Trauma PDF

Chapter Trauma 22 EYELID TRAUMA 908 TRAUMA TO THE GLOBE 913 CHEMICAL INJURIES 929 Periocular haematoma 908 Introduction 913 Introduction 929 Laceration 908...

Chapter Trauma 22 EYELID TRAUMA 908 TRAUMA TO THE GLOBE 913 CHEMICAL INJURIES 929 Periocular haematoma 908 Introduction 913 Introduction 929 Laceration 908 Blunt trauma 914 Aetiology 929 Penetrating trauma 923 Pathophysiology 929 ORBITAL TRAUMA 910 Enucleation/evisceration 925 Management 930 Orbital oor fracture 910 Supercial foreign body 926 Roof fracture 913 THERMAL BURNS 931 Intraocular foreign body 927 Blow-out medial wall fracture 913 Bacterial endophthalmitis 929 Lateral wall fracture 913 Orbital haemorrhage 913 907 908 Eyelid Trauma EYELID TRAUMA Periocular haematoma A ‘black eye’, consisting of a haematoma (focal collection of blood) and/or periocular ecchymosis (diuse bruising) and oedema (Fig. 22.1A), is the most common blunt injury to the eyelid or forehead and is generally innocuous. It is, however, critical to exclude the following more serious conditions:  Trauma to the globe or orbit. It is easier to examine the globe before the lids become oedematous. Once swelling is established, gentle sustained pressure to open the lids will often displace tissue fluid sufficiently to allow visualization of the anterior segment. It is critical not to apply any force on the globe itself until its integrity has been confirmed. A Urgent imaging such as computed tomography (CT), mag- netic resonance imaging (MRI) or bedside ultrasonogra- phy (taking meticulous care to avoid applying pressure on the globe) should be considered if there is suspicion of an underlying injury to the eyeball and adequate clinical visu- alization is not possible.  Orbital roof fracture, especially if the black eye is associated with a subconjunctival haemorrhage without a visible poste- rior limit (which would indicate the anterior extension of a posterior bleeding point) (Fig. 22.1B).  Basal skull fracture, which may give rise to characteristic bilateral ring haematomas (‘panda eyes’ – Fig. 22.1C). TIP Bilateral periocular haematoma (‘panda’ eyes) can be a sign of a skull-base fracture. B Laceration The presence of a lid laceration, however insignificant, man- dates careful exploration of the wound and examination of the globe and adnexal structures. Any lid defect should be repaired by direct closure whenever possible, even under tension, since this affords the best functional and cosmetic result (Fig. 22.2A and B).  Supercial lacerations parallel to the lid margin without gap- ing can be sutured with 6-0 black silk or nylon. e sutures are removed aer 5–6 days.  Infection is always a risk, even from a small laceration (Fig. 22.2C).  Lid margin lacerations invariably gape without careful closure and to prevent notching must be sutured with optimal align- ment (see Fig. 2.57C): { A 5-0 silk vertical mattress suture is inserted in line with C the meibomian gland orices, about 2 mm from the wound edges and 2 mm deep and le untied. Fig. 22.1 (A) Lower lid haematoma with subconjunctival haem- { Tarsal plate edges are brought together with partial- orrhage; (B) subconjunctival haemorrhage with no visible thickness lamellar 5-0 absorbable (e.g. polyglactin) sutures, posterior limit; (C) ‘panda eyes’. which are tied anteriorly. { e lid margin silk suture is then tied so that the cut edges e overlying skin is closed with interrupted 6-0 or 7-0 nylon slightly pucker the wound. e ends are le fairly long, e.g. or absorbable sutures, securing the ends of the silk suture to direct 2 cm. these and its knot away from the cornea.  CHAPTER Trauma 22 909 A A B Fig. 22.3 (A) Lower lid laceration involving the canaliculus (arrow); (B) monocanalicular silicone stent needed to bridge the laceration. B  Lacerations with extensive tissue loss may require major reconstructive procedures similar to those used following resection of malignant tumours (see Ch. 2).  Canalicular lacerations should be repaired within 24 hours (Fig. 22.3A). e laceration is bridged by silicone tubing (Crawford tube), which is threaded down the lacrimal system and tied in the nose, following which the laceration is sutured. Alternatively, repair of a single canaliculus can be performed using a monocanalicular stent (e.g. Mini Monoka – Fig. 22.3B) and, if necessary, suturing its footplate to the lid using 8-0 material. e tubing is le in situ for 3–6 months.  Tetanus status. Ensure that the patient’s tetanus immunization status is satisfactory aer any injury. Without prior immuniza- tion, 250 units of human tetanus immunoglobulin are given intramuscularly (IM). If previously immunized but a booster has not been administered within the last 10 years, subcutane- ous tetanus toxoid should be given. C  Foreign body. If there is any suspicion of a foreign body in Fig. 22.2 (A) Lid laceration; (B) postoperative result; (C) orbital the so tissues of the lid or orbit (Fig. 22.4A and C), a CT scan cellulitis secondary to small laceration. should be undertaken (Fig. 22.4B and D).  Lacerations with mild tissue loss just sucient to pre- vent direct primary closure can usually be managed by TIP There is always a risk of orbital cellulitis after a penetrating lid laceration, particularly if there is a retained performing a lateral cantholysis in order to increase lateral foreign body. mobility. 910 Orbital Trauma A B C D Fig. 22.4 (A) Small upper lid laceration in a child showing the tip of a coloured pencil; (B) axial CT scan showing the broken tips (arrows); (C) penetrating injury to the left upper lid with an intact globe; (D) axial CT scan showing a retrobulbar glass shard. Diagnosis ORBITAL TRAUMA  Visual function, especially acuity, should be recorded and Orbital oor fracture monitored.  Periocular signs include variable ecchymosis, oedema (Fig. Introduction 22.5B) and occasionally subcutaneous emphysema (a crackling A blow-out fracture of the orbital oor is typically caused by a sud- sensation on palpation due to air in the subcutaneous tissues). den increase in the orbital pressure from an impacting object that  Infraorbital nerve anaesthesia involving the lower lid, cheek, is greater in diameter than the orbital aperture (about 5 cm), such side of nose, upper lip, upper teeth and gums is common as the as a st or tennis ball, so that the eyeball itself is displaced and fracture frequently involves the infraorbital canal. transmits rather than absorbs the impact (Fig. 22.5A). Since the  Diplopia may be caused by one of the following mechanisms: bones of the lateral wall and the roof are usually able to withstand { Haemorrhage and oedema in the orbit may cause tighten- such trauma, the fracture most frequently involves the oor of the ing of the septa connecting the inferior rectus and inferior orbit along the thin bone covering the infraorbital canal. Occa- oblique muscles to the periorbita, thus restricting move- sionally, the medial orbital wall may also be fractured. Fractures ment of the globe. Ocular motility usually improves as the of the orbital rim and adjacent facial bones require appropriately haemorrhage and oedema resolve. tailored management. Clinical features vary with the severity of { Diplopia typically occurs in both upgaze (Fig. 22.6A trauma and the interval between injury and examination. Care and C) and downgaze secondary to mechanical entrap- should be taken to ensure that a full evaluation for head and sys- ment within the fracture of the inferior rectus or inferior temic injury has been performed and any necessary interspecialty oblique muscle or adjacent connective tissue and fat (Fig. referrals initiated. 22.6D).  