This document classifies and describes various types of eye injuries. It discusses blunt injuries which can cause corneal abrasions, hyphema, retinal detachment, and glaucoma. Perforating injuries by sharp objects may lacerate tissues or cause iris and lens damage. Foreign bodies can mechanically or chemically damage tissues depending on their material. Chemical injuries depend on the substance and exposure time but can cause burns, conjunctivitis, and corneal necrosis. Sympathetic ophthalmitis is a rare inflammatory response where an injured eye causes inflammation in the other eye.

1. Eye
Injuries

2. Classification:-
Eye Injuries are classified into:
(1) Blunt injuries.
(2) Perforating injuries.
(3) Injuries by foreign bodies.
(4) Chemical injuries.

3. [1] Injuries By Blunt Objects
(Contusions)
Common Objects: fist, tennis ball, a stick etc…
Results: vary from a small corneal abrasion which heals
in a few hours, to a rupture globe.
The effect of injury may appear:
1) Immediately following the trauma.
2) Delayed complications:
1- Macular degeneration. 2- Retinal detachment.
3- Post traumatic irido cyclitis.
4- Post traumatic glaucoma (angle recession
glaucoma).

4. The results of such injuries may be:
(1) The Orbit:
1) Fracture of bones.
2) Traumatic proptosis: due to:
1- retro bulbar haemorrhage.
2- Surgical emphysema.
3- carotid cavernous fistula.
3) Pulsating exophthalmos.
4) Orbital cellulitis.

5. Peri orbital sub cutaneous peri ocular ecchymosis and
emphysema. oedema with traumatic
enophthalmos

6. (2) The Lids:
1) Ecchymosis of the lid (Black Eye).
2) Surgical emphysema.
3) Traumatic ptosis: may be:
1- Mechanical ptosis due to ecchymosis or emphysema.
2- Paralytic due to injury to levator or its nerve.
4) Contused wounds:
1- Horizontal wounds along the direction of the fibers
of the orbicularis, do not gap and produce less scar.
2- Vertical wounds tend to gap and produce a bigger
scar.

7. Lid Margin Laceration
Before repair After repair

8. (3) The Conjunctiva:
1) Lacerated wound: it must be sutured.
2) Sub conjunctival haemorrhage, may be due to:
1- Local trauma leading to rupture of a small
conjunctival vessels.
2- Fracture of the base of the skull

9. Sub Conjunctival Haemorrhage
Due to fracture baseDue to local trauma
Trauma to the head
Loss of consciousness
Delayed
Triangular, apex to cornea
Dark red
Cannot be seen
Trauma to the eye
Not affected
Immediate
Triangular, base to cornea
Bright red
Definite
History
. Trauma
. Consc.
. Onset
Shape
Colour
Posterior
limit

10. (4) The Cornea:
1) Corneal abrasion:
Presentation: severe pain, lacrimation, and blepharospasm.
Diagnosis: stained with flourescein stain.
Treatment: bandage + antibiotics + cycloplegic.
2) Deep corneal opacity: may result from:
1- corneal edema.
2- folds in Descemet's membrane.
3- Rupture in Descemet’s membrane.
The condition disappears in a few weeks. No special
treatment.

11. 3) Blood staining of the cornea:
Etiology: occurs if two factors fulfilled: hyphema + increased IOP
Signs: .The cornea is at first red, later it becomes brown, then
orange, then yellow, then grey.
.Clearing occurs from the periphery to the center.
.Complete clearing takes up to 2 years.
Treatment: Keratoplasty.
4) Rupture of the cornea:
If occurs, the cornea must be sutured.

12. (5) The Sclera: (Rupture of the sclera)
Etiology: As a result of the trauma, the intra ocular
pressure rises and the sclera ruptures at its weakest
part i.e. up and in 2-3 mm from the limbus and
concentric with it.
Sequelae:
. Conjunctiva may rupture or remains intact.
. Iris commonly prolapses.
. Lens may be extruded or become dislocated
under the conjunctiva.
. Vitreous commonly prolapses.
. Severe intra ocular haemorrhage may occur.

13. Scleral rupture with Rupture globe with
Uveal prolapse grossly damaged eye

14. Treatment:
1) In hopeful cases:
1- Excise all prolapsed tissues.
2- Suture the wound accurately.
3- Close the conjunctiva.
4- Give local and general antibiotics.
2) In Non hopeful cases: (If the eye is grossly damaged)
Enucleation is done (to avoid sympathetic
ophthalmitis).

