Trauma The Orbit & Globe

Orbital Trauma

Orbital floor fracturecaused by a sudden increase in the orbital pressure from an impacting object that is greater in diameter than the orbital aperture (about 5 cm), such as a fist or tennis ball , so that the eyeball itself is displaced and transmits rather than absorbs the impact

Diagnosis

1.Visual function• should be recorded and monitored as necessary, particularly in

the acute situation.

2.Periocular signs • ecchymosis, oedema and occasionally subcutaneous

emphysema .

3.Infraorbital nerve anaesthesia • involving the lower lid, cheek, side of nose, upper lip, upper

teeth and gums is very common as the fracture frequently involves the infraorbital canal.

4. Diplopia : ○ Haemorrhage and oedema in the orbit .

○ Mechanical entrapment within the fractureDiplopia typically occurs in both upgaze and downgaze. Forced duction and the differential (IOP) test are positive. Improve if it is mainly due to entrapment of oedematous connective tissue and fat.persists if there is significant involvement of the muscles themselves.

. ○ Direct injury to an extraocular muscle, negative forced duction test. The muscle fibres usually regenerate and normal function often returns within about 2 months.

5. Enophthalmos :- if the fracture is severe, although it tends to manifest only after a few days as initial oedema resolves.

In the absence of surgical intervention, enophthalmos may continue to increase for about 6 months as post-traumatic orbital tissue degeneration and fibrosis develop.

• 6. Ocular damage (e.g. hyphaema, angle recession, retinal dialysis) should be

excluded by careful examination of the globe, although this is relatively uncommon in association with a blowout fracture.

Treatment• Initial treatment • observation, with the

prescription of oral antibiotics; ice packs and nasal decongestants .

• The patient should be instructed not to blow his or her nose, because of the possibility of forcing infected sinus contents into the orbit.

• Systemic steroids are occasionally required for severe orbital oedema, particularly if this is compromising the optic nerve.

• Subsequent treatment ○ Small cracks unassociated with herniation

do not require treatment .

○ Fractures involving up to one-half of the orbital floor, with little or no herniation, no significant enophthalmos and improving diplopia, also do not require treatment.

○ Fractures involving more than one-half of the orbital floor will usually develop significant enophthalmos if left untreated.

o Fractures with entrapment of orbital contents, enophthalmos of greater than 2 mm, and/or persistent and significant diplopia in the primary position should be repaired within 2 weeks. If surgery is delayed, the results are less satisfactory due to secondary fibrotic changes.

o Early marked enophthalmos may also be an indication for urgent repair.

‘White-eyed’ fracturea subgroup for which urgent repair is

required to avoid permanent neuromuscular damage.

The scenario is generally seen in patients less than 18 years of age, typically with little visible external soft tissue injury, and usually affects the orbital floor.

It involves the acute incarceration of herniated tissue in a trap-door effect occurring due to the greater elasticity of bone in younger people.

Patients may experience acute nausea, vomiting, and headache; persistent activation of the oculocardiac reflex can occur.

CT features may be subtle.

Eight year old male patient with "White eyed blowout fracture" left. Preoperative view (A).CT show trap door type orbital floor fracture Preoperative extraocular muscle 1 month postoperative view limitation was improved (B) .

Surgical repair a transconjunctival or subciliary incision or the maxillary sinus, with elevation of the periosteum from the orbital floor, freeing of trapped orbital contents and repair of the bony defect with a synthetic implant.

Treatment Small fractures may not require treatment but it is important to exclude a CSF leak, which carries a risk of meningitis. Sizeable bony defects with downward displacement of fragments usually warrant reconstructive surgery.

Roof fracture Roof fractures are rare. Isolated fractures, caused by falling on a sharp object or sometimes a relatively minor blow to the brow or forehead, are most common in children and often do not require treatment. Diagnosis A haematoma of the upper eyelid with periocular ecchymosis.Large fractures may be associated with pulsation of the globe due to transmission of (CSF) pressure, best detected with applanation tonometry.

