Ординатура / Офтальмология / Английские материалы / Clinical Ophthalmology A Systematic Approach 7th Edition_Kanski, Bowling_2011

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1Corneal 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.

2Acute 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.

3Tears in Descemet membrane are usually vertical and most commonly arise as the result of birth trauma (Fig. 21.12D).

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)

Hyphaema

1Signs

•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).

2Treatment 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’.

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Fig. 21.13 Traumatic hyphaema. (A) Bleeding fromthe 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.

1Pupil. 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).

3Ciliary body (see below).

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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.

Lenticular

1Cataract 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.

2Subluxation 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.

3Dislocation 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.

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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.

Fig. 21.16 Ruptured globe

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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).

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.

1Dialysis 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).

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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

1Traumatic 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.

aClassification. 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.

bMechanisms 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.

cPresentation. 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.

dInvestigation. 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.

eTreatment. 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.

2Optic 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

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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.

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.

1Presentation is frequently with irritability, lethargy and vomiting which may be initially misdiagnosed as gastroenteritis or other infection because the history of injury is withheld.

2Systemic 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.

3Ocular 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 preor 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.

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

(Courtesy of R Bates)

Penetrating trauma

Causes

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.

1Small 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.

2Medium-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.

4With 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.

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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

1Anterior 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.

2Posterior 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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