Orbital trauma

Ocular trauma is a common cause of unilateral blindness in children and young adults Young adults, (men) are the most likely victims of penetrating ocular injuries Domestic accidents, violent assaults, exploding batteries, sports-related injuries, and MVAs are the most common circumstances

Initial Examination of Ocular Trauma

History should indicate an estimate of visual acuity prior to and immediately after the injury
Note whether any visual loss was slowly progressive or sudden in onset Intraocular foreign body must be suspected if there is history of hammering, grinding or explosions Injury in a child with a history that is not appropriate for the injury sustained should raise suspicion of child abuse

 Physical Examination
Measurement and documentation of visual acuity If visual loss is severe, check for light perception, two-point discrimination, and the presence of an afferent pupillary defect Test ocular motility and periorbital skin sensation Palpate for bony defects in the orbital rim Check for enopthalmos by viewing profiles of the corneas while patient is lying down Corneal surface is check for foreign bodies, wounds and abrasions Bulbar conjunctiva checked for hemorrhage, foreign material, or lacerations Depth and clarity of anterior chamber is noted Size, shape and light reaction of pupil is assessed Soft eye, vision of hand movement or worse, an afferent pupillary defect or vitreous hemorrhage is suggestive of globe rupture If no slitlamp is available
Penlight, loupe, direct ophthalmoscope to examine tarsal surfaces of the lids and anterior segment

Photographic documentation is useful for medicolegal purposes The apparently uninjured eye should also be carefully examined

Immediate Management
If with obvious rupture of the globe
Avoid further manipulation until surgical repair can be done

No cycloplegic agents or topical antibiotics should be instilled prior to surgery to avoid potential toxicity to intraocular tissues A Fox shield of bottom third of paper cup is taped over the eye and systemic broad spectrum antibiotics are started (oral ciprofloxacin, 500 mg 2x daily) Analgesics, antiemetics, tetanus antitoxin are given as needed Induction of GA should not include depolarizing neuromuscular blocking agents (transiently increase pressure on the globe, thus augment tendency to herniate) Small children may also be better examined initially with the aid of short acting GA Topical anesthetics, dyes, and other medications placed in an injured eye must be sterile

Orbit Anatomy
The orbit is a pear-shaped cavity, the stalk of which is the optic canal. A pyramid with four walls that converge posteriorly
Intraorbital portion of the optic nerve is longer (25 mm) than the distance between the back of the globe and the optic canal (18 mm)
Allows for significant forward displacement of the globe without excessive stretching of the nerve. Roof Lateral Wall Floor Medial Wall Superior Orbital Fissure Inferior Orbital Fissure

Orbit Anatomy

 Superior Orbital Fissure

between the greater and lesser wings of the sphenoid bone
Superior portion contains the lacrimal, frontal and trochlear nerves, and the superior ophthalmic vein Inferior portion contains the superior and inferior divisions of the oculomotor nerve, the abducens and nasociliary nerves and sympathetic fibres from the cavernous plexus

Inferior Orbital Fissure

between the greater wing of the sphenoid and the maxilla
the maxillary nerve, the zygomatic nerve and branches of the pterygopalatine ganglion, inferior ophthalmic vein

Lids: Abrasions and Lacerations

Particulate matter must be removed, irrigate with saline, covered with antibiotic ointment and sterile dressing Excellent vascularity of the lids, healing is good with minimal chance of ischemic necrosis Partial-thickness lacerations not involving lid margin may be surgically repaired same as other skin lacerations Full-thickness lid lacerations must be repaired carefully to prevent marginal lid notching and trichiasis
Requires precise approximation of lacerated lid margin, tarsal plate and skin

If primary repair is not achieved within 24 hours, edema will necessitate delayed closure
Clean the wound, apply antibiotics, once swelling has subsided, do repair

Injury near inner canthus frequently involve canaliculi

Repair should be prompt as tissue more difficult to identify when swollen

Foreign Bodies:
Surface and Corneal Abrasions
Corneal foreign bodies, abrasions and corneal epithelial defects cause pain and irritation
Prominent on eye and lid movement Use of Fluorescein to identify exposed basement membrane and aqueous leakage Corneal vertical scratch marks suggests matter embedded on tarsal conjunctiva of upper lid