15. (6) The Anterior Chamber:
1) Hyphema:
Source: commonly comes from an iris vessel.
Clinically: blood in the anterior chamber with a horizontal upper
level.
Complications: secondary glaucoma → blood staining of cornea.
Treatment: 1- complete bed rest.
2- Corticosteroids for irido cyclitis.
3- Diamox or paracentesis for secondary glaucoma.
2) Anterior dislocation of lens: discussed later.

16. Hyphema

17. (7) The Iris:
1) Traumatic miosis:
1- Initial event in all contusions.
2- Due to irritation of the third nerve fibers supplying the
constrictor muscle.
2) Traumatic mydriasis:
1- It is due to paralysis of the third nerve fibers.
2- It may be transient or permanent.
3- It may be accompanied with paralysis of the ciliary muscle.
4- It leads to difficult near work.

18. 3) Lacerations of the Iris:
Clinically: V- shaped tears at the pupillary border.
Treatment: No treatment ( no mydriatics as they enlarge the tears)
4) Iridodialysis:
Definition: detachment of a part of the iris root from its
attachment into the ciliary body.
Clinically:
1- Symptoms: Uni ocular diplopia ( if the iridodialysis is large or
not covered by the upper lid).
2- Signs: . Black area at the periphery of the iris with D- shaped pupil
. Visible red reflex through the black area.

19. Sphincter tear Irido dialysis

20. 4- Treatment:
a- Medical treatment: Rest and atropine.
b- if troublesome diplopia, do either:
. Suturing of the iris to the sclera; or
. Iridectomy; or
. Colored contact lens.
5) Traumatic aniridia: The iris is completely torn from the
ciliary body and sinks as a minute ball to the bottom of the
anterior chamber where it may be invisible.

21. 6) Anti flexion of the iris: occurs in iridodialysis when the
dialysed part is rotated and the pigment faces forwards.
7) Retro flexion of the iris: the iris is driven backwards and
is incarcerated between the lens equator and the ciliary body.
8) Iridodonesis (tremulous iris): occurs in traumatic
displacement of the lens ( subluxation and posterior
dislocation).
9) Post traumatic irido cyclitis: may take a long course
and may lead to atrophia bulbi.

22. (8) Ciliary Body:
1) Traumatic spasm of accommodation: with
temporary myopia.
2) Traumatic paralysis of accommodation: with
defective near work.
3) Suppression of aqueous humour secretion: due to
vasomotor instability with ciliary body shock
(Traumatic hypotony).
4) Ciliary Body injury near the angle: with angle
recession glaucoma or hyphema.
5) Post traumatic irido cyclitis: may lead to atrophia
bulbi.

23. (9) The Lens:
1) Vossius ring: it is a ring of pigment on the anterior lens
capsule. It corresponds to the size of the pupil.
2) Traumatic cataract.
3) Displacement of the lens:
1- subluxation:
2- dislocation: anterior, or posterior.

24. Vossius ring Traumatic cataract Lens
subluxation

25. (10) The Vitreous:
1) Vitreous haemorrhage.
2) Vitreous opacities or floaters (Muscae Volitenates).
3) Vitreous herniation into the anterior chamber: It
occurs through a ruptured zonule with lens subluxation.
Vitreous
Haemorrhage

26. (11) The Choroid:
1) Rupture of the choroid:
Clinical picture:
1- Vision: is markedly affected if the choroid is ruptured near the
macula.
2- Fundus: white crescent (white color of the sclera) is seen on
the temporal side of the disc and is concentric with
it.
Treatment: needs no specific treatment.

27. 2) Choroidal haemorrhage.
3) Traumatic choroiditis.
4) Choroidal effusion or detachment.

28. (12) The Retina:
1) Retinal oedema: (Commotio retinea or Berlin’s oedema)
Cause: blunt trauma with counter – coop to the posterior pole
of the eye → vascular disturbance → retinal oedema.
Clinical picture:
1- Vision: rapid failure of vision to hand movement.
2- Fundus: a- Retina: milky white posterior part.
b- Macula: Cherry red spot (other causes).
Fate:
1- Resolution: within few days.
2- Macular degeneration.