CHAPTER Trauma 22 911 A B Fig. 22.5 Orbital oor blow-out fracture. (A) Diagram to illustrate the mechanism; (B) marked periocular ecchymosis, oedema and subconjunctival haemorrhage. { Forced duction and the dierential intraocular pressure test (increasing IOP as a restricted muscle presses on the globe) are positive. Diplopia may subsequently improve if it is mainly due to entrapment of oedematous connec- tive tissue and fat, but usually persists if there is signicant involvement of the muscles themselves. A { Direct injury to an extraocular muscle, associated with a negative forced duction test. e muscle bres usually regenerate and normal function oen returns within about 2 months.  Enophthalmos (Fig. 22.6B) may be present if the fracture is severe, although it tends to manifest only after a few days as initial oedema resolves. Late enophthalmos is uncom- mon, even in large fractures. Six months after a large B orbital floor fracture only 20% will have enophthalmos of more than 2 mm.  Ocular damage (e.g. hyphaema, angle recession, retinal dialy- sis) should be excluded by careful examination of the globe, although this is relatively uncommon in association with a blow-out fracture.  Hess chart testing (Fig. 22.7) to map eye movements is useful in assessment and monitoring. C  CT with coronal sections (Fig. 22.8 and see Fig. 22.6D) aids in evaluation of the extent of a fracture and determination of the nature of maxillary antral so tissue densities, which may rep- resent prolapsed orbital fat, extraocular muscles, haematoma or unrelated antral polyps. Treatment  Initial treatment generally consists of observation, with the D prescription of oral antibiotics. Ice packs and nasal decon- gestants may be helpful. e patient should be instructed not Fig. 22.6 Orbital floor blow-out fracture. (A) Restricted ele- vation right eye; (B) mild right enophthalmos; (C) white to blow his or her nose, because of the possibility of forcing eye blow-out fracture of the left orbit in a child; (D) coro- infected sinus contents into the orbit. Systemic steroids are nal CT scan showing entrapment of the left inferior rectus occasionally required for severe orbital oedema, particularly if muscle. this is compromising the optic nerve. 912 Orbital Trauma Fig. 22.7 Hess chart of a left orbital oor blow-out fracture showing restriction of left upgaze (superior rectus and inferior oblique) and restriction on downgaze (inferior rectus). There is also secondary overaction of the right eye. { Fractures involving more than one-half of the orbital oor may develop enophthalmos if le untreated. { Fractures with entrapment of orbital contents, enophthal- mos of greater than 2 mm and/or persistent and signicant diplopia in the primary position should be repaired within 2 weeks. However, it has recently been reported that in patients with enophthalmos of less than 2 mm there is no dierence in outcome between those undergoing surgery at 2 weeks and those undergoing surgery aer 6 months. In patients with diplopia and tissue incarceration but with- out muscle entrapment, improvement oen occurs with- out surgery. If the diplopia persists, delayed surgery is still likely to achieve resolution of diplopia except in extreme upgaze.  ‘White-eyed’ fracture is a subgroup for which urgent repair is required to avoid permanent neuromuscular damage. e Fig. 22.8 CT of orbital oor blow-out fracture – coronal view showing a defect in the orbital oor and the ‘tear drop’ sign scenario is generally seen in patients less than 18 years of age, due to soft tissue prolapse into the maxillary antrum (arrow). typically with little visible external so tissue injury and usu- ally aects the orbital oor (see Fig. 22.6C). It involves the acute incarceration of herniated tissue in a ‘trap-door’ eect and occurs because of the greater elasticity of bone in younger  Subsequent treatment is aimed at the prevention of per- people (see Fig. 22.6D). Patients may experience acute nau- manent vertical diplopia and/or cosmetically unacceptable sea, vomiting, headache and persistent activation of the oculo- enophthalmos. cardiac reex can occur. CT features may be subtle. { Small cracks without herniation do not require treatment  Surgical repair is performed via a transconjunctival or sub- as the risk of permanent complications is small. ciliary incision or via the maxillary sinus, with elevation of { Fractures involving up to one-half of the orbital oor, with the periosteum from the orbital oor, freeing of trapped little or no herniation, no signicant enophthalmos and orbital contents and repair of the bony defect with a synthetic improving diplopia, also do not require treatment. implant.  CHAPTER Trauma 22 913 Roof fracture Introduction Roof fractures are rarely encountered by ophthalmologists. Iso- lated fractures, caused by falling on a sharp object or sometimes a relatively minor blow to the brow or forehead, are most common A in children and oen do not require treatment. Fractures due to major trauma, with associated displacement of the orbital rim or signicant disturbance of other craniofacial bones, typically aect adults. Diagnosis A haematoma of the upper eyelid is typical, together with peri- ocular ecchymosis. ese oen develop over the course of a few B hours and may progressively spread to the side opposite the frac- ture. Other features of orbital wall fracture as discussed above may Fig. 22.9 Blow-out fracture of the left medial wall and oor. be present. Large fractures may be associated with pulsation of the (A) Defective left abduction; (B) CT coronal view showing fractures of the medial wall (arrow) and oor (arrowhead). globe due to transmission of cerebrospinal uid (CSF) pressure, (Courtesy of A Pearson.) best detected with applanation tonometry. local anaesthetic block performed to facilitate intraocular surgery. Treatment Rare causes include bleeding from vascular anomalies and occa- Small fractures may not require treatment, but it is important to sionally spontaneous haemorrhage due to poor clotting. exclude a CSF leak, which carries a risk of meningitis. Sizeable bony defects with downward displacement of fragments usually Diagnosis warrant reconstructive surgery. General management is similar to Proptosis, eyelid oedema and ecchymosis, haemorrhagic chemo- that of an orbital oor fracture (see above). sis, ocular motility dysfunction, decreased visual acuity, elevated intraocular pressure, optic disc swelling and a relative aerent pupillary defect are among the possible signs. Blow-out medial wall fracture Medial wall orbital fractures are usually associated with oor frac- Treatment tures. It is uncommon to nd an isolated fracture of the medial Treatment should be started immediately if progressive visual wall. Signs include periorbital ecchymosis and frequently subcuta- deterioration occurs. Canthotomy alone is rarely adequate. neous emphysema, which typically develops on blowing the nose.  Canthotomy. Aer clamping the incision site for 60 seconds, Defective ocular motility involving abduction and adduction is scissors are used to make a 1–2 cm horizontal full-thickness present if the medial rectus muscle is entrapped. CT will demon- incision under local anaesthesia (e.g. 1–2 ml lidocaine 1–2% strate the fracture. Treatment involves release of incarcerated tis- with adrenaline) at the angle of the lateral canthus (Fig. sue and repair of the bony defect (Fig. 22.9). 22.10A).  