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Chapter 21 Trauma

EYELID TRAUMA 872
Periocular haematoma 872
Laceration 872
ORBITAL FRACTURES 873
Blow-out orbital floor fracture 873
Blow-out medial wall fracture 875
Roof fracture 875
Lateral wall fracture 877
TRAUMA TO THE GLOBE 877
Introduction 877
Blunt trauma 878
Shaken baby syndrome 885
Penetrating trauma 885
Superficial foreign bodies 886
Intraocular foreign bodies 888
Enucleation 891
Bacterial endophthalmitis 891
CHEMICAL INJURIES 891
Causes 891
Pathophysiology 891
Management 892
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Eyelid trauma

Periocular haematoma

A ‘black eye’, consisting of a haematoma (focal collection of blood) and/or periocular ecchymosis (diffuse bruising) and oedema is the most common blunt injury to the eyelid or forehead and is generally innocuous. It is, however, very important to exclude the following more serious conditions:

1 Trauma to the globe or orbit. It is easier to examine the integrity of the globe before the lids become oedematous (Fig. 21.1A). Once oedema is established, gentle sustained pressure to open the lids will often displace oedema sufficiently to allow visualization of the anterior segment; it is critical not to allow any force on the globe itself until its integrity has been confirmed.
2 Orbital roof fracture, especially if the black eye is associated with a subconjunctival haemorrhage without a visible posterior limit (Fig. 21.1B).
3 Basal skull fracture, which may give rise to characteristic bilateral ring haematomas (‘panda eyes’ – Fig. 21.1C).
image

Fig. 21.1 (A) Periocular haematoma and oedema; (B) periocular haematoma and subconjunctival haemorrhage; (C) ‘panda eyes’

(Courtesy of R Bates – fig. A)

Laceration

The presence of a lid laceration, however insignificant, mandates careful exploration of the wound and examination of the globe. Any lid defect should be repaired by direct closure whenever possible, even under tension, since this affords the best functional and cosmetic results.

1 Superficial lacerations parallel to the lid margin without gaping can be sutured with 6-0 black silk; the sutures are removed after 5 days.
2 Lid margin lacerations invariably gape and must therefore be very carefully sutured with perfect alignment to prevent notching as follows (Fig. 21.2A and B).
a Pass a 5-0 silk vertical mattress suture in the plane of the meibomian gland orifices about 2 mm from the wound edges and 2 mm deep, and leave untied.
b Close the tarsal plate with partial-thickness lamellar 5-0 Vicryl (polyglactic acid) sutures and tie the sutures anteriorly.
c Tie the silk suture so that the cut edges slightly pucker but leave the suture long.
d Close the overlying skin with interrupted 7-0 nylon or Vicryl sutures incorporating the tag ends of the silk suture to keep its knot away from the cornea.
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3 Lacerations with mild tissue loss just sufficient to prevent direct primary closure can usually be managed by performing a lateral cantholysis in order to increase lateral eyelid mobility.
4 Lacerations with extensive tissue loss may require major reconstructive procedures such as are used following lid resection for malignant tumours (see Ch. 1).
5 Canalicular lacerations should be repaired within 24 hours. The laceration is bridging by silicone tubing (Crawford), which is threaded down the lacrimal system and tied in the nose, following which the laceration is sutured. Alternatively, repair of a single canaliculus is performed by using a monocanalicular stent (e.g. Mini Monoka) and, if necessary, securing its footplate to the lid using 8-0 suture material. The tubing is left in situ for 3–6 months.
image

Fig. 21.2 Repair of lid laceration. (A) Initial approximation of the tarsal plate with an absorbable suture and lid margin with a silk suture; (B) completed repair

(Courtesy of J Nerad, K Carter and M Alford, from Oculoplastic and Reconstructive Surgery, in Rapid Diagnosis in Ophthalmology, Mosby 2008)

It is very important to ensure that the patient’s tetanus immunization status is satisfactory after any injury. Without any prior immunization (unlikely) give 250 units of human tetanus immunoglobulin intramuscularly (IM); if previously immunized but a booster has not been administered within the last 10 years, give IM or subcutaneous tetanus toxoid.

Orbital fractures

Blow-out orbital floor fracture

A blow-out fracture of the orbital floor is typically caused by a sudden increase in the orbital pressure by an impacting object which is greater in diameter than the orbital aperture (about 5 cm), such as a fist or tennis ball (Fig. 21.3), so that the eyeball itself is displaced and transmits rather than absorbs the impact. Since the bones of the lateral wall and the roof are usually able to withstand such trauma, the fracture most frequently involves the floor of the orbit along the thin bone covering the infraorbital canal. Occasionally, the medial orbital wall may also be fractured; a ‘pure’ blow-out fracture does not involve the orbital rim whereas an ‘impure’ fracture involves the rim and/or adjacent facial bones. Clinical features vary with the severity of trauma and the time interval between injury and examination.

