Ocular Trauma


Blunt Trauma

Andrew Mick

image     THE DISEASE


Trauma to the eye from a blunt object results in a concussive shock wave throughout the orbit and globe. The mechanical forces exerted on the globe have the potential to produce damage in all orbital structures.

Common causes include fist fights, airbags, golf balls, baseballs, racquet balls, and bungee cords. Rocks and snowballs are common causes of blunt trauma in children. Greater damage often occurs with smaller objects because the force is more concentrated into the orbital structures. Smaller objects are also able to fit within the protective orbital rim. Larger objects dissipate a large amount of their force into the bones of the face and orbital rim.

The Patient

Significant History

  • Recent eye trauma

Clinical Symptoms

1. Pain

  • Sharp and sectoral: Corneal abrasion, laceration of the conjunctiva or lid
  • Dull aching: Orbital blowout, retrobulbar hemorrhage
  • Photophobia: Traumatic iritis

2. Watery discharge

3. Double vision

  • Entrapment of extraocular muscles (EOMs)
  • Damage to controlling cranial nerve
  • Retrobulbar hemorrhage

4. Decreased vision

  • Damage to cornea, lens, retina, or optic nerve
  • Intraocular bleeding: Hyphema or vitreous hemorrhage

Clinical Signs

1. Reduced visual acuity

2. EOM abnormalities

  • EOM restriction: muscle entrapment secondary to an orbital fracture, damage to controlling cranial nerve, retrobulbar hemorrhage

3. Lid involvement

  • Ecchymosis and swelling
  • Lid lacerations: Injury from a sharp or penetrating object
  • Crepitus or subcutaneous emphysema: Introduction of air into periocular tissues suggesting orbital blowout fracture

4. Globe involvement

  • Globe rupture: More likely with trauma from smaller, sharp, high speed objects (Fig. 12-1)
  • Conjunctival laceration
  • Subconjunctival hemorrhage

5. Intraocular pressure (IOP) abnormality

  • Low IOP: Ruptured globe, retinal detachment, or iritis
  • High IOP: Intraocular hemorrhage, inflammation, lens subluxation into the anterior chamber, retinal detachment, or angle recession

6. Corneal involvement


Figure 12-1. Globe rupture.

7. Anterior chamber involvement

  • Anterior chamber cell/flare
  • Hyphema
  • Abnormal anatomical position of tissues

8. Grading anterior uveitis

  • Subclinical: No cells or flare
  • Trace: Any cells or barely noticeable flare
  • Grade 1: 5 to 10 cells per high-power field
  • Grade 2: 11 to 20 cells per high-power field
  • Grade 3: 21 to 50 cells per high-power field
  • Grade 4: Cells too numerous to count, fibrinous/plasmoid aqueous

9. Hyphema (Fig. 12-2)

  • Microhyphema

    Figure 12-2. Hyphema.

    • No layering of red blood cells in the inferior angle
    • Visible red blood cells suspended throughout the anterior chamber

  • General hyphema

    • Grade I: less than 1/3 of the anterior chamber
    • Grade II: 1/3 to 1/2 of the anterior chamber
    • Grade III: greater than 1/2, but less than total
    • Grade IV: Total (100%) hyphema (a.k.a. 8-ball hyphema)

10. Iris involvement

  • Iridodialysis: Iris disinsertion at scleral spur (Fig. 12-3)
  • Sphincter or dilator muscle tears
  • Transillumination defects: Possible site of intraorbital foreign body entrance

11. Lens involvement

  • Subluxation
  • Anterior segment displacement
  • Opacification: Secondary to blunt trauma or penetrating foreign body

12. Vitreous involvement

  • Posterior vitreous detachment
  • Vitreous hemorrhage: Increases likelihood of associated retinal detachment/tear

13. Retinal involvement

14. Choroidal involvement

  • Choroidal rupture: Breaks of the inner choroid and overlying RPE, often curvilinear and concentric to optic nerve, may be associated with subretinal hemorrhage or serous detachment of the retina, short- and long-term risk of choroidal neovascular membranes (Fig. 12-5)
  • Chorioretinitis sclopetaria: Choroidal rupture caused by shock waves from high velocity, grazing object passing adjacent to the globe

15. Optic nerve involvement

  • Traumatic optic neuropathy: Most common injury site is at orbital apex, afferent pupillary deficit (APD), sluggish or absent pupillary responses, decreased vision, color vision abnormality, visual field defects, acutely may be normal but progressive atrophy develops over several weeks, damage can be direct or indirect

    Figure 12-4. Commotio retinae.


    Figure 12-5. Choroidal rupture.