Cantholysis. Following canthotomy, the lower lid is retracted downwards and the inferior crus of the lateral canthal tendon Lateral wall fracture is cut (Fig. 22.10B) using blunt-tipped scissors, directed infe- Acute lateral wall fractures (see Fig. 22.11D) are rarely encoun- riorly and inserted adjacent and parallel to the lateral orbital tered by ophthalmologists. Because the lateral wall of the orbit is rim between conjunctiva and skin and angled away from the more solid than the other walls, a fracture is usually associated eyeball. Blood is gently encouraged to drain. If necessary, the with extensive facial damage. superior limb of the tendon can also be cut, but this carries a substantial risk of damage to adnexal structures. Orbital haemorrhage TRAUMA TO THE GLOBE Introduction Introduction Orbital (retrobulbar) haemorrhage is important chiey due to the associated risk of acute orbital compartment syndrome with com- Terminology pressive optic neuropathy and can lead to irreversible blindness of  Closed injury is commonly due to blunt trauma. e corneo- the aected eye in severe cases. It can occur without or in associa- scleral wall of the globe is intact. tion with an orbital bony injury. Iatrogenic orbital haemorrhage  Open injury involves a full-thickness wound of the corneo- is not uncommon, typically resulting from a peri- or retrobulbar scleral envelope. 914 Trauma to the Globe A B Fig. 22.10 Surgical treatment of acute retrobulbar haemorrhage. (A) Lateral canthotomy (arrow showing anterior orbital rim); (B) disinsertion of inferior crus of the lateral canthal tendon.  Contusion is a closed injury resulting from blunt trauma. passed since the original injury and there is the suspicion of a Damage may occur at or distant to the site of impact. retained intraocular foreign body (IOFB).  Rupture is a full-thickness wound caused by blunt trauma. e globe gives way at its weakest point, which may not be at the TIP MRI scanning should not be undertaken if a ferrous site of impact. metallic foreign body is suspected in a patient with a  Laceration is a full-thickness defect in the eye wall produced penetrating injury. by a tearing injury, usually as the result of a direct impact.  Lamellar laceration is a partial-thickness laceration.  Incised injury is caused by a sharp object such as glass or a Blunt trauma knife. e most common causes of blunt trauma are sporting injuries  Penetrating injury refers to a single full-thickness wound, and assault. Severe blunt trauma to the globe results in anteropos- usually caused by a sharp object, without an exit wound. A terior compression with simultaneous expansion in the equato- penetrating injury may be associated with intraocular reten- rial plane (Fig. 22.12) oen associated with a transient but severe tion of a foreign body. increase in IOP. Although the impact is primarily absorbed by the  Perforation consists of two full-thickness wounds, one entry lens–iris diaphragm and the vitreous base, damage can also occur and one exit, usually caused by a missile. to the posterior pole. e extent of ocular damage depends on the severity of trauma. e prognosis varies, but is usually determined Investigation by the extent of retinal injury.  Plain radiographs may be taken when the presence of a for- eign body is suspected (Fig. 22.11A). A metallic foreign body Cornea which is within the eye will move up and down if the radio-  Corneal abrasion involves a breach of the epithelium (Fig. graphs are taken in upgaze and downgaze. 22.13A) and stains with uorescein (Fig. 22.13B). It is a pain-  Ultrasonography may be useful in the detection of intraocu- ful condition, exacerbated by ocular movement. If located lar foreign bodies, globe rupture, suprachoroidal haemorrhage over the pupillary area, vision may be signicantly impaired. and retinal detachment. It should be performed as gently as Details of treatment are discussed under ‘Recurrent corneal possible if there is a possibility of an open globe injury, taking epithelial erosion’ in Chapter 7 great care not to apply pressure on the globe.  Acute corneal oedema may develop following blunt trauma,  CT is superior to plain radiography in the detection and local- secondary to focal or diuse dysfunction of the endothelium ization of intraocular foreign bodies (Figs 21.11B–D). It is also and is sometimes seen underlying a large abrasion. It is com- of value in determining the integrity of intracranial, facial and monly associated with folds in Descemet membrane and stro- intraocular structures (see Fig. 22.11C). mal thickening, but usually clears spontaneously.  MRI is more accurate than CT in the detection and assessment  Tears in Descemet membrane are usually vertical (Fig. of injuries of the globe itself, such as an occult posterior rup- 22.13C) and most commonly arise as the result of birth trauma. ture, though not for bony injury. However, MRI should not be performed if a ferrous metallic foreign body is suspected. Hyphaema  Electrodiagnostic tests may be useful in assessing the integ- Hyphaema (haemorrhage in the anterior chamber) is a common rity of the optic nerve and retina, particularly if some time has complication of blunt ocular injury. e source of bleeding is  CHAPTER Trauma 22 915 A B C D Fig. 22.11 Imaging of ocular trauma. (A) Plain radiograph showing a lead air gun pellet; (B) axial CT showing a localized intraocular foreign body in the right eye; (C) 3-dimensional CT recon- struction of a facial shotgun injury; (D) coronal CT showing left lateral orbital wall fracture. (Courtesy of S Chen – gs B and C; A Pearson – g. D.) typically the iris root or ciliary body face. Characteristically, the blood settles inferiorly with a resultant ‘uid level’ (Fig. 22.14A), except when the hyphaema is total (Fig. 22.14B). Uncontrolled high IOP can result in ischaemic optic neuropathy and staining of the cornea (Fig. 22.14C) (see Ch. 11). Anterior uvea  Pupil. e iris may momentarily be compressed against the anterior surface of the lens by severe anteroposterior force, with resultant imprinting of pigment from the pupillary mar- gin. Transient miosis accompanies the compression, evidenced by the pattern of pigment corresponding to the size of the constricted pupil (Vossius ring – Fig. 22.15A). Damage to the iris sphincter may result in traumatic mydriasis, which can be temporary or permanent. e pupil reacts sluggishly or not at all to both light and accommodation. Radial tears in the pupil- lary margin are common (Fig. 22.15B).  Iridodialysis is a dehiscence of the iris from the ciliary body Fig. 22.12 Pathogenesis of ocular damage by blunt trauma. at its root. e pupil is typically D-shaped and the dialysis is 916 Trauma to the Globe A A B B C C Fig. 22.13 Corneal complications of blunt trauma. (A) Small un- Fig. 22.14 Traumatic hyphaema. (A) Small hyphaema from stained corneal abrasion; (B) large corneal abrasion stained a leaking vessel superiorly; (B) total hyphaema; (C) corneal with uorescein; (C) tears in Descemet membrane. (Courtesy blood staining due to sustained high intraocular pressure of C Barry – g. B.) associated with a total hyphaema. TIP If the intraocular pressure is low in the presence of a full hyphaema an occult posterior scleral rupture should be suspected.  CHAPTER Trauma 22 917 A B C D Fig. 22.15 Iris complications of blunt trauma. (A) Vossius ring; (B) radial sphincter tears; (C) iridodialysis; (D) retroillumination of iridodialysis. seen as a dark biconvex area near the limbus (Fig. 22.15C). Lens Retroillumination shows the extent of the injury (Fig.  Cataract formation is a common sequel to blunt trauma. Postu- 22.15D). An iridodialysis may be asymptomatic if it is lated mechanisms include direct damage to the lens bres them- covered by the upper lid. However, monocular diplopia selves and minute ruptures in the lens capsule with an inux of and glare sometimes ensue if the dehiscence is exposed aqueous humour, hydration of lens bres and consequent opaci- in the palpebral aperture. Traumatic aniridia (360° irido- cation. A ring-shaped anterior subcapsular opacity may underlie a dialysis) is rare. In a pseudophakic eye, the detached iris Vossius ring. Commonly opacication occurs in the posterior sub- may be ejected through the cataract surgical incision (Fig. capsular cortex along the posterior sutures, resulting in a ower- 22.16A). The symptoms of glare can be reduced and the shaped (‘rosette’) opacity (Fig. 22.18A) that may subsequently cosmetic appearance can be improved by inserting a pros- disappear, remain stationary or progress to maturity (Fig. 22.18B). thetic iris (Fig. 22.16B). Cataract surgery may be necessary for visually signicant opacity.  