Updated: Dec 27, 2022
Injuries to the eye can pose a serious threat to vision if not treated appropriately and in a timely manner. Ocular trauma is also an easily tested topic in the Duke-Elder exam. Here, we summarise the important classes of ocular trauma to learn about: eyelid trauma; orbital trauma; trauma to the globe; and chemical injuries.
A periocular hematoma (a ‘black eye’), is the most common blunt injury to the eyelid or forehead. It consists of a haematoma (focal collection of blood) and/or periocular ecchymosis (diffuse bruising) and oedema.
Periocular hematomas are generally innocuous, but the following more serious conditions must be excluded:
Trauma to the globe/orbit
Orbital roof fracture
Basal skull fracture
Any lid laceration, whatever the size, requires careful exploration of the wound and examination of the globe and adnexal structures. Where possible, any lid defect should be repaired by direct closure under tension, since this offers the best functional result and cosmetic appearance.
Infection is a risk to be aware of, even with small lacerations, which could potentially lead to orbital cellulitis. Retained foreign bodies increase the risk of orbital cellulitis, thus, a CT scan is warranted if there is suspicion of a foreign body in the soft tissues of the lid.
It is also important to make sure each patient is up-to-date with their tetanus immunisations.
Orbital floor fracture
Orbital floor fractures are caused by a sudden increase in orbital pressure from an impacting object. An object greater in diameter than the orbital aperture (〜5cm) causes the eyeball to be displaced rather than absorb the impact. The floor of the orbit, along the thin bone covering the infraorbital canal, is most susceptible to fracture; the bones of the lateral wall and roof are stronger and usually able to withstand the trauma. Rarely, the medial orbital wall can also be fractured.
Orbital floor fractures are typically caused by a ball/fist to the eye
The soft tissue of the globe is pushed into the maxillary sinus
The inferior rectus can become entrapped —> vertical diplopia and restriction of eye elevation
Haemorrhage and oedema in the orbit —> tightening of the septa connecting the inferior oblique muscles and inferior rectus to the periorbita —> restricting ocular motility. As the bleeding and oedema resolve with time, movement of the globe improves.
💡 When an extraocular muscle is entrapped, the antagonistic movement is restricted. For example, when the inferior rectus is trapped, upgaze is restricted.
Periorbital bruising and oedema, occasionally subcutaneous emphysema (a crackling sensation on palpation due to air under the skin)
Vertical diplopia and inferior rectus muscle entrapment
Enophthalmos (posterior displacement of the eyes - ‘sunken-in’ eyes)
Infraorbital nerve anaesthesia (since the fractures often involve the infraorbital canal) - anaesthesia of the lower lid, cheek, side of nose, upper lip/teeth/gums
CT with coronal sections show a classical ‘tear drop’ sign representing soft tissue prolapse in the maxillary antrum
Hess charts (which are used to diagnose ocular motility defects) are used for monitoring and follow-up
Observation + oral antibiotics
Surgery may be required for severe fractures with entrapment of orbital contents, significant exophthalmos (>2mm) or persistent diplopia
💡 Patients must be instructed NOT to blow their nose, and this could force infected sinus contents in the orbit.
Roof fractures are rare
Isolated roof fractures are most common in children. There are classically caused by falling on a sharp object, or a minor blow to the forehead, and often no treatment is required
Roof fractures resulting from major trauma with extensive facial damage typically affect adults
Signs: haematoma of the upper eyelid, periocular bruising, other features of orbital wall fracture (discussed above), pulsation of the globe in large fractures (due to transmission of CSF pressure)
Management: same general management as an orbital floor fracture. No surgery required for small fractures; reconstructive surgery for extensive damage. A CSF leak must be excluded, due to risk of meningitis.
Blow-out medial wall fracture
Normally associated with orbital floor fractures
Signs: periorbital bruising, subcutaneous emphysema, impaired ocular motility (involving abduction and adduction) if the medial rectus muscle is entrapped
Management: surgical release of incarcerated tissue and repair of the bony defect
Lateral wall fracture
Rare, because the lateral wall of the orbit is stronger than other walls
Fractures are usually associated with severe facial damage
Retrobulbar (orbital) haemorrhage
Retrobulbar (also known as orbital) haemorrhage, RBH, is a rare, rapidly progressive ophthalmic emergency that can cause irreversible blindness in severe cases.
Blood accumulation in the orbit can lead to a sharp rise in intraorbital pressure since the bony orbit is a fixed, rigid chamber. Raised intraorbital pressure restricts blood flow and can stretch the optic nerve —> optic nerve damage. This can be thought of as an acute orbital compartment syndrome.