image

Fig. 21.3 Mechanism of an orbital floor blow-out fracture

Diagnosis

1 Periocular signs include variable ecchymosis (Fig. 21.4A), oedema and occasionally subcutaneous emphysema.
2 Infraorbital nerve anaesthesia involving the lower lid, cheek, side of nose, upper lip, upper teeth and gums is very common because the fracture frequently involves the infraorbital canal.
3 Diplopia may be caused by one of the following mechanisms:
• Haemorrhage and oedema in the orbit may cause the septa connecting the inferior rectus and inferior oblique muscles to the periorbita to become taut and thus restrict movement of the globe. Ocular motility usually improves as the haemorrhage and oedema resolve.
• Mechanical entrapment within the fracture of the inferior rectus or inferior oblique muscle, or adjacent connective tissue and fat. Diplopia typically occurs in both upgaze (Fig. 21.4B) and downgaze (double diplopia). In these cases forced duction and the differential intraocular pressure tests are positive. Diplopia may subsequently improve if it is mainly due to entrapment of connective tissue and fat, but usually persists if there is significant involvement of the muscles themselves.
• Direct injury to an extraocular muscle is associated with a negative forced duction test. The muscle fibres usually regenerate and normal function returns within about 2 months.
4 Enophthalmos (Fig. 21.4C) may be present if the fracture is severe, although it tends to manifest only after a few days as the initial oedema resolves. In the absence of surgical intervention, enophthalmos may continue to increase for about 6 months as post-traumatic orbital degeneration and fibrosis develop.
5 Ocular damage (e.g. hyphaema, angle recession, retinal dialysis), although relatively uncommon, should be excluded by slit-lamp and fundus examination.
6 CT with coronal sections (Fig. 21.4D) is particularly useful in evaluating the extent of the fracture, as well as determining the nature of maxillary antral soft-tissue densities which may represent prolapsed orbital fat, extraocular muscles, haematoma or unrelated antral polyps.
7 Hess test (Fig. 21.5) is useful in assessing and monitoring the progression of diplopia.
image

Fig. 21.4 Right orbital floor blow-out fracture. (A) Mild bruising and superficial laceration; (B) restricted elevation; (C) mild enophthalmos; (D) CT coronal view shows a defect in the orbital floor (arrow) and the ‘tear drop’ sign in the antrum

(Courtesy of A Pearson – fig. D)

image

Fig. 21.5 Hess chart of a left orbital floor blow-out fracture shows restriction of left upgaze (superior rectus and inferior oblique) and restriction on downgaze (inferior rectus). There is also secondary overaction of the right eye

Treatment

1 Initial treatment is conservative with antibiotics; ice packs and nasal decongestants may be helpful. The patient should be instructed not to blow the 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.
2 Subsequent treatment is aimed at prevention of permanent vertical diplopia and/or cosmetically unacceptable enophthalmos. The three factors that determine the risk of these late complications are fracture size, herniation of orbital contents into the maxillary sinus and muscle entrapment. Although there may be some overlap, most fractures fall into one of the following categories:
• Small cracks unassociated with herniation do not require treatment as the risk of permanent complications is small.
• Fractures involving up to one-third 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-third of the orbital floor will usually develop significant enophthalmos if left untreated.
• 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.
• A subgroup, the ‘white-eyed’ fracture, requires urgent repair to avoid permanent neuromuscular damage. This 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 which occurs 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 as the orbital floor often appears intact.
• Early marked enophthalmos may also be an indication for urgent repair.
3 Technique of surgical repair
a A transconjunctival or subciliary incision is made (Fig. 21.6A).
b The periosteum is elevated from the floor of the orbit and all entrapped orbital contents are removed from the antrum (Fig. 21.6B).
c The defect in the floor is repaired by using synthetic material such as Supramid®, silicone or Teflon® (Fig. 21.6C).
d The periosteum is sutured (Fig. 21.6D).
image

Fig. 21.6 Technique of repair of an orbital floor blow-out fracture

Blow-out medial wall fracture

Medial wall orbital fractures are usually associated with floor fractures; isolated fractures are less common.

1 Signs
• Periorbital ecchymosis (Fig. 21.7A) and frequently subcutaneous emphysema, which typically develops on blowing the nose.
• Defective ocular motility involving abduction (Fig. 21.7B) and adduction (Fig. 21.7C), if the medial rectus muscle is entrapped in the fracture.
2 CT will show the extent of damage (Fig. 21.7D).
3 Treatment involves release of entrapped tissue and repair of the bony defect.
image

Fig. 21.7 Blowout fracture of the left medial wall and floor. (A) Periorbital haematoma and ptosis; (B) defective left abduction; (C) defective left adduction; (D) CT coronal view shows fractures of the medial wall (red arrow) and floor (white arrow)

(Courtesy of A Pearson)

Roof fracture

Roof fractures are rarely encountered by ophthalmologists. Isolated fractures, caused by falling on a sharp object (Fig. 21.8) or a blow to the brow or forehead, are most common in children. Complicated fractures, caused by major trauma with associated displacement of the orbital rim or significant disturbance of other craniofacial bones, typically affect adults.