Ciliary body (see below).  Subluxation of the lens may occur, secondary to tearing of the suspensory ligament. A subluxated lens tends to deviate Intraocular pressure towards the meridian of intact zonules. e anterior chamber It is important for IOP to be monitored carefully, particularly in may deepen over the area of zonular dehiscence if the lens the early period following trauma (see Ch. 11). Elevation of IOP rotates posteriorly. e edge of a subluxated lens may be vis- can occur for a variety of reasons, including hyphaema and inam- ible under mydriasis (see Fig. 22.18B) and trembling of the iris mation. In the presence of hypotony, it is important to exclude an (iridodonesis) or lens (phakodonesis) may be seen on ocular occult open injury. Tears extending into the face of the ciliary body movement. Subluxation of magnitude sucient to render the (angle recession) are associated with a 6–9% risk of late glaucoma pupil partly aphakic may result in uniocular diplopia. Lenticu- (Fig. 22.17). lar astigmatism due to tilting may occur. 918 Trauma to the Globe A B Fig. 22.16 Traumatic aniridia in a pseudophakic eye. (A) Retroillumination showing lens implant and ciliary processes; (B) prosthetic iris. (Courtesy of C Barry.) is asymmetry of anterior chamber depth. e anterior chamber of an aected eye is classically deep, with posterior rotation of the iris–lens diaphragm and IOP in the aected eye is low. e rupture is oen found slightly behind the insertion of the rectus muscles where the sclera is thinnest. Gentle B-scan ultrasonogra- phy can demonstrate a posterior rupture, but CT or MRI may be necessary. e principles of repair of a rupture in the sclera are described later. Vitreous haemorrhage Vitreous haemorrhage may occur, commonly in association with posterior vitreous detachment. Pigment cells (‘tobacco dust’) can be seen oating in the anterior vitreous and though not necessar- ily associated with a retinal break, should always prompt careful retinal assessment. Fig. 22.17 Gonioscopic appearance of angle recession Commotio retinae (arrowheads indicate the extent of the recession). Commotio retinae is caused by concussion of the sensory retina resulting in cloudy swelling that gives the involved area a grey  Dislocation due to 360° rupture of the zonular bres is rare. appearance (Fig. 22.20A and B). It most frequently aects the tem- e lens may dislocate into the vitreous (Fig. 22.18C), or poral fundus. If the macula is involved, a ‘cherry-red spot’ may be less commonly, into the anterior chamber (Fig. 22.18D). An seen at the fovea. Severe involvement may be associated with intra- underlying predisposing condition such as pseudoexfoliation retinal haemorrhage that can involve the macula. e prognosis in should considered. mild cases is good, with spontaneous resolution in around 6 weeks. Severe commotio may result in progressive pigmentary degenera- Globe rupture tion (Fig. 22.20C) and macular hole formation. Rupture of the globe may result from severe blunt trauma. e prognosis is poor if the initial visual level is light perception Chorioretinitis sclopetaria or worse. e rupture is usually anterior, in the vicinity of the is term describes a closed globe injury that follows a high- Schlemm canal, with prolapse of structures such as the lens, velocity projectile passing into the orbit close to the outside of the iris, ciliary body and vitreous (Fig. 22.19A and B). An anterior globe. Deformation from the sudden force causes the chorioretinal rupture may be masked by extensive subconjunctival haemor- layers to split and retract leaving the intact sclera exposed (Fig. rhage. Rupture at the site of a surgical wound (e.g. cataract, kera- 21.20D). Complications include vitreous haemorrhage and, occa- toplasty, vitrectomy) commonly follows substantial blunt force. sionally, retinal detachment. e prognosis depends on the cause An occult posterior rupture can be associated with little visible of the injury (low muzzle energy has a worse prognosis than a high damage to the anterior segment, but should be suspected if there muzzle injury), the location of damage and whether the macula is  CHAPTER Trauma 22 919 A B C D Fig. 22.18 Lens complications of trauma. (A) Flower-shaped cataract; (B) dense traumatic cataract with ruptured anterior capsule and prolapsed lens contents; (C) dislocation into the vitreous in a pseudophakic eye with pseudoexfoliation (arrowheads show the edge of the capsule); (D) dislocation into the anterior chamber. A B Fig. 22.19 Ruptured globe. (A) Localized rupture with uveal prolapse and subconjunctival haemorrhage; (B) large corneal rupture with signicant prolapse of intraocular structures. (Courtesy of RSR Naik – g. A.) 920 Trauma to the Globe A B C D Fig. 22.20 Non-ruptured globe injuries. (A) Commotio retinae: acute peripheral cloudy swell- ing of the retina (arrows show the demarcation); (B) commotio retinae involving the macula; (C) 3 months after blunt injury in a dierent patient showing chorioretinal scarring and atrophy; (D) chorioretinitis sclopetaria showing bare sclera and chorioretinal scarring. involved. Most patients experience improvement of vision aer the Retinal breaks and detachment injury, but only 15% achieve 6/6 vision. Trauma is responsible for about 10% of all cases of retinal detach- ment (RD) and is the most common cause in children, particularly Choroidal rupture boys. A variety of breaks may develop in traumatized eyes either at Choroidal rupture involves the choroid, Bruch membrane and the time of impact or subsequently. retinal pigment epithelium (RPE). It may be direct or indi-  A retinal dialysis (Fig. 22.22A) is a break occurring at the ora rect. Direct ruptures are located anteriorly at the site of impact serrata, caused by traction from the relatively inelastic vitre- and run parallel with the ora serrata. Indirect ruptures occur ous gel along the posterior aspect of the vitreous base. e tear opposite the site of impact. e visual prognosis is poor if the may be associated with avulsion of the vitreous base, giving fovea is involved (Fig. 22.21A). A fresh rupture may be partially rise to an overhanging ‘bucket-handle’ appearance compris- obscured by subretinal haemorrhage (Fig. 22.21B), which may ing a strip of ciliary epithelium, ora serrata and the immediate break through the internal limiting membrane with resultant post-oral retina into which basal vitreous gel remains inserted. subhyaloid or vitreous haemorrhage. Weeks to months later, A traumatic dialysis occurs most frequently in the superona- on absorption of the blood, a white crescentic vertical streak sal and inferotemporal quadrants. Although they occur at the of exposed underlying sclera concentric with the optic disc time of injury, they do not inevitably result in RD. In cases becomes visible (Fig. 22.21C and D). An uncommon late com- where detachment occurs, subretinal uid commonly does not plication is the development of a choroidal neovascular mem- develop until several months later and progression is typically brane in the region of the rupture. slow.  CHAPTER Trauma 22 921 A B C D Fig. 22.21 Choroidal rupture. (A) Acute rupture in the macular region with subretinal haemor- rhage; (B) acute parapapillary rupture (arrow) with subretinal haemorrhage; (C) foveal disrup- tion with resorbing subretinal and sub-RPE haemorrhage; (D) old rupture.  