29. 2) Retinal haemorrhage: may be
1- superficial flame shaped haemorrhage.
2- deep rounded haemorrhage.
3- pre retinal (sub hyaloid) haemorrhage.
3) Retinal tears, or dialysis :
May occur particularly in myopic or senile degeneration of the
retina , which may lead to retinal detachment.

30. Commotio Avulsion of vitreous Equatorial
Retinae & retinal dialysis Tears

31. (13) The Optic Nerve:
1) Avulsion of the Optic nerve: complete rupture of the
optic nerve.
2) Injury of the Optic nerve: In fracture of the base of
skull.
3) Oedema of the optic nerve.

32. (15) Lacrimal Apparatus:
1) Lacrimal gland displacement.
2) Lacrimal passages lacerations
(16) Intra ocular pressure:
1) Traumatic glaucoma.
2) Traumatic hypotony.
(17) Extra ocular muscles: Paralytic squint.

33. [2] Injuries by sharp instruments
(Perforating Injuries)
Definition: are those produced by sharp
instruments; such as knifes, scissors, needles,
nails etc…
Types:
(1) Wounds of the Lids: are sutured.
(2) Wounds of the Conjunctiva: are sutured.

34. (3) Corneal wound:
1) May be small and leads to anterior synechiae.
2) May be large and accompanied with prolapse of
the iris. Lens injury may occur.

35. (4) Scleral wound:
If large may lead to prolapse of the iris, ciliary body,
or choroid. Retinal tears may occur and lead to
retinal detachment.

36. [3] Injuries by Foreign Bodies
1] Extra Ocular F.B.
(1) F.B. of the Conjunctiva:
Types: pieces of stone, glass, steel, etc…
Site: may lodge anywhere in the conjunctival sac. Commonest
sites are the fornix and the sulcus sub tarsalis.
(2) F.B. of the Cornea:
May penetrate the epithelium or a variable depth of the stroma.
It leads to pain, photophobia, and lacrimation.

37. Complications:
(1) Corneal complications:
1) Corneal ulcer. 1)Rust ring (if iron F.B.).
3) Ring abscess. 4) Corneal opacities.
(2) Conjunctival complications:
1) granuloma. 2) implantation cyst.
Treatment:
Removal of the F.B.

38. 2] Intra Ocular F.B.
Common I.O.F.B.: iron and steel (90%), glass, lead,
bullets, etc…
Damage induced by F.B.:
(1) Mechanical effect: the I.O.F.B. may enter through the cornea
or sclera.
1) Corneal entry:
2) Scleral entry:

39. (2) Ocular Infections:
Common with a contaminated F.B. as a stone or wood.
(3) Specific chemical action on the ocular tissues:
1) Siderosis bulbi:
Causes: iron after a latent period becomes dissolved in the
ocular fluid and stains the ocular tissues by a rusty colour, for
example:
1- cornea: iron deposits.
2- iris: greenish then reddish brown discolouration.
3- lens: .iron rust deposits (the earliest clinical sign).
. Cataract (late).
4- retina: pigmentary retinal degeneration .
Symptoms: 1- impairment of vision. 1- night blindness (other
causes).

40. 2) Chalcosis bulbi:
Symptoms: little impairment of vision (as there is no
degenerative changes).
Signs:
1- cornea: Kayser – Fleischer’s ring (other causes) of golden
brown colour at the periphery.
2- lens: sun flower cataract of golden green colour.
(4) Sympathetic Ophthalmitis:

41. Diagnosis of I.O.F.B.:
(1) History: of ocular trauma with a foreign body.
(2) Clinical examination:
1) Slit – lamp: wound of entry, iris hole, foreign body, etc…
2) Gonioscopy: foreign body in the angle.
3) Ophthalmoscopy: reveals intra ocular foreign body if the
media are clear.
(3) Localization of the foreign body:
1) Plane x – ray: plane film may show a radio opaque F.B.
2) Ultra sonography: Accurate method.
3) Computed tomography: Accurate method. Which is highly
indicated for retinal FB..

42. Treatment of I.O.F.B.:
(1) Foreign body extraction:
1) Foreign body in the anterior segment:
1- In the anterior chamber: can be removed through a limbal
incision.
2- Entangled in the iris: removal or through iridectomy.
3- In the lens: Extraction of the lens.
2) Foreign body in the posterior segment:
1- Magnetic F.B.: is extracted by a giant electro – magnet after
making a small scleral incision over the pars plana.