1 Presentation is with a haematoma of the upper eyelid and periocular ecchymosis which develop after a few hours and may later spread to the opposite side (see Fig. 21.1C).
2 Signs
• Inferior or axial displacement of the globe.
• Large fractures may be associated with pulsation of the globe, best detected on applanation tonometry, due to transmission of CSF pressure.
3 Treatment
• Small fractures may not require treatment but it is important to exclude a CSF leak as this carries a risk of meningitis.
• Sizeable bony defects with downward displacement of fragments usually require reconstructive surgery.
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image

Fig. 21.8 Pre-operative image of a patient with a roof fracture caused by a ball-point pen

(Courtesy of R Bates)

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 (Fig. 21.9).

image

Fig. 21.9 Lateral wall fracture. (A) Severe facial trauma; (B) CT axial view shows a left lateral wall fracture

(Courtesy of A Pearson)

Trauma to the globe

Introduction

Definitions

1 Closed injury is commonly due to blunt trauma. The corneoscleral wall of the globe is intact.
2 Open injury involves a full-thickness wound of the corneoscleral envelope.
3 Contusion is a closed injury resulting from blunt trauma. Damage may occur at or distant to the site of impact.
4 Rupture is 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.
5 Laceration is a full-thickness defect in the eye wall produced by a tearing injury, usually as the result of a direct impact.
6 Lamellar laceration is a partial-thickness laceration.
7 Incised injury is caused by a sharp object such as glass or a knife.
8 Penetrating injury refers to a single full-thickness wound, usually caused by a sharp object, without an exit wound. A penetrating injury may be associated with intraocular retention of a foreign body.
9 Perforation consists of two full-thickness wounds, one entry and one exit, usually caused by a missile.

Principles of evaluation

1 Initial assessment should be performed in the following order:
a Determination of the nature and extent of any life-threatening problems.
b History of the injury, including the circumstances, timing and likely object.
c Thorough examination of the eyes and the orbits.
2 Special investigations
a Plain radiographs may be taken when a foreign body is suspected (Fig. 21.10A).
b CT is superior to plain radiography in the detection and localization of intraocular foreign bodies (Fig. 21.10B). It is also of value in determining the integrity of intracranial, facial and intraocular structures.
c MR is more accurate than CT in the detection and assessment of injuries of the globe itself such as an occult posterior rupture, though not for bony injury. MRI should never be performed if the presence of a ferrous metallic foreign body is suspected.
d US may be useful in the detection of intraocular foreign bodies (Fig. 21.10C), globe rupture, suprachoroidal haemorrhage and retinal detachment; it should be performed as gently as possible if there is a risk of an open globe injury, strictly avoiding any pressure on the globe. It is also helpful in planning surgical repair, for example regarding placement of infusion ports during vitrectomy and whether drainage of suprachoroidal haemorrhage is required.
e Electrodiagnostic tests may be useful in assessing the integrity of the optic nerve and retina, particularly if some time has passed since the original injury and there is suspicion of a retained intraocular foreign body.
image

Fig. 21.10 Imaging of foreign bodies. (A) Plain radiograph shows an air gun pellet; (B) CT axial view shows a left intraocular foreign body; (C) US shows an intraocular foreign body

Blunt trauma

The most common causes of blunt trauma are squash balls, elastic luggage straps and champagne corks. Severe blunt trauma to the globe results in anteroposterior compression with simultaneous expansion in the equatorial plane (Fig. 21.11) associated with a transient but severe increase in intraocular pressure. 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. The extent of ocular damage depends on the severity of trauma and tends largely to be concentrated to either anterior or posterior segment. Apart from obvious ocular damage, blunt trauma commonly results in long-term effects; the prognosis is therefore necessarily guarded.

image

Fig. 21.11 Pathogenesis of ocular damage by blunt trauma

Corneal

1 Corneal abrasion involves a breach of the epithelium (Fig. 21.12A), which stains with fluorescein (Fig. 21.12B). If over the pupillary area, vision may be grossly impaired. Details of treatment are discussed under ‘recurrent corneal epithelial erosions’ in Chapter 6.
2 Acute corneal oedema may develop, secondary to focal or diffuse dysfunction of the corneal endothelium. It is commonly associated with folds in Descemet membrane and stromal thickening (Fig. 21.12C), but usually clears spontaneously.
3 Tears in Descemet membrane are usually vertical and most commonly arise as the result of birth trauma (Fig. 21.12D).
image

Fig. 21.12 Corneal complications of blunt trauma. (A) Small unstained corneal abrasion; (B) large abrasion stained with fluorescein: (C) stromal oedema and folds in Descemet membrane; (D) tears in Descemet membrane

(Courtesy of R Curtis – fig. D)

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Hyphaema

1 Signs
• Hyphaema (haemorrhage into the anterior chamber) is a common complication.
• The source of the bleeding is the iris or ciliary body (Fig. 21.13A).
• Characteristically, the red blood cells sediment inferiorly with a resultant ‘fluid level’ (Fig. 21.13B), except when the hyphaema is total (Fig. 21.13C).
2 Treatment is aimed at prevention of secondary haemorrhage and control of any elevation of intraocular pressure that may result in corneal blood staining (Fig. 21.13D). Details of treatment are described in Chapter 10 under ‘traumatic glaucoma’.
image

Fig. 21.13 Traumatic hyphaema. (A) Bleeding from the ciliary body; (B) small hyphaema; (C) total hyphaema; (D) corneal blood staining

(Courtesy of R Curtis – fig. A; Krachmer, Mannis and Holland, from Cornea, Mosby 2005 – fig. D)

Anterior uvea

The anterior uvea may sustain structural and/or functional damage.

