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Common ocular emergencies (C7911)

Dr Iain Phillips describes the clinical features and management of a range of ocular emergencies resulting from trauma to the eye and surrounding tissues. Module C7911.

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The aim of this article is to provide a brief overview of the initial management of ocular trauma. If someone is concerned about a patient, they should be referred to their GP, local A&E department or ophthalmology service as appropriate.

Severe ocular trauma is often associated with other injuries. The principles behind the management of any trauma starts with basic life support, with airway, breathing and circulation. If a patient has other serious injuries, these should be managed before the eye is attended to.

Lid lacerations

As a general rule, a lid laceration (Figure 1) is overlying a penetrating eye injury until proven otherwise and requires referral to the local A&E department. It is important to know the date of the patient’s last tetanus immunisation. If the laceration involves more than the superficial skin of the lid margin, it requires an ophthalmology opinion. If there is a suspicion of an orbital fracture or foreign body the patient requires imaging. These wounds must be cleaned, subcutaneous local anaesthetic used to anaesthetise the skin, any necrotic tissue removed and then the laceration sutured with fine suture material.

Injury to the orbit

The eye is well protected by its bony surroundings. Direct trauma to the eye increases orbital pressure and can cause orbital damage, most commonly to the base of the orbit, known as a ‘blow-out fracture’. Damage to the roof of the orbit can occur with a blow to the forehead or falling on a sharp object. A ‘pure’ blow-out fracture does not involve the rim of the orbit, an ‘impure’ fracture does.1
Clinical features of a blow-out fracture to the orbit include the limitation of eye movement, diplopia and pain on moving the affected eye. Gazing upward can cause discomfort as the inferior rectus muscle catches on the rough surface of the fractured bone in the orbit base. The infra-orbital nerve can be damaged, leading to paraesthesia to the skin below the eye. Surgical emphysema is the presence of subcutaneous air, which suggests the air sinus has been fractured and enophthalmos can occur. Any damage to the medial canthus, such as a laceration, requires exclusion of trauma to the lacrimal canaliculi. If there is a suspicion of a penetrating eye injury, no pressure should be applied to the globe of the eye.

CT imaging is the gold standard investigation to identify the extent of bony injury. Fractures to the roof or medial wall of the orbit require reconstructive surgery, often to release the trapped tissue. When there is damage to the floor of the orbit, some surgeons aim to operate early, while others allow the swelling to reduce so an accurate assessment of the degree of enophthalmos and loss of ocular movement can take place. The more severe the fracture, the more likely surgery will be necessary.

Trauma to the eye

If there has been ocular trauma, the conjunctivae should be examined to exclude the presence of an abrasion or laceration, particularly in the presence of a sub-conjunctival haemorrhage (Figure 2). Examination of the cornea with fluorescein will show an abrasion and a concentration of fluorescein could suggest a leak of aqueous through a penetrating wound. Corneal abrasions heal quickly and chloramphenicol is routinely given to prevent infection. On healing, some patients experience recurrent pain as a consequence of defect healing of the wound. Recurrent corneal erosions can be prevented by regular use of lubricants and a sub-epithelial scar can be treated using laser therapy.
Both blunt and penetrating eye trauma can cause haemorrhage into the anterior chamber of the eye. The hyphaema shows a collection of blood and a fluid level. Traumatic mydriasis may occur in response to blunt trauma to the eye. The pupil may be an abnormal shape if the iris has plugged a penetrating wound.

The lens can be dislocated. A sign of this is iridodinesis, where the diaphragm of the eye flutters as the eye moves. On examination with a slit lamp, a transient posterior subcapsular cataract may occur. Cataracts can develop quickly after penetrating trauma (Figure 3).
The fundus should be examined with a fully dilated pupil only if there is no neurological deficit and there is no suspicion of a penetrating eye injury. A lack of detail on fundoscopy suggests a vitreous haemorrhage. Blunt trauma can cause separation of the retina from the pars plana of the ciliary body (retinal dialysis) (Figure 4), as well as areas of retinal haemorrhage and oedema (commotio retinae). A macular hole can occur destroying the fovea and leading to vision loss.

Tearing of the choroid leads to sub-retinal haemorrhage and scarring. Damage to the peripheral retina should be excluded using indirect ophthalmoscopy or slit-lamp microscopy. Traumatic optic nerve damage can occur, particularly through damage to its blood supply, and on examination the disc appears pale.

Imaging of ocular trauma depends on the clinical scenario. X-ray and CT scans can be used to assess the damage around the eye or to identify a foreign body. Any suggestion of a metallic foreign body is a contraindication for the use of magnetic resonance imaging (MRI). Trials are now being carried out to assess the compatibility of ultrasound to assess ocular trauma and identify the complications such as retinal detachment.2
Trauma to the globe should be urgently referred to an ophthalmologist, with the necessary treatment defined by the extent of the injury. Less serious injuries, for example, may be monitored and reviewed regularly in clinic. Penetration of the globe will require suturing, and further surgery may be required to remove a foreign body, cataract or to repair a detached retina.

Trauma that causes a penetrative injury in the eye has a poor prognosis and is likely to result in permanent vision loss, particularly if iron foreign bodies are involved as their presence leads to destruction of the retina. Secondary glaucoma can develop if the trabecular meshwork is damaged.