43. 2- Non – Magnetic F.B.: is extracted through pars plana vitrectomy.
(2) Enucleation: if the eye is seriously damaged with
multiple foreign bodies and no perception of light.
Removal of IOFB
By pars plana vitrectomy

44. Sympathetic Ophthalmitis
Definition: It is a bilateral granulomatous pan -
uveitis.
Aetiology: perforating eye injury with incarceration
of the uveal tissue in the wound.
Pathogenesis: Trauma → some pigment from the
uveal tract reach the circulation → the body will
form antibody against the pigment → these
antibodies will circulate in the blood and reach
both eyes where they react with the uveal
pigment → UVEITIS.

45. Clinical Picture:
Onset: 4 – 8 weeks after the injury. It may be delayed for many
years up to 40 years. The traumatised eye is called “exciting
eye”, the other eye is called “sympathising eye”.
Prodromal symptoms: they are better seen in the sympathising
eye. The eye becomes irritable and photophobic.
The Full picture:
1- bilateral anterior uveitis which may be mild or severe and
granulomatous.
2- bilateral multifocal choroiditis and exudative retinal
detachment may occur in severe cases.

46. Treatment:
(1) Prophylaxis:
1) A hopeless injured eye must be removed.
2) Intra ocular F.B. must be removed.
3) If the eye is possible to save, all prolapsed uveal tract must be
excised and the wound is closed with no incarceration.
4) If the injured eye is still inflamed 2 weeks after the trauma we
better excise it.
5) If prodromal signs appear in the good eye, the exciting eye
must be removed.
(2) Treatment of established cases:
1) Topical: treatment of anterior uveitis is with steroids and
cycloplegics.

47. 2) Systemic:
1- systemic steroids (1 – 2 mg / kg / day).
2- Immunosuppressive may be required.

48. [4] Chemical Injuries
The eye may be injures by the following chemicals:
(1) Acids: sulphoric and hydrochloric acid.
(2) Alkalies: sodium and potassium hydroxide,
ammonia, or lime.
(3) Other chemicals: phenol, aniline dye, Iodine,
and benzene

49. Clinical Effects:
(1) Immediate effects: ( depends on the amount and
concentration of the chemical agent and the duration of exposure).
1) Eye lids: burns with dermatitis and blepharitis.
2) Conjunctiva: Hyperemia, chemosis, and necrotic areas.
3) Cornea: 1- oedema, ulceration, necrosis, and sloughing.
2- vasularized scarring on healing.
4) Intra ocular changes: 1- hyphema, miosis, and irido cyclitis.
2- secondary glaucoma.
(2) Delayed effects:
1) Eye lids: cicatricial entropion or ectropion, epiphora,
2) Conjunctiva: Xerosis, and symblepharon.
3) Cornea: corneal opacities and ectasia.
4) Intra ocular changes: irido cyclitis, secondary glaucoma,
atrophia bulbi.

50. Treatment:
(1) First aid treatment:
1) If the chemical substance is known: its specific antidote is used to
wash the conjunctival sac.
1- Acids: weak alkaline as sodium bicarbonate.
2- Alkalies: weak acid as boric acids 4% or milk.
3- Lime: a- Pick with a forceps any remaining particle.
b- avoid water.
c-- solution of sodium salt of ethylene diamine tetra acetic acid
(EDTA).
d-- if EDTA not available → saturated solution of sugar.
4- Iodine: starch or milk.
5- Aniline dyes: wash with a weak solution of alcohol 10% then
use glycerin drops 10%.
2) If the chemical substance is unknown, or the specific antidote is
not available: 1- sterile saline solution.
2- tap water. 3- milk.

51. (2) Local medications:
1) Antibiotic eye ointment: to prevent infection.
2) Atropine eye ointment: for corneal burns.
3) Steroid eye ointment: to diminish the inflammatory reaction
and adhesion.
(3) Prevention of symblepharon:
1) Steroid eye ointment.
2) Glass rod coated with antibiotic ointment is passed in the
fornices 1 – 3 times daily.
3) Soft contact lens.

52. (4) Treatment of complications:
1) Secondary glaucoma: 1- Diamox (early).
2- Trabeculectomy (late).
2) Corneal opacities: keratoplasty.