1 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 – Fig. 21.14A). 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 (Fig. 21.14B).
2 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 (Fig. 21.14C). 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 a cataract surgical incision.
3 Ciliary body (see below).
image

Fig. 21.14 Iris complications of blunt trauma. (A) Vossius ring; (B) radial sphincter tears; (C) iridodialysis

Intraocular pressure

It is important for IOP to be monitored carefully, particularly in the early period following trauma. Elevation can occur for a variety of reasons including hyphaema (above) and inflammation (see Ch. 10). In contrast, the ciliary body may react to severe blunt trauma by temporary cessation of aqueous secretion (‘ciliary shock’) resulting in hypotony; it is important for an occult open injury to be excluded as the cause of the hypotony. Tears extending into the face of the ciliary body (angle recession) are associated with a risk of later glaucoma.

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Lenticular

1 Cataract formation is a common sequel to blunt trauma. Postulated mechanisms include traumatic damage to the lens fibres themselves, and minute ruptures in the lens capsule with influx of aqueous humour, hydration of lens fibres and consequent opacification. 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 (Fig. 21.15A) which may subsequently disappear, remain stationary or progress to maturity. Cataract surgery may be necessary for visually significant opacity.
2 Subluxation of the lens may occur, secondary to tearing of the suspensory ligament. 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. The edge of a subluxated lens may be visible under mydriasis and trembling of the iris (iridodonesis) or lens (phakodonesis) may be seen on ocular movement. Subluxation of magnitude sufficient to render the pupil partly aphakic (Fig. 21.15B) may result in uniocular diplopia; lenticular astigmatism due to tilting may occur.
3 Dislocation due to 360° rupture of the zonular fibres is rare and may be into the vitreous, or less commonly, into the anterior chamber (Fig. 21.15C); an underlying predisposing condition should be suspected.
image

Fig. 21.15 Lens complications of blunt trauma. (A) Flower-shaped cataract; (B) inferior subluxation; (C) dislocation into the anterior chamber

(Courtesy of C Barry – fig. B)

Globe rupture

Rupture of the globe may result from severe blunt trauma. 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 (Fig. 21.16); an anterior rupture may be masked by extensive subconjunctival haemorrhage. 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 intraocular pressure 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 intraocular foreign body. The principles of scleral rupture repair are described later.

image

Fig. 21.16 Ruptured globe

Vitreous haemorrhage

Vitreous haemorrhage may occur, often 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 a careful retinal assessment.

Commotio retinae

Commotio retinae is caused by concussion of the sensory retina resulting in cloudy swelling which gives the involved area a grey appearance. Commotio most frequently affects the temporal fundus (Fig. 21.17A). If the macula is involved, a ‘cherry-red spot’ may be seen at the fovea (Fig. 21.17B). Severe involvement may be associated with intraretinal haemorrhage, sometimes affecting the macula. The prognosis in mild cases is good with spontaneous resolution within 6 weeks. Sequelae to more severe commotio may include progressive pigmentary degeneration and macular hole formation (Fig. 21.17C).

image

Fig. 21.17 Commotio retinae. (A) Peripheral; (B) central; (C) macular hole following resolution

(Courtesy of C Barry – fig. C)

Choroidal rupture

Choroidal rupture involves the choroid, Bruch membrane and retinal pigment epithelium (RPE); 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 (Fig. 21.18A), 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 (Fig. 21.18B) which may result in haemorrhage, scarring and further visual deterioration.

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Fig. 21.18 Choroidal rupture. (A) Acute with subretinal haemorrhage; (B) old with secondary choroidal neovascularization

(Courtesy of J Donald M Gass, from Stereoscopic Atlas of Macular Diseases, Mosby 1997 – fig. B)

Retinal breaks and detachment

Trauma is responsible for about 10% of all cases of retinal detachment (RD) and is the most common cause in children, particularly boys. A great variety of breaks may develop in traumatized eyes either at the time of impact or subsequently.

1 Dialysis is a break occurring at the ora serrata, and is caused by traction of the relatively inelastic vitreous gel along the posterior aspect of the vitreous base with tearing of the retina. This may be associated with avulsion of the vitreous base, giving rise to a ‘bucket-handle’ appearance (Fig. 21.19A) which comprises 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 (Fig. 21.19B). Although they occur at the time of injury they do not inevitably result in RD. In cases that detach, subretinal fluid frequently may not develop until several months later, and progression is typically slow.
2 Equatorial breaks (Fig. 21.19C) are less frequent and are due to direct retinal disruption at the point of scleral impact.
3 Macular holes may occur either at the time of injury or following resolution of commotio retinae (see Fig. 21.17C).
image

Fig. 21.19 (A) Dialysis; (B) avulsion of the vitreous base; (C) equatorial breaks

(Courtesy of C Barry – fig. A; P Rosen – fig. B; S Milewski – fig. B)

Optic nerve

1 Traumatic optic neuropathy (TON) presents following ocular, orbital or head trauma as sudden visual loss which cannot be explained by other ocular pathology. It occurs in up to 5% of cases of facial fracture.
a Classification. Injury can be (a) direct, due to blunt or sharp optic nerve damage from a foreign body such as a projectile, or (b) indirect, occurring secondarily to impacts upon the eye, orbit or other cranial structures.
b Mechanisms include 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.
c Presentation. Though major head injury is not unusual, associated trauma may be deceptively minor. Vision is often very poor from the outset, with only perception of light (PL) 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.
d Investigation. Assessment should be individualized. Some clinicians request CT, MR or both for all cases, others limit imaging to patients with visual decline. CT is superior for the demonstration of optic canal fracture, but MRI for soft tissue changes (e.g. haematoma); very thin sections are recommended.
e 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. Several treatments have been advocated but no clear benefit has been shown, and all carry significant risks.
• 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.
• Optic nerve decompression (e.g. endonasal, transethmoidal) may be advocated in some circumstances such as ongoing deterioration despite steroids, or bilateral visual loss. Compression by bony fragment or haematoma may also be an indication; however, optic canal fracture is a poor prognostic indicator and there is no evidence that surgery improves the outlook.
• Optic nerve sheath fenestration has been tried in some centres.
2 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 (Fig. 21.20). There is no treatment; the visual prognosis depends on whether avulsion is partial or complete.
image