RBH has several causes:
Trauma to the orbit
Iatrogenic: usually due to a peri- or retrobulbar local anaesthetic block performed for intraocular surgery
Bleeding from vascular anomalies
Spontaneous haemorrhage due to poor clotting (rare)
Painful loss of visual acuity
Restricted ocular movements
Eyelid oedema and ecchymosis
Relative afferent pupillary defect (RAPD)
Raised intraocular pressure
Optic disc swelling
Imaging can help with diagnosis, but this shouldn’t delay treatment.
Surgical management has better outcomes than medical management. It is essential to immediately decompress the orbit and relieve pressure to prevent compartment syndrome and permanent visual loss
1st-line: lateral canthotomy and cantholysis (LCC). Lateral canthotomy is exposure of the lateral cantonal tendon. Cantholysis involves dis-insertion of the lateral cantonal tendon (by cutting the inferior crus of the lateral cantal tendon), which releases intraorbital pressure.
If LCC doesn’t work, inferior septectomy and/or surgery can be performed
Some use medical management as an adjunct to surgery: IV acetazolamide + IV hydrocortisone
Trauma to the globe
The cornea and sclera remain intact. Usually caused by blunt trauma.
Involves a full-thickness defect of the cornea and/or sclera
A closed injury caused by blunt trauma. The damage can occur at the site of impact or at a distant site
A full-thickness wound caused by blunt trauma. The globe gives way at its weakest point (which may not be at the site of impact).
Caused by a sharp object e.g. a knife or glass.
An injury with an entry wound but no exit wound, usually caused by a sharp object.
An injury with both entry and exit wounds, usually caused by a missile.
A full-thickness eye wall defect caused by a tearing injury, usually caused by direct impact.
A partial-thickness laceration.
Consider the following investigations in cases of globe trauma:
X-ray - where a foreign body is suspected
Ultrasound - useful to detect intraocular foreign bodies, globe rupture, retinal detachment and suprachoroidal haemorrhage
CT - provides a more detailed view than simple radiographs for detecting and localising intraocular foreign bodies. It is also useful to view the integrity of intracranial, intraocular and facial structures
MRI - better than CT for assessing injuries of the globe itself (but not for bony injury)
Electrodiagnostic tests - to assess the function of the optic nerve and retina
💡An MRI should NEVER be performed if there is suspicion of a ferrous metallic foreign body in the eye.
Common causes: sporting injuries, assault
Mechanism: blunt trauma to the globe —> anteroposterior compression with concurrent expansion in the equatorial plane. This is often associated with a temporary but severe increase in intraocular pressure.
Prognosis usually depends on the extent of retinal injury
The table below summarises potential consequences of blunt trauma to the globe.
Breech of the corneal endothelium. Stains with fluorescein.
Acute corneal oedema
Develops secondary to focal/diffuse dysfunction of the corneal endothelium after blunt trauma. Usually self-resolves.
Haemorrhage in the anterior chamber - the blood settles inferiorly and a ‘fluid level’ is usually seen. The iris root or ciliary body face is usually the source of bleeding.
The iris can be compressed against the anterior surface of the lens by the anteroposterior force of blunt trauma —> transient miosis. Damage to the iris sphincter —> temporary/permanent traumatic miosis. Reaction of the pupil to light and accommodation is sluggish/absent.
Dehiscence of the iris from the ciliary body.
Can be elevated due to hyphaema or inflammation, hence careful monitoring of IOP is vital.
Common. Characteristically a ‘flower-shaped’ (’rosette’) opacity is seen. See our notes on ‘Secondary and traumatic cataract’ for more detail.
Tearing of the suspensory ligament —> subluxation of lens. Rarely the lens may dislocate into the vitreous or anterior chamber.
Caused by severe blunt force. Has a poor prognosis if the initial visual acuity is light perception or worse. Globe rupture is usually anterior, close of the Schlemm canal, with prolapse of the lens, iris, ciliary body and vitreous.
Often occurs together with posterior vitreous detachment. In the anterior vitreous, pigment cells (described as “tobacco dust”) may be seen.
Involves the choroid, Bruch membrane and retinal pigment epithelium. If the fovea is involved, visual prognosis is poor.
Retinal breaks and detachment
〜10% of retinal detachments are caused by trauma. Retinal breaks caused by trauma may occur either at the time of impact, or they can develop later on. A retinal dialysis is disinsertion of the retina at the ora serrata (the serrated junction between the choroid and ciliary body), caused by traction of the relatively inflexible vitreous gel along the posterior aspect of the vitreous base. Traumatic dialyses are more common in the inferotemporal and superonasal quadrants.