Lateral wall fracture Acute lateral wall fractures are rarely encountered by

ophthalmologists. Because the lateral wall of the orbit is more solid than the other walls, a fracture is usually associated with

extensive facial damage.

Blunt trauma

• Severe blunt trauma to the globe results in anteroposterior compression with simultaneous expansion in the equatorial plane associated with a transient but severe increase in IOP.

• Although the impact is primarily absorbed by the lens–iris diaphragm and the vitreous base, damage can also occur at a distant site such as the posterior pole.

Cornea• Corneal abrasion involves a breach of the epithelium, and stains well with fluorescein . If located over the pupillary area, vision may be grossly impaired.

• Acute corneal oedema :- secondary to focal or diffuse dysfunction of the endothelium and is sometimes seen underlying a large abrasion. It is commonly associated with folds in Descemet membrane and stromal thickening, but usually clears spontaneously.

• Tears in Descemet membrane are usually vertical and most commonly arise as the result of birth trauma.

HyphaemaHyphaema is a common complication of blunt ocular injury. The source of bleeding is typically the iris root or ciliary body face.

Characteristically, the blood settles inferiorly with a resultant ‘fluid level’ except when the hyphaema is total .

Treatment is aimed at the prevention of secondary haemorrhage and control of any elevation of IOP , which as well as optic neuropathy can lead to staining of ocular tissues, particularly the cornea

Anterior Uvea• Pupil :- The iris may momentarily be compressed against the anterior surface of the lens by severe anteroposterior force, with resultant imprinting of pigment from the pupillary margin. Transient miosis accompanies the compression, evidenced by the pattern of pigment corresponding to the size of the miosed pupil (Vossius ring ). Damage to the iris sphincter may result in traumatic mydriasis, which can be temporary or permanent; the pupil reacts sluggishly or not at all to both light and accommodation. Radial tears in the pupillary margin are common

•Iridodialysis • is a dehiscence of the iris from the ciliary body at its root. •The pupil is typically D-shaped and the dialysis is seen as a dark biconvex area near the limbus .

• An iridodialysis may be asymptomatic if covered by the upper lid; if exposed in the palpebral aperture, uniocular diplopia and glare sometimes ensue, and may necessitate surgical repair of the dehiscence.

•Traumatic aniridia (360° iridodialysis) is rare; in a pseudophakic eye, the detached iris may be ejected through the cataract surgical incision

Lens• Cataract formation:- is a common sequel to blunt trauma. •A ring-shaped anterior subcapsular opacity may underlie a Vossius ring.• Commonly opacification occurs in the posterior subcapsular cortex along the posterior sutures, resulting in a flower-shaped (‘rosette’) opacity that may subsequently disappear, remain stationary or progress to maturity .

• Subluxation of the lens A subluxated lens tends to deviate towards the meridian of intact zonule; the anterior chamber may deepen over the area of zonular dehiscence, if the lens rotates posteriorly. trembling of the iris (iridodonesis) or lens (phakodonesis) may be seen on ocular movement.

• Dislocation :- due to 360° rupture of the zonular fibres is rare . an underlying predisposing condition such as pseudoexfoliation should be suspected.

• Globe rupture • Rupture of the globe may result from severe blunt trauma;

the prognosis is poor if the initial visual level is light perception or worse.

• Anterior :- The rupture is usually anterior, in the vicinity of the Schlemm canal, with prolapse of structures such as the lens, iris, ciliary body and vitreous ,

• may be masked by extensive subconjunctival haemorrhage .• Rupture at the site of a surgical wound (e.g. cataract,

keratoplasty, vitrectomy) is common with substantial blunt force.

• Posterior :- • An occult posterior rupture can be associated

with little visible damage to the anterior segment, but should be suspected if there is asymmetry of anterior chamber depth – the anterior chamber of an affected eye is classically deep, with posterior rotation of the iris– lens diaphragm – and IOP in the affected eye is low.

• Gentle B-scan ultrasonography may demonstrate a posterior rupture, but CT or MR may be necessary; MR is not performed if there is a risk of ferrous IOFB.

Vitreous haemorrhage • may occur, commonly in association with posterior vitreous detachment.