Equatorial breaks are less frequent and are due to direct reti- { Indirect, in which force is transmitted secondarily to the nal disruption at the point of scleral impact. nerve without apparent direct disruption due to impacts  RD secondary to a giant tear may occasionally be seen (Fig. upon the eye, orbit or other cranial structures. 22.22B).  Mechanisms include contusion, deformation, compression or  A macular hole may occur either at the time of injury or fol- transection of the nerve, intraneural haemorrhage, shearing lowing resolution of commotio retinae (Fig. 22.22C). (acceleration of the nerve at the optic canal where it is teth-  Choroidal detachment. is can occur in a so eye aer a ered to the dural sheath, thought to rupture the microvascular severe injury and needs to be distinguished from a retinal supply), secondary vasospasm, oedema and transmission of a detachment (Fig. 22.22D). shock wave through the orbit.  Presentation. ough major head injury is not unusual, asso- Traumatic optic neuropathy ciated trauma may be deceptively minor. Indirect neuropathy Traumatic optic neuropathy follows ocular, orbital or head is considerably more common than direct. Vision is oen very trauma and presents with sudden visual loss that cannot be poor from the outset, with only perception of light in around explained by other ocular pathology. It occurs in up to 5% of 50%. Typically, the only objective nding is an aerent pupil- facial fractures. lary defect. e optic nerve head and fundus are initially nor-  Classication mal, with pallor developing over subsequent days and weeks { Direct, due to blunt or sharp optic nerve damage from (Fig. 22.23). It is important to exclude reversible causes of trau- agents such as displaced bony fragments, a projectile, or matic visual loss such as compressive orbital haemorrhage (see local haematoma. above). 922 Trauma to the Globe A B C D Fig. 22.22 Retinal breaks and detachment. (A) Dialysis with retinal detachment; (B) giant reti- nal tear (arrow showing edge of detached retina); (C) traumatic macular hole; (D) subretinal haemorrhage associated with extensive choroidal detachment.  Investigation. Assessment should be individualized. Some clinicians request CT, MR or both for all cases, others limit imaging to patients with observed visual decline. CT is more eective in the demonstration of bony abnormalities such as optic canal fracture, but MRI is superior for so tissue changes (e.g. haematoma). With either modality, very thin sections are recommended.  Treatment. Spontaneous visual improvement occurs in up to about half of patients with an indirect injury. However, if there is initially no light perception the prognosis is poor. Several treatment options have been advocated but no clear benet has been shown and all carry signicant risks. { Steroids (intravenous methylprednisolone) should be considered for otherwise healthy patients with severe visual loss or in those with delayed visual loss. If used, Fig. 22.23 Optic atrophy secondary to a fracture within the these should be started within the rst 8 hours, but the optic canal. optimal regimen has not been determined and their  CHAPTER Trauma 22 923 A B Fig. 22.24 Optic nerve avulsion. (A) Acute injury showing peripapillary haemorrhages; (B) later stage showing a cavity where the optic nerve head (arrow) has retracted from the dural sheath. (Courtesy of J Donald M Gass, from Stereoscopic Atlas of Macular Diseases, Mosby 1997 – g. B.) use remains controversial. In a trial of high-dose corti- TIP A small child with characteristic ophthalmic features costeroid treatment of patients with acute brain injury of abusive head trauma (especially unexplained retinal (CRASH study) patients receiving steroids were at higher haemorrhages) should be examined in conjunction with a risk of death. specialist paediatrician. { Optic nerve decompression (e.g. endonasal, transeth- moidal) may be considered if there is progressive visual  Presentation is frequently with irritability, lethargy and vom- deterioration despite steroids. Compression of the nerve by iting, which may be initially misdiagnosed as gastroenteritis or bony fragment or haematoma may also be an indication. other infection because the history of injury is withheld. However, optic canal fracture is a poor prognostic indi-  Systemic features may include signs of impact head injury, cator and there is no evidence that surgery improves the ranging from skull fractures to so tissue bruises. Subdural outlook, whilst carrying a signicant risk of complications. and subarachnoid haemorrhage is common and many survi- Optic nerve avulsion vors suer substantial neurological handicap. Multiple rib and long bone fractures may be present. In some cases, examina- Optic nerve avulsion is rare and typically occurs when an object tion ndings are limited to the ocular features. intrudes between the globe and the orbital wall, displacing the  Ocular features eye. Postulated mechanisms include sudden extreme rotation or { Periocular bruising and subconjunctival haemorrhages anterior displacement of the globe. Avulsion may be isolated or (Fig. 22.25A). occur in association with other ocular or orbital injuries. Fundus { Retinal haemorrhages, bilateral or unilateral (20%), are the examination shows a striking cavity where the optic nerve head most common feature. e haemorrhages typically involve has retracted from its dural sheath (Fig. 22.24A and B). ere is no multiple layers and may also be pre- or subretinal (Fig. treatment and the visual prognosis depends on whether avulsion 22.25B). ey are most obvious in the posterior pole, but is partial or complete. oen extend to the periphery. { Poor visual responses and aerent pupillary defects. Abusive head trauma { Visual loss occurs in about 20% of cases, largely as a result Abusive head trauma (‘shaken baby’ syndrome) is a form of physi- of cerebral damage. cal 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, Penetrating trauma oen in association with impact injury to the head. ese children should be examined in conjunction with a specialist paediatrician Introduction whenever characteristic ophthalmic features are identied. e Penetrating injuries are three times more common in males than pattern of injury results from rotational acceleration and decelera- females and typically occur in a younger age group (50% aged tion of the head, in contrast to the linear forces generated by a fall. 15–34). e most frequent causes are assault, domestic/occupa- Direct trauma is not the main mechanism of brain damage. Brain- tional accidents and sport. Serious eye trauma can be prevented by stem traction injury causes apnoea and the consequent hypoxia the appropriate use of protective eyewear. e extent of the injury is leads to raised intracranial pressure and ischaemia. determined by the size of the object, its speed at the time of impact 924 Trauma to the Globe A B Fig. 22.25 Abusive head trauma (shaken baby syndrome). (A) Subconjunctival haemorrhage; (B) fundus haemorrhages involving dierent levels. (Courtesy of G Kontos – g. A; R Bates – g. B.) and its composition. Sharp objects such as knives cause well-  With iris involvement. If possible, the iris should be carefully dened cuts in the globe. However, the extent of damage caused repositioned. However, excision of the prolapsed portion may by ying foreign bodies is determined by their kinetic energy. For be required, particularly if it appears necrotic or if there is a example, an air gun pellet is large and although relatively slow- risk of contamination by foreign material (Fig. 22.26B). moving has a high kinetic energy and can thus cause considerable  With lens damage (Fig. 22.26C) Wounds are treated by rst ocular damage. Of paramount importance is the risk of infection suturing the laceration then removing the lens by phacoemul- that may follow any penetrating injury. Endophthalmitis or pan- sication or with a vitreous cutter. Primary implantation of ophthalmitis, oen more severe than the initial injury, may ensue an intraocular lens is frequently associated with a favourable with loss of the eye. Risk factors include delay in primary repair, visual outcome and a low rate of postoperative complications. ruptured lens capsule and a dirty wound. Prophylactic intravit-  Late scarring. If the injury involves the visual axis (Fig. real antibiotics (see Ch. 10) should be considered; vancomycin is 22.26D), penetrating keratoplasty may be needed. a common choice. As with eyelid trauma, tetanus status should be ascertained. An eye with an open injury should be covered by a Scleral protective eye shield. Signs of an occult scleral wound are described in the section above discussing globe injury in blunt trauma.  