Management
Antibiotic ointment for simple epithelial defects, with pressure patch to immobilize lids For removal of foreign body
Topical anesthetic, fine-gauge needle, done under slit lamp Cotton-tipped applicator not recommended, further damage to epithelium Metallic/rust rings surrounding copper or iron, use drill with burr tip Deeply embedded fragments and presence of aqueous leak needs OR

Wound should be examined daily for evidence of infection

 Never give a topical anesthetic solution to the patient for repeated use after a corneal injury
Delays healing, masks further damage and can cause permanent corneal scarring Can also cause corneal infiltrates and ulceration No steroids if with present epithelial defect

Recurrent epithelial erosions sometimes follow corneal injuries and are treated with patching, bandage contact lens, corneal micropuncture or excimer laser phototherapeutic keratectomy

Foreign Bodies:
Intraocular
Suspect when there is complaint of discomfort or blurred vision paired with history of
Striking metal upon metal Explosion High-velocity projectile injury

Anterior portion of eye should be inspected with a loupe or slit lamp to localize wound of entry Direct or indirect ophthalmoscopic visualization of intraocular foreign body must be attempted Xray, ultrasound or CT, never MRI Once localized, removal should be done
Iron (siderosis) and Copper (chalcosis) can lead to disorganization of ocular tissues Glass or porcelain may be tolerated indefinitely Organic foreign matter must be removed as these cause inflammation and abscess formation

 Treatment
Foreign body is anterior to lens zonules
Removed through a limbal incision from the anterior chamber

Foreign body located behind lens and anterior to equator

Removed through the pars plana nearest to it

Foreign body posterior to the equator

Removed with pars plana vitrectomy and intraocular forceps, there are special forceps for spherical pellets or ones with magnetic tips Damaged retina warrants further treatment to prevent retinal detachment

Contusions of the Eyeball

Rupture of the eyeball can occur as a result of blunt contusive force Blunt trauma
Produces a rise in orbital and intraocular pressure with deformation of the globe Rapid decompression occurs when the eye wall ruptures or the orbital contents herniate into adjacent sinuses Superonasal limbus is the most common site of globe rupture (contrecoup effect lower temporal quadrant most exposed to trauma) Blunt injury generally has worse prognosis
Higher incidence of retinal detachment and intraocular tissue avulsion and herniation

 Other than rupture of the scleral wall, contusive forces can lead to
Motility disorders Subconjunctival hemorrhage Corneal edema Iritis Hyphema
blood in the anterior chamber

Posterior structure injury

Vitreous and retinal hemorrhages Retinal edema Retinal holes Vitreous base avulsions Retinal detachment Choroidal rupture Optic nerve contusion or avulsion

Angle-recession glaucoma Traumatic mydriasis Rupture of the iris sphincter Iridodialysis

localized separation or tearing away of the iris from its attachment to the ciliary body

Paralysis of accommodation Lens dislocation Cataract

Penetrating Injury of the Eyeball

Rupture of the eyeball can occur as a result of sharp penetrating injury Most penetrating injuries cause a marked loss of vision, injuries due to small high-velocity particles might present with only minimal pain and blurring Other signs include
Hemorrhagic chemosis, conjunctival laceration, shallow anterior chamber with or without eccentrically placed pupil, hyphema, or vitreous hemorrhage, IOP may be low, normal or rarely high.

 Treatment
Except for injuries involving rupture of the eyeball itself, most of the effects of contusion of the eye do not require immediate surgical treatment Any injury that causes intraocular hemorrhage increases risk for
Delayed secondary hemorrhage Intractable glaucoma Permanent damage to eyeball

Anterior segment wounds

Microsurgical techniques Samples for culture are taken if bacterial superinfection is suspected (organic foreign body or farmwork related) Lends remnants and blood are removed Anterior chamber reformation during repair achieved with viscoelastics, air, or physiologic intraocular fluids

 Prognosis for traumatic retinal detachment is poor

Macular injury Giant retinal tears Formation of intravitreal fibrovascular membranes (penetrating injury)
Generate sufficient contractile force to detach retina Vitrectomy is warranted