    • Direct optic nerve damage: Penetrating objects or bone fractures.
    • Indirect optic nerve damage: Mechanical shearing, nerve sheath hemorrhage, orbital/retrobulbar hemorrhage, orbital emphysema, ischemia from damaged blood vessels, secondary inflammation (Fig. 12-6)

  • Optic nerve avulsion: Globe rotated and pulled forward resulting in tearing of the lamina cribrosa and nerve fibers at the disc margin, acute partial ring of hemorrhage surrounding the optic nerve, late fibrous proliferation fills area surrounding avulsion site


Figure 12-6. Retrobulbar hemorrhage.


Blunt trauma is more common in men than women and has a higher prevalence in the younger age groups. Work environments and recreational activities that put eyes at risk of trauma also increase the prevalence of injuries.

Ancillary Tests


Figure 12-7. Left inferior orbital floor fracture.

The Treatment

1. Corneal abrasion

  • Antibiotic coverage

    • Noncontact lens wearer: Polymyxin B/trimethoprim solution four times a day
    • Contact lens wearer needs antipseudomonal coverage: besifloxacin 0.6% (Besivance: Bausch and Lomb, Madison, NJ): moxifloxacin 0.5% (Vigamox: Alcon, Ft Worth, TX), gatifloxacin 0.3% (Zymar: Allergan, Irvine, CA), ofloxacin, ciprofloxacin, tobramycin four times a day

  • Cycloplegia

    • Cyclopentolate 1% three times a day
    • Scopolamine 0.25% two times a day

  • Bandage contact lens
  • Débridement of loose epithelium

2. Orbital fracture

3. Hyphema

4. Traumatic uveitis

  • Treatment guidelines:

    • Subclinical: Cycloplegic such as cyclopentolate 1% four times a day
    • Grade 1: Cycloplegic such as homatropine 5% three times a day, topical steroids such as prednisolone acetate 1% three times a day
    • Grade 2: Cycloplegic such as homatropine 5% four times a day or scopolamine 0.25% twice a day, topical steroids such as prednisolone acetate 1% four times a day
    • Grades 3 and 4: Cycloplegic such as atropine 1% once daily or scopolamine 0.25% twice daily, topical steroids such as prednisolone acetate 1% four times a day, consider longer acting steroid-containing ointment nightly such as sulfacetamide/prednisolone (Vasociden: Novartis, Switzerland) gentamicin/prednisolone (Pred-G: Allergan, Irvine, CA) tobramycin/dexamethasone (Tobradex: Alcon, Ft Worth, TX)
    • Presence of elevated IOP associated with iritis: β-blockers are first line of therapy without contraindications, consider α-agonists and topical carbonic anhydrase inhibitors, avoid prostaglandin analogs as they promote inflammation, no miotics as they increase vascular permeability and risk of posterior synechiae formation

5. Lens subluxation

  • Subluxation of the lens into the anterior chamber can cause marked increase in IOP secondary to pupil block. Prior to referral for repositioning or removal of the lens, the following should be done to decrease IOP:

    • Cyloplegia with appropriate agent
    • Treat elevated IOP with β-blocker, α-agonist, topical or oral carbonic anhydrase inhibitor (acetazolamide 250 four times a day, 500 mg sequel twice a day, methazolamide 25 mg twice a day), or oral hyperosmotic agent (isosorbide 1 to 3 gm/kg, not metabolized to glucose)

6. Ruptured globe

  • Advise patient to not touch or squeeze eyes, position eye shield, advise the patient to not consume any food or water, immediately refer patient to ophthalmic surgeon for surgical repair

7. Commotio retinae

8. Retinal tears and detachments

  • B-scan ultrasonography: When retina cannot be visualized because of media opacity, an APD may be an early indicator of possible detachment, referral for retinopexy or vitreal-retinal surgery as the extent of damage warrants.

9. Choroidal rupture

  • There is no specific treatment for this condition
  • Periodic examination for the development of a choroidal neovascular membrane at the site of RPE disruption that can occur months after the injury or years later, immediate referral to a retinal specialist if choroidal neovascular membrane detected

10. Optic nerve trauma

  • There is no specific treatment for this condition
  • High-dose intravenous steroids administered in the first hours after trauma or surgical decompression of the optic canal have been advocated; treatment therefore will vary with different treating physicians

Corneal Abrasion

Andrew Mick

image     THE DISEASE


The cornea is composed of five distinct layers, including the epithelium, Bowman’s membrane, stroma, Descemet’s membrane, and the endothelium. A defect in the most superficial layer, the epithelium, is classified as a corneal abrasion. Any object that strikes the cornea can produce a superficial abrasion. Common causes are fingernails, tree branches, mascara brushes, and paper cuts.