Anterior scleral lacerations have a better prognosis than those pos- TIP Most penetrating eye injuries need urgent surgical repair, terior to the ora serrata. A foreign body may be found in the wound usually under general anaesthesia. (Fig. 22.27A). An anterior scleral wound may be associated with serious complications such as iridociliary prolapse (Fig. 22.27B Corneal and C) and vitreous incarceration (Fig. 22.27D). e latter, unless Peaking of the pupil and shallowing of the anterior chamber are appropriately managed, may result in subsequent brous prolifera- key signs, though full-thickness corneal penetration may be pres- tion along the plane of incarcerated vitreous, with the development ent without these signs. e technique of primary repair depends of tractional RD. Viable uveal tissue should be reposited and pro- on the extent of the wound and associated complications such as lapsed vitreous cut ush with the wound, with subsequent vitreo- iris incarceration, at anterior chamber and damage to intraocular retinal assessment. 8-0 nylon or 7-0 absorbable material such as contents. polyglactin should be used for scleral suturing in this setting.  Small shelving wounds with a formed anterior chamber may  Posterior scleral lacerations are frequently associated with not always require suturing as they can heal spontaneously or retinal damage. Primary repair of the sclera to restore globe with the aid of a so bandage contact lens (Fig. 22.26A). integrity should be the initial priority.  Medium-sized wounds should be sutured without delay, espe- cially if the anterior chamber is shallow or at. 10-0 nylon Prognosis is used, with shorter stitches near the visual axis opposing is is dependent on the severity of the injury and the complica- perpendicular edges rst and apical portions of wounds last. tions that arise secondary to the injury. In particular, the prognosis A postoperative bandage contact lens may be applied. e is inuenced by: (a) the initial visual acuity, (b) the presence of a corneoscleral junction should be sutured with 9-0 nylon. relative pupillary defect, (c) the presence of an intraocular foreign  CHAPTER Trauma 22 925 A B C D Fig. 22.26 Penetrating corneal wounds. (A) Small penetrating injury at the limbus. When the metallic foreign body is removed the anterior chamber may shallow and a single corneal suture may then need to be inserted; (B) severe corneal slicing injury with extensive iris pro- lapse (arrow); (C) associated with lens damage, showing linear cut in the lens and prolapsed lens contents (arrow); (D) late scarring within the visual axis. body, (d) the presence of infection and (e) the presence of a retinal injury/detachment. Enucleation/evisceration Primary enucleation or evisceration should be considered for Retinal detachment extremely severe injuries, especially when it is impossible to Traumatic tractional RD following a penetrating injury may result repair the sclera and where there is no prospect of retention of from vitreous incarceration in the wound. Subsequent broblastic vision (see Fig. 4.49). This usually reduces the rehabilitation proliferation is exacerbated by the presence of blood in the vitre- time and allows a rapid return to work. Secondary enucleation ous gel. Contraction of the resultant epiretinal brosis can progress or evisceration may be considered following primary repair to cause an anterior tractional RD. A retinal break may develop if the eye is blind and irreversibly damaged, particularly if it several weeks later, leading to a more rapidly progressing rheg- is also unsightly and uncomfortable. In both instances, the matogenous detachment. surgery is safe with a low complication and infection rate. Based on anecdotal evidence, it has been recommended that if enucleation or evisceration is to be performed it should TIP To prevent extrusion of the intraocular contents when take place within 10–14 days of the original injury in order to repairing a penetrating injury, it is important not to exert any prevent the rare complication of sympathetic ophthalmia (see pressure on the eye. Ch. 12). 926 Trauma to the Globe A B C D Fig. 22.27 Penetrating scleral wounds. (A) Scleral laceration secondary to wood splinter; (B) corneoscleral laceration with iris prolapse; (C) large scleral cut with iris prolapse; (D) anterior scleral laceration with vitreous prolapse (arrow). TIP In a patient with a small lid wound who has been working Corneal with tools, always lift the lids to check for a small penetrating  Clinical features. Marked ocular grittiness is characteristic. injury in the sclera. Magnication is oen required (Fig. 22.28D). Leukocytic inl- tration is typically seen around the embedded foreign body and ferrous particles in situ for even a few hours cause rust Supercial foreign body staining of the bed of the abrasion. Mild secondary uveitis may occur, with associated irritative miosis and photophobia. Subtarsal  Management { A high index of suspicion should be maintained for the pres- A small foreign body, such as a particle of steel, coal or sand, oen impacts on the corneal or conjunctival surface. is may be ence of an IOFB. Posterior segment examination and if neces- washed along the tear lm into the lacrimal drainage system or sary plain X-ray imaging can be used to help to exclude this. { A slit lamp is preferred to determine the position and adhere to the superior tarsal conjunctiva (Fig. 22.28A) and abrade the cornea with every blink, when a pathognomonic pattern of depth of the foreign body and to guide removal using a linear corneal abrasions may be seen (Fig. 22.28B). Occasionally sterile hypodermic needle (oen 25-gauge). { A residual ‘rust ring’ is easiest to remove with a sterile burr. a barbed foreign body, such as an insect (Fig. 22.28C) or plant { Antibiotic ointment is instilled, subsequent duration of use material, will become deeply embedded, with resultant substantial discomfort. depending on severity. { A cycloplegic and topical non-steroidal anti-inammatory can be prescribed if required to promote comfort. TIP In a patient with a linear corneal abrasion, search for a { If a corneal foreign body is not removed, there is a sig- small foreign body on the tarsal surface. nicant risk of secondary infection and corneal ulceration.  