Radiation damage

Radiation from an arc lamp or sunlamp causes intense discomfort approximately six hours after exposure. On examination the cornea shows diffuse epithelial oedema and some punctate damage, which resolves spontaneously in 48 hours. Patients can be given chloramphenicol as prophylaxis and take simple analgesia.
Corneal foreign body

It is important to identify the source of any foreign body as organic materials can lead to infection, while metallic objects can lead to the formation of ‘rust rings’ and induce persistent inflammation in the eye.

When taking the history, it is necessary to understand the velocity of the object in order to assess the likelihood of a penetrating eye injury. Slit lamp assessment should identify the nature of the foreign body, its position and the possibility of a penetrating injury. The eye lid should be everted to exclude a hidden foreign body. Management includes removing the foreign body, using fluorescein to examine the extent of the damage to the epithelium. Topical antibiotics can be given, along with a cycloplegic agent. Patches are not commonly used. Topical anaesthesia should not be continued after the initial assessment.

Patients should be referred for an ophthalmology opinion within 24 hours if the foreign body is not removed. A corneal opacity suggesting abscess formation should be referred urgently. Patients should avoid contact lens use until the defect is completely healed.

Chemical burns

Chemical burns to the eye are a medical emergency. The more alkaline or acidic a substance is, the higher the risk of permanent damage. Alkaline injuries are more common and carry a higher risk of sight loss. The acid alters the pH of the surface of the cornea leading to corneal damage. The surface proteins are denatured, altering their shape and impairing their function. The proteins precipitate and coagulate (group) together. The coagulation of proteins causes the characteristic ground glass appearance of the corneal stroma following chemical injury. This is a protective mechanism, which prevents the deeper penetration of acid into the eye.

Alkaline chemical injuries are more severe because an alkaline substance penetrates deeper into the eye. Alkali substances inhibit membrane fatty acid, stromal collagen and glycosaminoglycan function. Tears hydrate these structures causing damage to the meshwork of the trabeculae, which can lead to raised intraocular pressure. Inflammatory mediators are released leading to further rises in intraocular pressure. Hydrofluoric acid is an acid that acts like an alkali. It dissociates in the eye and the fluoride ion acts as an alkaline substance. These interactions allow the alkaline substance deeper into the eye penetrating the cornea into the anterior segment.3

Patients present with a history of being exposed to a liquid or gas being splashed into the eye. Common complaints include severe pain, red eye, photophobia, excessive tear production and the sensation of a foreign body in the eye. At this point an examination of the eye should be deferred to allow proper and adequate irrigation of the eye. The aim is to normalise the pH of the eye, which involves irrigating the eye with large volumes of a neutral solution such as normal saline. The pH can be measured using universal indicator paper aiming for a pH as neutral as possible. If the patient has difficulty in opening the eye then topical anaesthesia can be used to allow irrigation.

On examining the eye, it is important to note the clarity and integrity of the cornea, the presence of any limbal ischaemia and the intraocular pressure. Any particulates of a foreign body act as reservoir of the chemical, worsening the injury. An initial assessment of visual acuity should be conducted. An initial decrease in vision can be due to excess tears, pain, local effects of injury (such as hazing) or epithelial damage. Despite normal visual acuity at the time of the accident, it can deteriorate over time.

Corneal damage ranges from a mild diffuse punctate keratitis to a complete corneal epithelial defect. After exposure to a chemical there may be stromal haze, these can range from minimal to complete inability to see through the cornea and examine the anterior chamber. Chemical injury stimulates inflammatory mechanisms. The more severe the level of vascular blanching at the limbus correlates to a more severe injury as the limbal stem cells are responsible for corneal regrowth. Other signs of severe injury include significant scleral ischaemia, an avascular limbus, conjunctival blanching and severe corneal haze.

Intraocular pressure can be raised due to damage to the trabeculae, anterior chamber inflammation or the degree of collagen damage. Chemical burns can cause scarring anywhere on the body; as a result, the eyelids can be damaged and scarred. If this occurs and the corneal surface cannot be adequately covered by the eyelid there is an increased likelihood of complications. The degree of limbal ischaemia is assessed by the degree of blanching.
Corneal opacification is rare at the first presentation of a chemical injury, but may develop weeks and months later, particularly in severe injuries with poor healing potential. Limbal transplants can be attempted and recent research in an animal model suggests stem cells could be used to re-epithelialise the eye. A small animal trial published this month has suggested that passing oxygen against the eye can reduce the risk of corneal perforation and delay the risk of ulceration, although previous studies using hyperbaric oxygen showed no statistical difference.4 ?

References

  1. Kanski J. Trauma. Clinical ophthalmology: A synopsis. 2004, pp383-6.
  2.  Rabinowitz R, Yagev R et al. Comparison between clinical and ultrasound findings in patients with vitreous hemorrhage. Eye. 2004, 18(3):253-6.
  3. Randleman J, Loft E et al. Chemical burns. Ophthalmology. www.emedicine.com 2006.
  4. Sharifipour F, Zamani et al. Oxygen therapy for severe corneal alkali burn in rabbits. Oct;26(9):1107-10.

? Dr Iain Phillips is an SHO in emergency medicine

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