Ocular Trauma

Blunt trauma

Mild – moderate “bruise” ocular tissues Eye wall intact

Moderate – severe Rupture eye wall Very severe consequences

Lacerating trauma (Sharp)

“cut” eye wall Outcome depends on extent and

location

Sources of Injury

Blunt objects - 30-40% rocks, fists, branches, champagne corks

Motor Vehicle Injuries - 9% Play or sports - 1/3

golf/squash balls, shoulder/elbow, bats/racquets, horse Falls - 4% Sharp objects - 18%

Globe involvement in 22% of cases

Location of Injury

Anterior Segment Posterior Segment Adnexa Orbital Structures

Anterior Segment

Conjunctiva Cornea Iris Lens

Posterior Segment

Vitreous Retina Optic nerve

Adnexa

Eyelids Lacrimal Structures

Orbital Structures

Extraocular muscles Bony walls

Initial ExaminationHISTORY

o mechanism of injury• abrasion, blunt force, penetrating object,

burnso symptoms o time of the injury

visual acuity prior to the injuryPrevious injuries

Past ocular history Past medical history

Initial Examination

PE:o Visual acuity o Eye examination

o Including uninjured eyeo Photodocumentation for medicolegal

purposes

Labs and imaging

ER Management

Stabilize patient Obtain history

Address eye injury–Avoid unnecessary manipulation

Use medications with caution

Chemical burns: IRRIGATE Check pH: 7.0 to 7.4

Lids and orbits

Assessment History

Detailed as possible Time and nature of injury

Missile, blunt, ? FB remaining, chemical etc

Past ocular history Previous VA and lid function remember trauma is a recurrent pathology

Med Hx ?tetanus, ? Anticoagulation

Examination

Rule out life threatening injuriesRule out globe threatening injuriesExamine both eyesAssess lid trauma - document +/-

photosPlan for repair

Examination - lids Tissue loss Layers of lid Lid Margin Canaliculi

Image

CT - fine cuts orbits

If ? FB If unable to determine posterior aspect

of wound If suspect orbital fracture/ other injuries

Repair Timing

Ideally within 12-24 hours of injury Can delay up to 1 week

Patient factors Gross swelling

– Ice packs to reduce– ? steroid

Anaesthesia GA / LA

Repair: General Principles

Clean wound Remove FB Minimal debridement Careful handling of tissues Careful alignment of anatomy

Lid margins, lash line, skin folds etc Close in layers

Simple laceration Minor, partial thickness

May be steri-stripped if not under tension Sutures

6.0/7.0 absorbable (gut or vicryl) or non absorbable Remove at 5 days if non absorbable

Deep lacerations Repair in layers as needed Identify septum and do not attach to muscle,skin or tarsus -

risk of lid lag

Lid Margin lacerations

Approximate lid margin Tarsal plate first 6.0 vicryl suture - can use as traction

3-4 sutures to plate Spatulated needle is useful

Align lashes - silk Skin - nylon or gut or vicryl

Canalicular Lacerations Upper

Controversial (loss may not affect pt) Either

repair laceration and ignore canaliculus, or Stent canaliculus (Mini Monoka) and repair lac

Lower Usually needs to be repaired Repair within 24-48 hours Stent

bicanalicular or monocanalicular Leave in for 3-6 months

8.0 or 9.0 vicryl to canaliculus

Complications Lid margin notching

If small may resolve, otherwise requires repair Lagophthalmos

Due to scarring or tissue loss or septum into wound Try massage, may need scar release

Hypertrophic scars May improve with time Consider steroid injection into 4-6/52

Infection Rare

Tearing canalicular damage, lid malposition, pump failure

Traumatic ptosis Myogenic or neurogenic

Orbital Fractures

Orbital #s classification

Open or closed Internal (orbital skeleton), rim, complex (internal +rim)