CHAPTER Trauma 22 927 A B C D Fig. 22.28 Supercial foreign bodies. (A) Retained subtarsal foreign body; (B) linear corneal abrasion stained with uorescein; (C) insect retained in the inner canthus; (D) recently embed- ded corneal foreign body. Any discharge, inltrate, or signicant uveitis should raise Diagnosis suspicion of secondary bacterial infection, with subse-  History. A careful history may be key to determining the ori- quent management as for bacterial keratitis. Metallic par- gin and nature of the foreign material. ticles seem to be associated with a lower risk of infection  Examination should pay special attention to possible sites of than organic and stone foreign bodies. entry or exit. Topical uorescein may be helpful to identify an entry wound. Projection from wounds may allow logical Intraocular foreign body deduction of the location of a foreign body. Gonioscopy and fundoscopy must be considered, taking care to minimize pres- Introduction sure on the eye. Associated signs such as lid laceration and An IOFB may traumatize the eye mechanically, introduce infection anterior segment damage should be noted.  CT with axial and coronal cuts is used to detect and local- or exert other toxic eects on the intraocular structures. It may lodge in any of the structures it encounters, thus may be located ize a metallic IOFB, providing cross-sectional images with a anywhere in the anterior (Fig. 22.29A and B) or posterior segments sensitivity and specicity superior to plain radiography and (Fig. 22.29C and D). Notable mechanical eects include cataract ultrasonography.  MRI is contraindicated in the context of a metallic (specically formation secondary to capsular injury, vitreous liquefaction and retinal haemorrhages and tears. Stones and organic foreign bodies ferrous) IOFB. are associated with a high rate of infection. Intravitreal antibiotic prophylaxis is generally recommended. Many substances are inert, Treatment including glass, plastics, gold and silver. However, iron and cop-  Magnetic removal of ferrous foreign bodies involves the cre- per may undergo dissociation and result in siderosis and chalcosis ation of a sclerotomy adjacent to the foreign body, with appli- respectively (see below). cation of a magnet followed by cryotherapy to the retinal break. 928 Trauma to the Globe A B C D Fig. 22.29 Intraocular foreign bodies. (A) In the anterior chamber; (B) in the lens; (C) in the vitreous (arrow) with retinal detachment; (D) retinal impaction, with localized inammation suggestive of early infection.  Forceps removal may be used for non-magnetic for- consisting of radially distributed iron deposits on the anterior eign bodies and magnetic foreign bodies that cannot be lens capsule (Fig. 22.30A), reddish-brown staining of the iris safely removed with a magnet. It involves pars plana vit- that may give rise to heterochromia iridis and pigmentary reti- rectomy and removal of the foreign body with forceps nopathy followed by atrophy of the retina and RPE (Fig. 22.30B), either through the pars plana or limbus depending on the potentially leading to profound visual loss. Trabecular damage circumstances. can cause glaucoma. Electroretinography shows progressive  Prophylaxis against infection (see below). attenuation of the b-wave over time. TIP A missed intraocular foreign body with a ferrous Chalcosis component can result in late visual loss secondary to siderosis. e ocular reaction to an IOFB with a high copper content involves a violent endophthalmitis-like picture, oen with pro- gression to phthisis bulbi. On the other hand, an alloy with a Siderosis relatively low copper content such as brass or bronze, results in Steel is the most common foreign body constituent and is typi- chalcosis. Electrolytically dissociated copper becomes deposited cally projected into the eye by hammering or power tool use. A intraocularly, resulting in a picture similar to that seen in Wilson ferrous IOFB undergoes dissociation with the consequent depo- disease. us, a Kayser–Fleischer ring develops and an anterior sition of iron in the intraocular epithelial structures, notably the ‘sunower’ cataract. Retinal deposition results in golden plaques lens epithelium, iris and ciliary body epithelium and the sensory visible ophthalmoscopically. Since copper is less retinotoxic than retina. It exerts a toxic eect on cellular enzyme systems, with iron, degenerative retinopathy does not develop and visual func- resultant cell death. Signs include anterior capsular cataract, tion may be preserved.  CHAPTER Trauma 22 929 A B Fig. 22.30 Siderosis oculi. (A) Lenticular deposits; (B) atrophy of the retina and RPE associated with an impacted ferrous foreign body. (Courtesy of J Donald M Gass, from Stereoscopic Atlas of Macular Diseases, Mosby 1997 – g. B.) remainder at home. Chemical injury is the second common- Bacterial endophthalmitis est cause of work-based eye injuries at 12%, behind ‘foreign Endophthalmitis develops in about 1 in 10 cases of penetrating body’ injuries at 43%. Alkali burns are twice as common as trauma with retained foreign body. acid burns, since alkalis are more widely used both at home  Risk factors include delay in primary repair, retained and in industry. The severity of a chemical injury is related IOFB and the position and extent of wounds. Clinical signs to the properties of the chemical, the area of affected ocular are the same as acute postoperative endophthalmitis (see surface, duration of exposure (including retention of particu- Ch. 10). late chemical on the surface of the globe or under the upper  Pathogens. Staphylococcus spp. and Bacillus spp. are isolated lid) and related effects such as thermal damage. Alkalis tend to from about 90% of culture-positive cases. penetrate more deeply than acids as the latter coagulate surface  Management proteins, forming a protective barrier. The most commonly { Prophylactic antibiotics (e.g. ciprooxacin 750 mg twice involved alkalis are ammonia, sodium hydroxide and lime. daily or moxioxacin 400 mg once daily) can be given Ammonia and sodium hydroxide characteristically produce for open globe injuries, together with topical antibiotic, severe damage because of rapid penetration. Hydrofluoric acid steroid and cycloplegia. used in glass etching and cleaning also tends to rapidly pene- { Prompt removal of a retained IOFB. trate the ocular tissues, whilst sulphuric acid may be compli- { Prophylactic intravitreal antibiotics, especially for high- cated by thermal effects and high velocity impacts associated risk cases (e.g. agricultural injuries). with car battery explosion. { Culture of a removed IOFB. { Treatment for established cases is the same as for acute postoperative bacterial endophthalmitis (see Ch. 10). Pathophysiology  Damage by severe chemical injuries tends to progress as below: { Necrosis of the conjunctival and corneal epithelium with CHEMICAL INJURIES disruption and occlusion of the limbal vasculature. Loss of limbal stem cells may lead to conjunctivalization and vas- Introduction cularization of the corneal surface, or persistent corneal A chemical eye injury should be considered an acute emergency epithelial defects with sterile corneal ulceration and perfora- that requires urgent treatment to reduce the risk of permanent tion. Longer-term eects include ocular surface wetting dis- visual loss. Early and appropriate treatment is fundamental to the orders, symblepharon formation and cicatricial entropion. successful management. { Deeper penetration causes the breakdown and pre- cipitation of glycosaminoglycans and stromal corneal opacication. Aetiology { Anterior chamber penetration results in iris and lens damage. Chemical injuries range in severity from trivial to potentially { Ciliary epithelial damage impairs secretion of ascorbate, blinding. The majority are accidental, but a few are due to which is required for collagen production and corneal repair. assault. Two-thirds of accidental burns occur at work and the { Hypotony and phthisis bulbi may ensue in severe cases. 