• Pigment cells (‘tobacco dust’) may be seen floating in the anterior vitreous, and though not necessarily associated with a retinal break, should always prompt careful retinal assessment.

Commotio retinae

• caused by concussion of the sensory retina resulting in cloudy swelling that gives the involved area a grey appearance .

• It most frequently affects the temporal fundus. If the macula is involved, a ‘cherry-red spot’ may be seen at the fovea.

• Severe involvement may be associated with intraretinal haemorrhage that can involve the macula.

• The prognosis in mild cases is good, with spontaneous resolution in around 6 weeks.

• Sequelae to more severe commotio may include progressive pigmentary degeneration and macular hole formation .

(A) Wide-field imaging showing typical appearance;

(B) associated with retinal haemorrhages

(C) macular hole following resolution of commotio at the posterior pole

Choroidal rupture involves the choroid, Bruch membrane and retinal pigment epithelium; it may be direct or indirect. Direct ruptures are located anteriorly at the site of impact and run parallel with the ora serrata. Indirect ruptures occur opposite the site of impact. A fresh rupture may be partially obscured by subretinal haemorrhage , which may break through the internal limiting membrane with resultant subhyaloid or vitreous haemorrhage. Weeks to months later, on absorption of the blood, a white crescentic vertical streak of exposed underlying sclera concentric with the optic disc becomes visible . The visual prognosis is poor if the fovea is involved. An uncommon late complication is choroidal neovascularization.

(A) Acute foveal disruption with subretinal and sub-RPE haemorrhage

(B ) old lesions

Retinal breaks and detachment • • A retinal dialysis • is a break occurring at the ora serrata, caused by

traction from the relatively inelastic vitreous gel along the posterior aspect of the vitreous base.

• The tear may be associated with avulsion of the vitreous base, giving rise to an overhanging ‘bucket-handle’ appearance comprising a strip of ciliary epithelium, ora serrata and the immediate post-oral retina into which basal vitreous gel remains inserted .

• Traumatic dialyses occur most frequently in the superonasal and inferotemporal quadrants. Although they occur at the time of injury they do not inevitably result in RD.

• In cases that detach, subretinal fluid commonly does not develop until several months later, and progression is typically slow.

Trauma is responsible for about 10% of all cases of retinal detachment (RD) and is the most common cause in children, particularly boys.

Dialysis with retinal detachment

avulsed vitreous base

• • Equatorial breaks • are less frequent; they are due

to direct retinal disruption at the point of scleral impact.

• • Macular holes :- • may occur either at the time of

injury or following resolution of commotio retinae.

equatorial retinal breaks

traumatic macular hole

Traumatic optic neuropathy • follows ocular, orbital or head trauma as sudden

visual loss that cannot be explained by other ocular pathology. It occurs in up to 5% of facial fractures.

• • Classification:- • (a) Direct, due to blunt or sharp optic nerve

damage from agents such as displaced bony fragments, a projectile, or local haematoma;

• (b) indirect, in which force is transmitted secondarily to the nerve without apparent direct disruption due to impacts upon the eye, orbit or other cranial structures.

Mechanisms

• contusion, deformation, compression or transection of the nerve, intraneural haemorrhage, shearing (acceleration of the nerve at the optic canal where it is tethered to the dural sheath, thought to rupture the microvascular supply), secondary vasospasm, oedema and transmission of a shock wave through the orbit.

Presentation• indirect neuropathy is considerably more common than direct. • Vision is often very poor from the outset, with only perception of light in

around 50%.• Typically, the only objective finding is an afferent pupillary defect; the optic

nerve head and fundus are initially normal, with pallor developing over subsequent days and weeks.

• It is important to exclude potentially reversible causes of traumatic visual loss such as compressive orbital haemorrhage;

• more controversially, some cases of compression – bony and possibly haemorrhagic – due to fracture within the optic canal or elsewhere may be amenable to intervention.

• Investigation. • CT is more effective in the demonstration of bony abnormalities such as optic

canal fracture.• MR is superior for soft tissue changes (e.g. haematoma); with both

modalities, very thin sections are recommended.