Type Blowout - typically 10-15mm behind rim, just medial

infraorbital canal Tripod - disruption of zygoma at z-f and z-m sutures & along

arch Enophthalmos, malar flattening, inf lat cantus displacement

Pathogenesis of orbital floor blow-out fracture

Evaluation of the orbit Eyelids

Telecanthus - tendon disruption or nasoethmoidal #, suspect nld involvement

Globe Displacement, proptosis

Motility - ductions and diplopia, include FDT Pupil - APD, efferent, mydriasis Palpate

Rim, crepitus, retropulsion Nerves - V1 & V2

• Periocular ecchymosis and oedema• Infraorbital nerve anaesthesia

• Ophthalmoplegia - typically in up- and down- gaze (double diplopia)

• Enophthalmos - if severe

Signs of orbital floor blow-out fracture

Imaging

CT Axial and coronal 3mm sections 1.5 through apex if suspect TON

MRI No good - bone, metal FB Subdural optic n haematoma

Anterior Segment Trauma

Assessment

History Forces involved Blunt, FB?, Penetrating Chemical

Acid? Alkali? Contact allergy?

Common Causes Abrasion

Minor trauma - lash, finger Recurrent Epithelial Erosion Syndrome Plant

Foreign body Grinding

Penetrating Injury Hammering metal on metal Explosion Dirty / clean

Blunt Fist Ball Bungy cord

Examination Visual Acuity Skin/lids

Evidence of severity of injury Evert lids

? Subtarsal FB Look for fine scratches on upper cornea

Conjunctiva Laceration Look carefully for scleral injury beneath Sub conj hemorrhage

Examination… Cornea

Fluorescein stain - abrasion/wound Leak Infiltrate FB

Anterior chamber Cells Hyphaema Hypopyon

Examination…. Iris

Transillumination defects Peaked pupil Dilated pupil Check for RAPD

Lens Red reflex Stability

IOP +/- angle

RAPD RAPD Relative afferent

pupillary defect

Corneal foreign body

Grinding most common cause Usually do not need surgery Treatment

Removal of foreign body with needle and/or burr

Children may require GA

Corneal Abrasion Common Usually resolve quickly Very painful initially Treatment

Exclude other injuries Chloramphenicol ointment Patch 24 hours +/- pain relief / sleeping tablets

w+XDwvc

Hyphaema Blunt injury Complications:

Raised IOP Angle recession Corneal staining Rebleed

Treatment Steroid Bed rest - debatable Frequent monitoring wrt IOP

Traumatic Uveitis

Ranges from Mild to SevereUsually other injuries as wellTreat as for normal uveitis but

may not require long taper

Iris Dialysis

Cataract

Contusions of the Eyeball

Hyphema

Subconjunctival Hemorrhage

Iridodialysis

Thermal Burn

Examples: Curling Iron Burn. UV Irradiation. Sun Viewing.

X-ray Radiation.Plan: Pressure patching and antibiotics.

Chemical trauma Alkali Alkali agents are lipophilic and therefore

penetrate tissues more rapidly than acids. They saponify the fatty acids of cell membranes, penetrate the corneal stroma and destroy proteoglycan ground substance and collagen bundles. The damaged tissues then secrete proteolytic enzymes, which lead to further damage

Acids Acids are generally less harmful than

alkali substances. They cause damage by denaturing and precipitating proteins in the tissues they contact. The coagulated proteins act as a barrier to prevent further penetration (unlike alkali injuries).[5].

The severity of ocular injury depends on four factors:

the toxicity of the chemicalhow long the chemical contact the depth of penetration the area of involvement

Patients with mild to moderate injury (Grade I and II) have a good prognosis and can often be treated successfully with medical treatment alone

The aims of medical treatment are to enhance recovery of the corneal epithelium and augment collagen synthesis, while also minimizing collagen breakdown and controlling inflammation

Treatments

Early irrigation is critical in limiting the duration of chemical exposure

The goal of irrigation is to remove the offending substance and restore the physiologic pH.

Standard Treatments Antibiotics Cycloplegic agents such as atropine

or cyclopentolate can help with comfort Artificial tears- and other lubricating eye

drops Steroid drops- In the first week

following injury, topical steroids can help calm inflammation and prevent further corneal breakdown.[14]