Fig. 21.20 Optic nerve avulsion

(Courtesy of J Donald M Gass, from Stereoscopic Atlas of Macular Diseases, Mosby 1997)

Shaken baby syndrome

Shaken baby syndrome (non-accidental head injury, abusive head trauma) is a form of physical abuse occurring typically in children under the age of 2 years. Mortality is more than 25%, and it is responsible for up to 50% of deaths from child abuse. It is caused principally by violent shaking, often in association with impact injury to the head, and should be considered in conjunction with a specialist paediatrician whenever characteristic ophthalmic features are identified. The pattern of injury results from rotational acceleration and deceleration of the head, in contrast to the linear forces generated by falls. It is thought that direct trauma is not the main mechanism of brain damage; brainstem traction injury causes apnoea, consequent hypoxia leading to raised intracranial pressure and ischaemia.

1 Presentation is frequently with irritability, lethargy and vomiting which may be initially misdiagnosed as gastroenteritis or other infection because the history of injury is withheld.
2 Systemic features may include signs of impact head injury, ranging from skull fractures to soft tissue bruises (Fig. 21.21A); subdural and subarachnoid haemorrhage is common and many survivors suffer substantial neurological handicap. Multiple rib and long bone fractures may be present. In some cases, examination findings are limited to the ocular features.
3 Ocular features are many and varied. The most important are:
• Retinal haemorrhages, bilateral or unilateral (20%), are the most common feature. The haemorrhages typically involve multiple layers and may also be pre- or subretinal (Fig. 21.21B). They are most obvious in the posterior pole, but often extend to the periphery.
• Periocular bruising and subconjunctival haemorrhages.
• Poor visual responses and afferent pupillary defects.
• Visual loss occurs in about 20% of cases, largely as a result of cerebral damage.
image

Fig. 21.21 Shaken baby syndrome. (A) Facial bruising; (B) fundus haemorrhages involving different levels

(Courtesy of R Bates)

Penetrating trauma

Causes

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Penetrating injuries are three times more common in males than females, and typically occur in a younger age group (50% aged 15–34). The most frequent causes are assault, domestic and occupational accidents, and sport. The extent of the injury is determined by the size of the object, its speed at the time of impact and its composition. Sharp objects such as knives cause well-defined lacerations of the globe. However, the extent of damage caused by flying foreign bodies is determined by their kinetic energy. For example, an air gun pellet is large and although relatively slow-moving has a high kinetic energy and can thus cause considerable ocular damage. In contrast, a fast-moving fragment of shrapnel has a low mass and therefore will cause a well-defined laceration with relatively less intraocular damage than an air gun pellet. 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. Any eye with an open injury should be covered by a protective eye shield upon diagnosis.

Corneal

The technique of primary repair depends on the extent of the wound and associated complications such as iris incarceration, flat anterior chamber and damage to intraocular contents.

1 Small shelving wounds (Fig. 21.22A) with formed anterior chamber may not require suturing as they often heal spontaneously or with the aid of a soft bandage contact lens.
2 Medium-sized wounds usually require suturing, especially if the anterior chamber is shallow or flat (Fig. 21.22B). 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.
3 With iris involvement (Fig. 21.22C) wounds usually require iris abscission.
4 With lens damage (Fig. 21.22D) wounds are treated by suturing the laceration and 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.
image

Fig. 21.22 Penetrating corneal wounds. (A) Small shelving with formed anterior chamber; (B) with flat anterior chamber; (C) with iris involvement; (D) with lens damage

(Courtesy of R Bates – fig. D)

Scleral

1 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 (Fig. 21.23A) and vitreous incarceration (Fig. 21.23B). The latter, unless appropriately managed, may result in subsequent fibrous proliferation along the plane of incarcerated vitreous (Fig. 21.23C) and tractional retinal detachment. Every attempt should be made to reposit viable uveal tissue and cut prolapsed vitreous flush with the wound. Use 8-0 nylon or 7-0 absorbable material such as polyglactin (Vicryl) should be used for scleral suturing in this setting.
2 Posterior scleral lacerations are frequently associated with retinal damage. Primary repair of the sclera should be the initial priority, with later vitreoretinal assessment.
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Fig. 21.23 Penetrating scleral wounds. (A) Anterior circumferential scleral laceration with iridociliary prolapse; (B) radial anterior scleral laceration with ciliary and vitreous prolapse; (C) fibrous proliferation

(Courtesy of Wilmer Institute – fig. A; EM Eagling and MJ Roper-Hall, from Eye Injuries, Butterworths 1986 – fig. B)

Retinal detachment

Traumatic tractional retinal detachment may result from vitreous incarceration in the wound and the presence of blood within the vitreous gel which acts as a stimulus to fibroblastic proliferation along the planes of incarcerated vitreous (Fig. 21.24A). The contraction of such anterior epiretinal membranes leads to a shortening and a rolling effect on the peripheral retina in the region of the vitreous base and eventually to an anterior tractional retinal detachment (Fig. 21.24B). A retinal break may develop several weeks later leading to a sudden extension of subretinal fluid and consequent visual loss.