Treatment• Spontaneous visual improvement occurs in up

to about half of indirect injury patients, but if there is initially no light perception this carries a very poor prognosis.

• Steroids (intravenous methylprednisolone) might be considered for otherwise healthy

patients with severe visual loss, or in those with delayed visual loss.

If used, these should be started within the first 8 hours, but the optimal regimen is undetermined and their use remains controversial !!!

• Optic nerve decompression :- (e.g. endonasal, transethmoidal) may be advocated in

some – poorly defined – circumstances such as ongoing deterioration despite steroids and bilateral visual loss.

Compression by bony fragment or haematoma may also be an indication;

optic canal fracture is a poor prognostic indicator and there is no evidence that surgery improves the outlook, whilst carrying a significant risk of complications.

• Optic nerve sheath fenestration has been tried in some centres.

Optic nerve avulsion Optic nerve avulsion is rare and typically occurs when an object intrudes between the globe and the orbital wall, displacing the eye.Postulated mechanisms include sudden extreme rotation or anterior displacement of the globe. Avulsion may be isolated or occur in association with other ocular or orbital injuries. Fundus examination shows a striking cavity where the optic nerve head has retracted from its dural sheath . There is no treatment; the visual prognosis depends on whether avulsion is partial or complete.

• Of paramount immediate importance is the risk of infection with any penetrating injury. Endophthalmitis or panophthalmitis, often more severe than the initial injury, may ensue with loss of the eye.

• Risk factors include delay in primary repair, ruptured lens capsule and a dirty wound.

• Prophylactic intravitreal antibiotics as for postoperative endophthalmitis should be considered, with the agent selected dependent on local microbiological advice; vancomycin is a common choice.

• tetanus status should be ascertained. • Any eye with an open injury should be covered by a

protective eye shield upon diagnosis

• Corneal • Peaking of the pupil and

shallowing of the anterior chamber are key signs, though full-thickness corneal penetration may be present without these.

• The technique of primary repair depends on

the extent of the wound associated complications such

as iris incarceration, flat anterior chamber

and damage to intraocular contents.

Small shelving wounds with a formed anterior chamber may not always require suturing as they can heal spontaneously or with the aid of a soft bandage contact lens.

Medium-sized wounds should almost always be sutured without delay, especially if the anterior chamber is shallow or flat. 10-0 nylon is used, with shorter stitches near the visual axis opposing perpendicular edges first and apical portions of wounds last. A postoperative bandage contact lens may be applied subsequently for a few days to ensure that the anterior chamber remains deep. The corneoscleral junction should be sutured with 9-0 nylon.

With iris involvement :-Abscission (excision) of the

prolapsed portion is commonly required , particularly if necrotic or there is a risk of contamination by foreign material.

With lens damage :-Wounds are treated by first

suturing the laceration then removing the lens by phacoemulsification or with a vitreous cutter.

Primary implantation of an intraocular lens is frequently associated with a favourable visual outcome and a low rate of postoperative complications.

• Scleral • • Anterior scleral lacerations have a better prognosis than those posterior to the ora serrata. An

anterior scleral wound may, nevertheless, be associated with serious complications such as iridociliary prolapse and vitreous incarceration. The latter, unless appropriately managed, may result in subsequent fibrous proliferation along the plane of incarcerated vitreous, with the development of tractional retinal detachment.

• Viable uveal tissue should be reposited and prolapsed vitreous cut flush with the wound, with subsequent vitreoretinal assessment.

• 8-0 nylon or 7-0 absorbable material such as polyglactin should be used for scleral suturing in this setting.

• • Posterior scleral lacerations are frequently associated with retinal damage. Primary repair of the sclera to restore globe integrity should be the

initial priority.

• Retinal detachment • Traumatic tractional retinal detachment following

a penetrating injury may result from vitreous incarceration in the wound, with associated fibroblastic proliferation being exacerbated by the presence of blood in the vitreous gel.

• Contraction of the resultant epiretinal fibrosis can progress to an anterior tractional retinal detachment.

• A retinal break may develop several weeks later, leading to a more rapidly progressing rhegmatogenous detachment.