930 Chemical Injuries  Healing  Grade 3 (Fig. 22.31C) manifests total loss of corneal epithe- { e epithelium heals by migration of epithelial cells origi- lium, stromal haze obscuring iris detail and between one- nating from limbal stem cells. third and one-half limbal ischaemia (guarded prognosis). { Damaged stromal collagen is phagocytosed by keratocytes  Grade 4 (Fig. 22.31D) manifests with an opaque cornea and more and new collagen is synthesized. than half of the limbus showing ischaemia (poor prognosis). Other features that should be noted at the initial assessment are the extent of corneal and conjunctival epithelial loss, iris changes, Management the status of the lens and the IOP. Emergency treatment Medical treatment A chemical burn requires urgent treatment by the rst person Most mild injuries (grade 1 and 2) are treated with topical anti- who sees the aected person. Immediate treatment is as follows: biotic ointment for about a week, with topical steroids and cyclo-  Copious irrigation is crucial to minimize duration of contact plegics if necessary. e main aims of treatment of more severe with the chemical and to normalize the pH in the conjuncti- burns are to reduce inammation, promote epithelial regenera- val sac as soon as possible. e speed and ecacy of irrigation tion and prevent corneal ulceration. For moderate–severe inju- is the most important prognostic factor following chemical ries, preservative-free drops should be used. injury. Topical anaesthetic should be instilled prior to irriga-  Steroids reduce inammation and neutrophil inltration tion, as this dramatically improves comfort and facilitates and address anterior uveitis. However, they also impair stro- cooperation. A lid speculum may be helpful. Tap water should mal healing by reducing collagen synthesis and inhibiting be used if necessary to avoid any delay, but a sterile balanced broblast migration. For this reason, topical steroids may be buered solution, such as normal saline or Ringer lactate, used initially (usually 4–8 times daily, strength depending on should be used to irrigate the eye for 15–30 minutes or until injury severity) but must be tailed o aer 7–10 days when the measured pH is neutral. sterile corneal ulceration is most likely to occur. Steroids  Double-eversion of the upper eyelid should be performed so may be replaced by topical non-steroidal anti-inammatory that any retained particulate matter trapped in the fornices is drugs, which do not aect keratocyte function. identied and removed.  Cycloplegia to improve comfort (e.g. atropine 1% twice daily).  Debridement of necrotic areas of corneal epithelium should  Preservative-free topical antibiotic drops are used for pro- be performed at the slit lamp to promote re-epithelialization phylaxis of bacterial infection (e.g. chloramphenicol four and remove associated chemical residue. times daily).  Admission to hospital is usually required for severe injuries  Ascorbic acid improves wound healing by promoting the (grade 3 and 4 – see below) in order to ensure adequate instil- synthesis of mature collagen by corneal broblasts. Topical lation of eye drops in the early stages. sodium ascorbate 10% can be given 2-hourly in addition to a systemic dose of 1–2 g vitamin C (L-ascorbic acid) four times TIP The initial management of a chemical injury to the eye daily (not in patients with renal disease). is immediate copious ocular irrigation. If available, instillation  Citric acid is a powerful inhibitor of neutrophil activity and of a topical anaesthetic improves comfort and facilitates reduces the intensity of the inammatory response. Chelation cooperation. of extracellular calcium by citrate also appears to inhibit colla- genase. For grade 3 and 4, topical sodium citrate 10% should be instilled 2-hourly for about 10 days and may also be given orally Grading of severity (2 g four times daily). e aim is to eliminate the second wave of Acute chemical injuries are graded in order to plan subsequent phagocytes, which normally occurs about 7 days aer the injury. treatment and to provide an indication of the prognosis. Currently, Ascorbate and citrate can be tapered as the epithelium heals. there are two classications used for grading chemical injuries:  Tetracyclines are eective collagenase inhibitors and also the Roper-Hall classication (see below) and the Dua classica- inhibit neutrophil activity and reduce ulceration. ey should tion. In the Roper-Hall classication, grading is performed on the be considered if there is signicant corneal melting and can basis of corneal clarity and severity of limbal ischaemia. e latter is be administered both topically (tetracycline ointment four assessed by observing the patency of the deep and supercial vessels times daily) and systemically (doxycycline 100 mg twice daily at the limbus. e Dua classication is more detailed and is based on tapering to once daily). Acetylcysteine 10% six times daily is the number of clock hours of aected limbus and the percentage of an alternative anticollagenase agent given topically. conjunctival involvement. is provides a better prognostic predic-  Symblepharon formation should be prevented as necessary by tor than the Roper-Hall classication, particularly for grade 4 cases. lysis of developing adhesions with a sterile glass rod or damp  Grade 1 (Fig. 22.31A) is characterized by a clear cornea cotton bud. (epithelial damage only) and no limbal ischaemia (excellent  IOP should be monitored, with treatment if necessary. Oral prognosis). acetazolamide is recommended to avoid adding further to the  Grade 2 (Fig. 22.31 B) shows a hazy cornea but with visible iris ocular surface burden. detail and less than one-third of the limbus being ischaemic  Periocular skin injury may require a dermatology (good prognosis). opinion.  CHAPTER Trauma 22 931 A B C D Fig. 22.31 Chemical burns. (A) Grade 1 – clear cornea with chemosis of the conjunctiva; (B) grade 2 – corneal haze but visible iris detail; (C) grade 3 – corneal haze obscuring iris details; (D) grade 4 – marked conjunctival ischaemia and an opaque cornea. Surgery { Correction of eyelid deformities such as cicatricial entro- pion (see Fig. 2.55B).  Early surgery may be necessary to promote revascularization of { Keratoplasty for corneal scarring (Fig. 22.32C) should the limbus, restore the limbal cell population and re-establish the be delayed for at least 6 months and preferably longer, to fornices. One or more of the following procedures may be used: allow maximal resolution of inammation. { Advancement of Tenon capsule with suturing to the lim- { In a very severely damaged eye (Fig. 22.32D) a keratopros- bus is aimed at re-establishing limbal vascularity to help to thesis may be required (see Fig. 8.11). prevent the development of corneal ulceration. { Limbal stem cell transplantation from the patient’s other eye (autogra) or from a donor (allogra) is aimed at restoring normal corneal epithelium. THERMAL BURNS { Amniotic membrane graing to promote epithelialization ermal injuries range in severity from trivial to potentially and suppression of brosis. blinding. Most involve the eyelids and face, but the surface of the { Gluing or keratoplasty may be needed for actual or cornea may be burnt resulting in severe corneal scarring (Fig. impending perforation. 22.33A and B). Most mild injuries are treated with topical antibi-  Late surgery may involve: otic drops for about a week with topical steroids and cycloplegics. { Division of conjunctival bands (Fig. 22.32A) and sym- Plastic surgery to the lids may be required if there is cicatrization blepharon (Fig. 22.32B). and abnormal lid position. Corneal scarring will usually require { Conjunctival or other mucous membrane graing. keratoplasty. 932 Thermal Burns A B C D Fig. 22.32 Late sequelae of chemical injury. (A) Conjunctival bands; (B) symblepharon; (C) corneal scarring with pannus; (D) extensive cicatrization. A B Fig. 22.33 Thermal burn. (A) To lids and anterior segment; (B) to cornea.