Traumatic optic neuropathy
Sudden visual loss after orbital/ocular/head trauma that cannot be explained by other ocular causes. The force may be directly or indirectly transmitted to the optic nerve. Visual acuity is reduced to light perception in 〜50% of cases, and an afferent pupillary defect may be the only sign. Pallor of the optic nerve develops over days-weeks. IV methylprednisolone may be considered within the first 8 hours.
Penetrating eye injuries are 3x more likely to occur in males than females, and are most often caused by occupational or domestic accidents, assault and sport. They can be prevented by wearing protective eyewear.
As well as causing direct trauma to the eye, a key issue with penetrating injuries is the risk of infection that may follow. Penetrating eye injuries can cause endophthalmitis or panophthalmitis, which are often more severe than the initial injury, and can cause loss of the eye. For this reason, prophylactic antibiotics (systemic ciprofloxacin, or in cases of contaminated IOFB, intravitreal vancomycin + ceftazidime) should be considered, and tetanus status investigated (as with eyelid trauma).
Most penetrating eye injuries need urgent surgical repair.
💡 Penetrating trauma cannot be excluded even if there are no entry wounds on examination
Intraocular foreign body (IOFB)
All patients with penetrating eye injuries should be considered for an IOFB. IOFBs can cause damage to the eye in several ways: mechanically; by having toxic effects on ocular structures; and by causing infection.
Copper IOFBs with a high copper content —> an aggressive endophthalmitis-like reaction, which may progress to phthisis bulbi (’end-stage eye’). An alloy with a fairly low copper content (e.g. brass/bronze) —> chalcosis. Intraocular copper deposits can lead to anterior ‘sunflower’ cataracts and Kayser-Fleischer rings (also ophthalmic signs of Wilson’s disease)
Iron IOFBs —> siderosis. Iron deposition in intraocular epithelium structures —> cell necrosis —> anterior capsular cataract (consisting of iron deposits on the anterior lens capsule). It also causes reddish-brown staining of the iris —> heterochromia iridis and pigmentary retinopathy —> atrophy of the retina and retinal pigment epithelium. Trabecular damage can lead to glaucoma.
Aluminium and zinc are mildly toxic
Glass, plastic, gold and silver are inert
X-ray and CT are useful to detect and localise the IOFB
MRI scans are contraindicated with metallic (particularly ferrous) IOFBs, as IOFBs may be magnetised
Topical fluorescein may help to identify an entry wound
Intravitreal antibiotic prophylaxis is recommended
Ferrous foreign bodies: a sclerotomy is created next to the foreign body, and the IOFB is removed magnetically, followed by cryotherapy to the retinal break
Non-magnetic foreign bodies: a pars plana vitrectomy is performed, followed by forceps removal of the IOFB (either through the pars plana or the limbus)
Chemical and thermal injuries can be severe, resulting in severe corneal scarring and permanent visual loss, hence timely management is critical.
Alkali burns are twice as common as acid burns (as they are more widely used in homes and in industry). The most commonly involved alkalis are sodium hydroxide, ammonia and lime. Sodium hydroxide and ammonia cause more severe damage due to rapid penetration.
Alkali injuries are more serious than acids, as they are lipophilic and hence penetrate more deeply than acids. This is because acids coagulate surface proteins, forming a protective barrier.
Alkalis cause damage via liquefactive necrosis
Acids cause damage via coagulative necrosis
Severe burns should be admitted to hospital.
Copious irrigation for 15-30 minutes, ****ideally with a sterile balanced buffered solution (e.g. normal saline or Ringer lactate), but tap water may be used if necessary - this minimises duration of contact with the chemical, and helps to normalise the pH in the conjunctival sac. The speed and efficacy of irrigation is the most important prognostic factor following chemical injury. Topical anaesthetic should be given before irrigation to make the procedure more comfortable and increase cooperation.
Double eversion of the upper eyelid - so that any trapped particles can be identified and removed
Debridement of necrotic areas of corneal epithelium
Administer topical antibiotics ± topical steroids and cycloplegics. Topical antibiotics are for prophylaxis of bacterial infection; steroids reduce inflammation; and cycloplegics may improve comfort.
Ascorbic acid (not to be used in acid burns) - improves wound healing by promoting collagen synthesis
Doxycycline - a proteinase inhibitor which helps healing
Long-term corneal healing problems
Corneal epithelium healing involves the migration of limbal stem cells. Consequently, if there is damage to the limbus, corneal healing is impaired. Possible solutions include:
Amniotic membrane grafting
Limbal stem cell transplant
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