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Fig. 21.24 Pathogenesis of traumatic tractional retinal detachment. (A) Penetrating injury resulting in vitreous prolapse and vitreous haemorrhage; (B) subsequent vitreoretinal proliferation and traction resulting in retinal detachment

Superficial foreign bodies

Subtarsal

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Small foreign bodies such as particles of steel, coal or sand often impact on the corneal or conjunctival surface. They may be washed along the tear film into the lacrimal drainage system or adhere to the superior tarsal conjunctiva (Fig. 21.25A) in the subtarsal sulcus and abrade the cornea with every blink, when a pathognomonic pattern of linear corneal abrasions may be seen (Fig. 21.25B).

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Fig. 21.25 (A) Subtarsal foreign body; (B) linear abrasions stained with fluorescein; (C) corneal foreign body with surrounding cellular infiltration

(Courtesy of R Fogla – fig. C)

Corneal

1 Clinical features. Corneal foreign bodies are extremely common and cause considerable irritation. Leukocytic infiltration may also develop around any foreign body of some duration (Fig. 21.25C). If a foreign body is allowed to remain, there is a significant risk of secondary infection and corneal ulceration. Mild secondary uveitis is common with irritative miosis and photophobia. Ferrous foreign bodies of even a few hours’ duration often result in rust staining of the bed of the abrasion. Any discharge, infiltrate, or significant uveitis should raise suspicion of secondary bacterial infection; subsequent management should be as for a corneal ulcer. Metallic foreign bodies are often sterile, perhaps due to acute rise in temperature during transit through the air; organic and stone foreign bodies carry a higher risk of infection.
2 Management
a Careful slit-lamp examination is essential to locate the exact position and depth of the foreign body.
b The foreign body is removed under slit lamp visualization using a sterile 26-gauge needle.
c Magnetic removal may be useful for a deeply embedded metallic foreign body.
d A residual ‘rust ring’, is easiest to remove with a sterile ‘burr’, if available.
e Antibiotic ointment is instilled together with a cycloplegic and/or typical NSAIDs to promote comfort.

Intraocular foreign bodies

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An intraocular foreign body (IOFB) may traumatize the eye mechanically, introduce infection or exert other toxic effects on the intraocular structures. Once in the eye, the foreign body may lodge in any of the structures it encounters; thus it may be located anywhere from the anterior chamber to the retina and choroid (Fig. 21.26). Notable mechanical effects include cataract formation secondary to capsular injury, vitreous liquefaction, and retinal haemorrhages and tears. Stone and organic foreign bodies are associated with a higher rate of infection, and this is particularly high with soil-contaminated or vegetable matter, when prophylaxis with intravitreal antibiotics is required. Many substances including glass, many plastics, gold and silver are inert. However, iron and copper may undergo dissociation and result in siderosis and chalcosis respectively.

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Fig. 21.26 Intraocular foreign bodies. (A) In the lens; (B) in the angle; (C) in the anterior vitreous; (D) on the retina with associated preretinal haemorrhage

(Courtesy of R Curtis – fig. B: EM Eagling and MJ Roper-Hall, from Eye Injuries, Butterworths 1986 – fig. D)

Initial management

1 Accurate history is vital to determine the origin of the foreign body. It may be helpful for the patient to bring any causative objects such as a chisel.
2 Examination is performed, paying special attention to possible sites of entry or exit. Topical fluorescein may be helpful to identify an entry wound. Alignment and projection of identified wounds may allow logical deduction of the probable location of a foreign body. Gonioscopy and fundoscopy must be performed. Associated signs such as lid laceration and damage to anterior segment structures must be noted.
3 CT with axial and coronal cuts is used to detect and localize a metallic intraocular FB (see Fig. 21.10B), providing cross-sectional images with a sensitivity and specificity that is superior to plain radiography and ultrasonography.
4 MR is contraindicated in the context of a metallic (specifically ferrous) intraocular foreign body.

Technique of removal

1 Magnetic removal of ferrous foreign bodies involves the creation of a sclerotomy adjacent to the foreign body, with application of a magnet followed by cryotherapy to the retinal break. Scleral buckling may be performed to reduce the risk of retinal detachment if this is judged to be high.
2 Forceps removal may be used for non-magnetic foreign bodies and magnetic foreign bodies that cannot be safely removed with a magnet. It involves pars plana vitrectomy and removal of the foreign body with forceps either through the pars plana or limbus (Fig. 21.27) depending on its size.
3 Prophylaxis against infection (see below).
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Fig. 21.27 Removal of foreign body through the limbus

(Courtesy of A Desai)

Siderosis

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Steel is the most common foreign body constituent, typically projected into the eye by hammering or power tool use. A ferrous IOFB undergoes dissociation resulting in the deposition of iron in the intraocular epithelial structures, notably the lens epithelium, iris and ciliary body epithelium and the sensory retina, where it exerts a toxic effect on cellular enzyme systems, with resultant cell death.

