are dissociated electrolytically and deposited under the membranous structures of the eye. Unlike iron ions these do,not enter into a chemical combination with the proteins of the cells and thus produce no degenerative changes.

Clinical manifestations: 1. Kayser-Fleischer ring: It is a golden brown ring which occurs due to deposition of copper under peripheral parts of the Descemet’s membrane of the cornea.

2. Sun-flower cataract: It is produced by deposition of copper under the posterior capsule of the lens. It is brilliant golden green in colour and arranged like the petals of a sun-flower.

3. Retina: It may show deposition of golden plaques at the posterior pole which reflect the light with a metallic sheen.

Reaction of an organic foreign bodies: The organic foreign bodies such as wood and other vegetative materials produce a proliferative reaction characterised by the formation of giant cells. Caterpillar hair produces ophthalmia nodosum which is characterised by a severe granulomatous iridocyclitis with nodule formation.

Sympathetic ophthalmitis

It is a serious bilateral granulmatous panuveitis, which follows a penetrating ocular trauma. The injured eye is called exciting eye and the fellow normal eye which also develops uveitis is called sympathizing eye. Predisposing factors: 1. It, almost always, follows a perforating wound.

2. Wounds in the ciliary region (the so-called dangerous zone) are more prone to it.

3. Wounds with incarceration of the iris, ciliary body or lens capsule are more vulnerable.

4. It is more common in children than in adults.

5. It does not occur when actual suppuration develops in the injured eye.

Pathology. Dalen-Fuch’s nodules are formed due to proliferation of the pigment epithelium (of the iris, ciliary body and choroid) associated with invasion by the lymphocytes and epitheloid cells. Retina shows perivascular cellular infiltration (sympathetic perivasculitis).

Clinical features. Sympathizing (sound) eye: It is usually involved after 4-8 weeks of injury in the other eye. Sympathetic ophthalmitis almost always manifests as acute plasdc iritis. Rarely it may manifest as neuroretinitis or choroiditis.

• Sensitivity to light (photophobia) and transient indistinctness of near objects (due to weakening of accommodation) are the earliest symptoms.

Prophylasis. Early excision of the injured eye is the best prophylaxis when there is no change of saving useful vision. Meticulous repair and use of steroids, where eye can be salvaged.

CHEMICAL AND RADIATIONAL INJURIES

Alkali burns

• In general, alkali bums are much more dangerous than acid burns.
• Alkalies dissociate and saponify fatty acids of the cell membrane and, therefore, destroy the structure of cell membrane of the tissues.
• The strong acids cause instant coagulation of all the proteins which then act as barrier and prevent deeper penetration of the acids into the tissues.

Radiational injuries

1. Ultraviolet radiations may cause (i) photo-ophthalmia and (ii) may be responsible for senile cataract.

2 Infra-red radiations may cause solar macular burns

3. Ionizing radiational injuries are caused following radiotherapy to the tumours in the vicinity of the eyes. The common ocular lesions include (i) radiation keratoconjunctivitis; (ii) radiation dermatitis of lid and (iii) radiation cataract.

MISCELLANEOUS POINTS

• The common sites of rupture of the globe are the limbus, the equator and especially under the rectus muscles, where the sclera in thinnest.
• The indication of early surgical intervention in traumatic cataract is secondary glaucoma.
• Prolapsed iris in perforating trauma should preferably be abscissed and not reposited because it will carry intraocular infection.
• Foreign bodies are the most common cause of eye injury.
• A piece of glass in the anterior chamber is exceptionally difficult to see because its transparency and refractive index differ little from the surrounding media.
• Intraocular foreign body of iron causes maximum damage to the eye.