Hyphema
Blood in the aqueous that settles out in a visible layer Usually from contusive forces that tear the iris vessels and damage the anterior chamber angle Can complicate into acute glaucoma if the trabecular meshwork is blocked by fibrin and cells or if there is clot formation that lead to pupillary block

 Treatment
Visible hyphema that fills more that 5% of anterior chamber
Rest, steroid drops, no aspirin or NSAIDs, do not dilate (risk for rebleeding) Assess for posterior segment damage, use ultrasound Examine for secondary bleeding, glaucoma, corneal blood staining from iron pigment Some studies suggest use of aminocaproic acid to stabilize clot formation reduces risk for rebleeding. Rebleeding occurs in 1620% of cases within 2-3 days, thus higher risk for glaucoma and iron staining

Hyphema may be surgically evacuated if intraocular pressure remains elevated (>37 mm Hg fir 7 days or 50 mm Hg fir 5 days)

Burns of the Eye

Chemical Burns
All chemical burns are ophthalmic emergencies Immediate tap-water lavage should be done at site of injury before patient is transported, remove any foreign bodies In ER, brief histoty and PE precedes copious (sterile isotonic saline) irrigation of ocular surfaces including conjunctival fornices Lid speculum and local anesthetic infiltration of the lids may be done to stop blepharospasm Analgesics, topical anesthetic and cycloplegic agents are indicated Use moistened cotton-tipped applicator and jeweler s forceps to remove remaining particulate matter Watch for respiratory distress due to swelling of upper airways pH check of ocular surface done by placing strip of indicator paper in fornix
Resume irrigation if pH is not between 7.3 and 7.7

After lavage, apply an antibiotic ointment and pressure dressing

 Alkali burns
Rapidly penetrates through ocular tissues and will continue to cause damage long after the injury is sustained
Dictates need for prolonged lavage and repeated pH checks

May cause immediate rise in intraocular pressure owing to contraction of the sclera and trabecular meshwork damage Secondary pressure rise occurs 2-4 hours later from release of prostaglandins, leading to uveitis, difficult to asses as there is an opaque cornea Corneal melting and perforation can occur from collagenase activity

Acid burns
Acid forms a barrier of precipitated necrotic tissue that tends to limit further penetration and damage

Treatment for Alkali burns

Topical steroids, antiglaucoma agents, and cycloplegics (first 2 weeks), steroids stopped after 2 weeks so as not to hinder reepithelialization Ascorbate and citrate drops are useful in alkali burns but only minimal effective in preventing corneal melting for severe cases or those with already persistent corneal defects Acetylcysteine (collagenase inhibitor) trial may be beneficial Corneal exposure and persistent epithelial defects are treated with artificial lubricants, tarsorrhaphy or bandage contact lens

 Long term complications of chemical burns

Glaucoma Corneal scarring Symblepharon Entropion Keratitis sicca (dry eye)

Competency of the conjunctival and scleral vasculature is of prognostic value

greater loss of perilimbal epithelium and conjunctival and scleral vasculature shows poor prognosis Transplantation of limbal epithelium can be done severe cases to facilitate corneal epithelialization

Thermal Burns
Treated with topical antibiotics and sterile dressings After 2-3 days, ectropion and lid retraction begin Tarsorrhaphies and moisture chambers should be done to protect the cornea Full thickness skin grafts are delayed until skin contraction is no longer progressing Ultraviolet Irradiation
- Moderate doses produces painful superficial keratitis - Pain often begins 6-12 hours after exposure - This keratitis follows exposure to an electric welding arc without the protection of a filter, short circuits in high voltage lines, or exposure to the reflections from snow without protective sunglasses ( snow blindness )

 For severe cases of flash burn, instillation of a sterile topical anesthetic is done prior to examination
Treatment is pressure patching with antibiotic ointment, if with iritis, a mydriatic is added

Infrared exposure rarely produces ocular reaction

Glassblower s cataract, rare today

Radiant energy from viewing the sun or a solar eclipse without an adequate filter may produce a serious burn of the macula leading to permanent impairment of vision Excessive exposure to X-ray produces cataractous changes that may not appear for many months after exposure, this is the same as with nuclear radiation

References: Kanski et. Al. and Grant s Dissector

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