Injury to orbital soft tissues

Damage to extraocular muscles

Avulsion of extraocular muscles is rare and usually results from a penetrating orbital injury with a "hooking" force, seen occasionally with deliberate attempts at enucleation during assault (Figure 14.11). CT scan allows an assessment of the state of the musculature, although repair is often difficult due to oedema, haemorrhage and retraction of the muscle into the orbit. When enucleation has been achieved, orbital oedema may be extreme and bacterial contamination likely; in these circumstances primary implantation of a ball is likely to fail and this should be deferred until both the oedema and the risk of infection has settled.

Explosive injuries result in ragged wounds with widespread intraorbital debris, and should be treated by extensive cleaning of tissues, debridement where necessary and repair of the globe and eyelids where possible. Where there has been a major loss of eyelid tissues, the principles of reconstruction are similar to those for eyelid repair after excision of tumours (Chapter 5), although this may need to be deferred until the acute oedema has improved; whilst awaiting reconstruction, the repaired globe should be kept moist with regular lubricant/antibiotic ointments and a "moisture chamber" such as, for example, a cling-film application over a Cartella shield.

Optic nerve injury

Injury to the optic nerve can either be direct, due to penetrating orbital foreign bodies or avulsion, or indirect as part of a major head injury, with fractures around the orbital apex - where bone fragments may impinge on the nerve - or actually involving the optic canal.

Optic nerve damage anterior to the entrance of the central retinal artery causes visual loss with retinal artery occlusion, whereas optic nerve avulsion (Figure 14.11) produces extensive peripapillary haemorrhage and a later fibroglial reaction.

The commonest site for injury to the posterior part of the optic nerve is in the bony canal (Figure 14.12) and, more rarely, in the intracranial nerve or chiasm. Optic neuropathy may occur with or without fracture of the canal and recent CT studies suggest that sphenoid fractures are more common than previously

Testicular Hammer

Figure 14.11 (a) Major avulsion of the globes and eyelids during assault with a claw-hammer, (b) the scleral defect is evident at the site of optic nerve avulsion.

Figure 14.11 (a) Major avulsion of the globes and eyelids during assault with a claw-hammer, (b) the scleral defect is evident at the site of optic nerve avulsion.

thought. It is believed that the energy of impact and shearing forces due to deceleration are transmitted to the area of the optic canal, resulting in axonal damage and tearing of the pial vessels supplying the intracanalicular optic nerve; oedema of the injured tissues and posttraumatic vasospasm will both exacerbate neural ischaemic damage and this forms a rational basis for the use of high-dose corticosteroids after such injuries. The role of optic canal decompression, however, remains in doubt.

Treatment of indirect optic neuropathy may be empirically based on the results for spinal cord injury: a loading dosage of 30mg/kg Methyl-prednisolone within 8 hours of injury is followed by an infusion of about 5mg/kg/hr for 24 hours after injury. A tailing dosage of prednisolone or dexamethasone may then be continued for a few days.

Optic Fracture
Figure 14.12 Fracture of the right optic nerve canal with severe optic neuropathy.

Surgery may be considered for removal of bone fragments, where these are thought to be causing a compressive optic neuropathy, and for drainage of intraorbital haematomas. Although visual improvement has been reported after drainage of haematomas from within the optic nerve sheath, there is no evidence that this procedure actually alters the natural course of the condition.

Decompression of the optic canal, by removal of the lateral wall of the sphenoid sinus where it overlies the optic canal, has not been shown to improve visual recovery after injury to the intracanalicular optic nerve; it may, however, have a role where vision deteriorates in the face of adequate medical therapy. Decompression may be achieved through a trans-cranial or a trans-ethmoidectomy approach and may be usefully incorporated as part of an open repair of craniofacial injuries. Because of the proximity of the internal carotid artery to the operative site, an otorhinolaryngologist or neurosurgeon familiar with the regional anatomy best performs the procedure.

Subperiosteal haematoma

A subperiosteal haematoma of the orbit may follow blunt trauma, is usually superiorly within the orbit and the presentation - with a slowly progressive displacement of the globe -may lead to delayed diagnosis (Figure 14.7). The haematoma should be drained through a transcutaneous approach and a vacuum drain left in place until the bleeding settles; compressive optic neuropathy, whilst rare, dictates urgent intervention.

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