1 Signs include anterior capsular cataract, consisting of radial iron deposits on the anterior lens capsule (Fig. 21.28A) and reddish brown staining of the iris (Fig. 21.28B) that may give rise to heterochromia iridis (Fig. 21.28C).
2 Complications include secondary glaucoma due to trabecular damage, and pigmentary retinopathy followed by atrophy of the retina and RPE (Fig. 21.28D), which can have a profound effect on vision. Electroretinography shows progressive attenuation of the b-wave over time.
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Fig. 21.28 Siderosis oculi. (A) Lenticular deposits; (B) severe iris involvement and advanced cataract; (C) heterochromia iridis; (D) atrophy of the retina and RPE

(Courtesy of W Lisch – fig. A; J Donald M Gass, from Stereoscopic Atlas of Macular Diseases, Mosby 1997 – fig. D)

Chalcosis

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The ocular reaction to an intraocular foreign body with a high copper content involves a violent endophthalmitis-like picture, often with progression to phthisis bulbi. On the other hand, an alloy such as brass or bronze, with a relatively low copper content, results in chalcosis. Electrolytically-dissociated copper becomes deposited intraocularly, resulting in a picture similar to that seen in Wilson disease. Thus a Kayser–Fleischer ring develops, as does an anterior ‘sunflower’ cataract. Retinal deposition results in golden plaques visible ophthalmoscopically. Since copper is less retinotoxic than iron, degenerative retinopathy does not develop and visual function may be preserved.

Enucleation

Primary enucleation should be performed only for very severe injuries, with no prospect of retention of vision when it is impossible to repair the sclera (see Fig. 21.16). Secondary enucleation may be considered following primary repair if the eye is severely and irreversibly damaged, particularly if it is also unsightly and uncomfortable. The time delay also allows the patient valuable time to mentally and emotionally adapt to the prospect of losing an eye. Based on anecdotal evidence, it has been recommended that enucleation should be performed within 10 days of the original injury in order to prevent the very remote possibility of sympathetic ophthalmitis (see Ch. 11). However, objective evidence for this is lacking.

Bacterial endophthalmitis

Endophthalmitis develops in about 8% of cases of penetrating trauma with retained foreign body.

1 Risk factors include delay in primary repair, retained intraocular foreign body, and the position and extent of the laceration. Clinical signs are the same as acute postoperative endophthalmitis (see Ch. 9).
2 Pathogens. Staphylococcus spp. and Bacillus spp. are isolated from about 90% of culture-positive cases.
3 Management
a Prophylaxis
• Ciprofloxacin 750 mg b.d. or moxifloxacin 400 mg daily is given for open globe injuries, together with topical antibiotic, steroid and cycloplegia.
• Prompt removal of retained intraocular foreign bodies.
• Intravitreal antibiotics for high-risk cases (e.g. agricultural injuries).
b Culture of removed intraocular foreign bodies (do not stick them in the clinical notes!).
c Treatment for established cases is the same as for acute bacterial endophthalmitis (see Ch. 9).

Chemical injuries

Causes

Chemical injuries range in severity from the trivial to the potentially blinding. The majority are accidental, and a few due to assault. Two-thirds of accidental burns occur at work and the remainder at home. Alkali burns are twice as common as acid burns since alkalis are more widely used both at home and in industry. The severity of a chemical injury is related to the properties of the chemical, the area of affected ocular surface, duration of exposure (including retention of particulate chemical on the surface of the globe or under the upper lid) and related effects such as thermal damage. Alkalis tend to penetrate more deeply than acids, as the latter coagulate surface proteins, forming a protective barrier. The most common involved alkalis are ammonia, sodium hydroxide and lime. The commonest acids implicated are sulphuric, sulphurous, hydrofluoric, acetic, chromic and hydrochloric. Ammonia and sodium hydroxide may produce severe damage because of rapid penetration. Hydrofluoric acid used in glass etching and cleaning also tends to rapidly penetrate the eye, whilst sulphuric acid may be complicated by thermal effects and high velocity impact after car battery explosions.

Pathophysiology

1 Damage by severe chemical injuries occurs in the following order:
• Necrosis of the conjunctival and corneal epithelium with disruption and occlusion of the limbal vasculature. Loss of limbal stem cells may result in conjunctivalization and vascularization of the corneal surface, or persistent corneal epithelial defects with sterile corneal ulceration and perforation. Other long-term effects include ocular surface wetting disorders, symblepharon formation and cicatricial entropion.
• Deeper penetration causes the breakdown and precipitation of glycosaminoglycans and stromal corneal opacification.
• Anterior chamber penetration results in iris and lens damage.
• Ciliary epithelial damage impairs secretion of ascorbate which is required for collagen production and corneal repair.
• Hypotony and phthisis bulbi may ensue in severe cases.
2 Healing of the corneal epithelium and stroma takes place as follows:
• The epithelium heals by migration of epithelial cells which originate from limbal stem cells.
• Damaged stromal collagen is phagocytosed by keratocytes and new collagen is synthesized.
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Management

Emergency treatment

A chemical burn is the only eye injury that requires emergency treatment without first taking a history and performing a careful examination. Immediate treatment is as follows:

1 Copious irrigation is crucial to minimize duration of contact with the chemical and normalize the pH in the conjunctival sac as soon as possible, and the speed and efficacy of irrigation is the most important prognostic factor following chemical injury. A sterile balanced buffered solution, such as normal saline or Ringer lactate should be used to irrigate the eye for 15–30 minutes or until pH is neutral (tap water should be used if necessary to avoid any delay). A topical anaesthetic should be instilled prior to irrigation, as this dramatically improves comfort and facilitates cooperation. A lid speculum may be helpful.
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2 Double-eversion of the upper eyelid should be performed so that any retained particulate matter trapped in the fornices is identified and removed.
3 Debridement of necrotic areas of corneal epithelium should be performed to promote re-epithelialization and remove associated chemical residue.
4 Admission to hospital will usually be required for severe injuries (grade 4 ± 3) in order to ensure adequate eye drop instillation in the early stages.