The Patient

Significant History

  • Trauma from vegetative matter: Increased risk of fungal infection
  • Contact lens wear: Increased risk of bacterial infection, especially Pseudomonas
  • Paper cuts or fingernail injuries: Increased risk of recurrent erosion after resolution
  • High-speed foreign body or associated blunt trauma: Increased risk of penetrating injury

Clinical Symptoms

  • Pain/foreign body sensation
  • Lacrimation
  • Light sensitivity

Clinical Signs

  • Positive fluorescein staining of defect
  • Negative Seidel’s test
  • Mild anterior chamber reaction
  • Swollen eyelid

The Treatment

Recurrent Corneal Erosion

Andrew Mick

image     THE DISEASE


Damage to Bowman’s membrane, the basement membrane of the epithelium, prevents normal adherence of the epithelium. This results in a weakened area of epithelium that regularly sloughs off. Bilateral anterior corneal dystrophies (epithelial basement membrane dystrophy, Meesmann’s dystrophy, Reis-Bucklers’ dystrophy) can result in a similar clinical presentation.


Erosions are recurrent epithelial defects that are secondary to poor adherence to the underlying basement membrane. They are commonly caused by prior abrasions of the cornea or corneal dystrophies.

The Patient

Significant History

  • History of corneal trauma
  • Previous episodes of similar symptoms

Clinical Symptoms

  • Recurrent pain and foreign body sensation, most prominent upon awakening
  • Lacrimation
  • Light sensitivity
  • Decreased vision

Clinical Signs

  • Negative and/or positive corneal staining with fluorescein dye
  • Injection of conjunctiva
  • Mild anterior chamber reaction
  • Presence of anterior corneal dystrophy


Recurrent corneal erosions secondary to previous abrasions can occur at any age. The demographics of erosions secondary to different corneal dystrophies vary:

Anterior Corneal Dystrophies

1. Epithelial basement dystrophy (map dot dystrophy)

  • Most cases not inherited, but may show autosomal dominant pattern
  • Intricate pattern of dots and lines throughout the epithelium
  • Most commonly seen in adults between the age of 40 and 70 years

2. Meesmann’s dystrophy

  • Autosomal dominant inheritance
  • Intraepithelial cysts especially concentrated in the interpalpebral space
  • Most commonly presents in first to second decade

3. Reis-Bucklers’ dystrophy

  • Autosomal dominant inheritance
  • Honeycomb appearance of central epithelium
  • Usually presents in first to second decade with painful erosions

Ancillary Tests


The Treatment

Initial Therapy

  • Cycloplegia: Cyclopentolate 1% four times a day or homatropine 5% twice a day
  • Polymyxin B/trimethoprim solution four times a day, polymyxin B/bacitracin ointment nightly
  • Copious artificial tears and ophthalmic lubricants
  • Consider tight-fitting bandage contact lens if erosion is large or patient is extremely symptomatic
  • Follow closely until reepithelialized

After Reepithelialization

  • Nonpreserved artificial tears during the day, lubricating ointment nightly
  • Consider 5% NaCl ointment nightly for 4 to 6 weeks and then as needed

Failure to Reepithelialize

  • Anesthetize and remove abnormal/loose epithelium on edge of erosion with sterile forceps
  • Apply bandage contact lens and treat as directed in the “After Reepitheliaztion” section
  • Consider oral doxycycline: 50 mg twice a day and mild topical steroid three times a day for 4 weeks: fluorometholone alcohol 0.1% and loteprednol 0.2% suspension (Alrex: Bausch and Lomb, Madison, NJ)
  • Continued recurrence
  • Consider oral doxycycline 50 mg twice a day and mild topical steroid three times a day for 4 weeks: fluorometholone alcohol 0.1% and loteprednol 0.2% suspension (Alrex: Bausch and Lomb, Madison, NJ)
  • Consider micropuncture therapy: Multiple punctures through Bowman’s membrane with 22-guage needle after removal of abnormal epithelium with forceps, large areas of the corneal involvement preferably not in optic axis, after application apply bandage contact lens and treat as directed earlier

Other Treatment Options

  • Superficial keratectomy or phototherapeutic keratectomy: When treatment zone is large or if affected area is in the optic axis

Superficial Ocular Foreign Body

Andrew Mick

image     THE DISEASE


A variety of materials in the environment can easily embed themselves into the cornea or conjunctiva. Evaluation of the type of material and its precise location in the eye is necessary to determine appropriate management.


Drilling, chopping, and sanding can produce particles that can become entrapped in superficial layers of the eye. Wind-borne particles are another source of this injury.

The Patient

Significant History

  • Report of getting something in the eye or employment/environment that entails exposure to debris

Clinical Symptoms

  • Foreign body sensation or pain
  • Lacrimation
  • Photophobia


Figure 12-8. Corneal foreign body.

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Oct 2, 2016 | Posted by in OPHTHALMOLOGY | Comments Off on Ocular Trauma

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