Grading of severity

Acute chemical injuries are graded to plan appropriate subsequent treatment and afford an indication of likely ultimate prognosis. Grading is performed on the basis of corneal clarity and severity of limbal ischaemia (Roper-Hall system); the latter is assessed by observing the patency of the deep and superficial vessels at the limbus (Fig. 21.29A).

Grade 1 is characterized by clear cornea (epithelial damage only) and no limbal ischaemia (excellent prognosis).
Grade 2 shows hazy cornea but with visible iris details (Fig. 21.29B) and less than one-third of the limbus being ischaemic (good prognosis).
Grade 3 manifests total loss of corneal epithelium, stromal haze obscuring iris details (Fig. 21.29C) and between one-third and half limbal ischaemia (guarded prognosis).
Grade 4 shows opaque cornea (Fig. 21.29D) and more than half limbal ischaemia (very poor prognosis).
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Fig. 21.29 Chemical burns. (A) Limbal ischaemia; (B) grade 2 – corneal haze but visible iris details; (C) grade 3 – corneal haze obscuring iris details; (D) grade 4 – total corneal opacification

Other features to note at initial assessment are the extent of corneal and conjunctival epithelial loss, iris changes, status of the lens and intraocular pressure.

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Medical treatment

Most mild (grade 1 and 2) injuries are treated with topical antibiotic ointment for about a week, with topical steroids and cycloplegics if necessary. The main aims of treatment of more severe burns are to reduce inflammation, promote epithelial regeneration and prevent corneal ulceration. For moderate-severe injuries, preservative-free drops should be used.

1 Steroids reduce inflammation and neutrophil infiltration, and address anterior uveitis. However, they also impair stromal healing by reducing collagen synthesis and inhibiting fibroblast migration. For this reason topical steroids may be used initially (usually 4–8 times daily, strength depending on injury severity) but must be tailed off after 7–10 days when sterile corneal ulceration is most likely to occur. Steroids may be replaced by topical NSAIDs, which do not affect keratocyte function.
2 Cycloplegia may improve comfort.
3 Topical antibiotic drops are used for prophylaxis of bacterial infection (e.g. chloramphenicol q.i.d.).
4 Ascorbic acid reverses a localized tissue scorbutic state and improves wound healing, promoting the synthesis of mature collagen by corneal fibroblasts. Topical sodium ascorbate 10% is given 2-hourly in addition to a systemic dose of 1–2 g vitamin C (L-ascorbic acid) q.i.d. (not in patients with renal disease).
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5 Citric acid is a powerful inhibitor of neutrophil activity and reduces the intensity of the inflammatory response. Chelation of extracellular calcium by citrate also appears to inhibit collagenase. Topical sodium citrate 10% is given 2-hourly for about 10 days, and may also be given orally (2 g four times daily). The aim is to eliminate the second wave of phagocytes, which normally occurs about 7 days after the injury. Ascorbate and citrate can be tapered as the epithelium heals.
6 Tetracyclines are effective collagenase inhibitors and also inhibit neutrophil activity and reduce ulceration. They should be considered if there is significant corneal melting and can be administered both topically (tetracycline ointment q.i.d.) and systemically (doxycycline 100 mg b.d. tapering to once daily). Acetylcysteine 10% drops 6 times daily are an alternative topical anticollagenase agent.
7 Symblepharon formation should be prevented as necessary by lysis of developing adhesions with a sterile glass rod or damp cotton bud.
8 Monitor IOP and treat if necessary; oral acetazolamide is recommended.
9 Periocular skin injury may require a dermatology opinion.

Surgery

1 Early surgery may be necessary to promote revascularization of the limbus, restore the limbal cell population and re-establish the fornices. One or more of the following procedures may be used:
• Advancement of Tenon’s capsule and suturing to the limbus is aimed at re-establishing limbal vascularity thus preventing the development of corneal ulceration.
• Limbal stem cell transplantation from the patient’s other eye (autograft) or from a donor (allograft) is aimed at restoring normal corneal epithelium.
• Amniotic membrane grafting to promote epithelialization and suppression of fibrosis.
• Gluing or keratoplasty may be needed for actual or impending perforation.
2 Late surgery may involve the following procedures:
• Division of conjunctival bands (Fig. 21.30A) and treating symblepharon (Fig. 21.30B).
• Conjunctival or mucous membrane grafts.
• Correction of eyelid deformities (Fig. 21.30C).
• Keratoplasty should be delayed for at least 6 months and preferably longer to allow maximal resolution of inflammation.
• Keratoprosthesis (Fig. 21.30D) may be required in very severely damaged eyes because the results of conventional grafting are poor.
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Fig. 21.30 (A) Conjunctival bands; (B) symblepharon; (C) cicatricial entropion of the upper eyelid; (D) keratoprosthesis

(Courtesy of R Bates – fig. D)