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Ординатура / Офтальмология / Учебные материалы / Clinical Diagnosis and Management of ocular trauma

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186

 

Clinical Diagnosis and Management of Ocular Trauma

 

Commotio Retinae

 

 

 

 

Commotio retinae is also known as Berlin’s edema or

 

 

concussion edema. It is caused by blunt trauma (a

 

 

contrecoup injury), with the force being transmitted

 

 

through the vitreous and finally onto the retina and

 

 

choroids. With this condition, there will be a confluent

 

 

area of retinal whitening due to outer photoreceptor

 

 

disruption and RPE damage, but not edema. Blood

 

 

vessels are seen distinctly and are undisturbed under

 

 

the retinal whitening. The retinal opacification gradually

 

 

subsides over several weeks and visual function usually

 

 

returns to its pretrauma level. However, a permanent

 

 

loss of vision is not unusual and can be associated with

 

 

changes in the retinal pigment epithelium.

 

 

Choroidal Rupture

Fig. 30.7: Traumatic cataract with rupture of anterior capsule and lens matter in anterior chamber

Choroidal rupture is detectable as a yellow or white crescent-shaped subretinal streak that is often concentric with the optic nerve. The rupture can be single (Fig. 30.9) or multiple and may be obscured for several days to weeks by overlying preor subretinal hemorrhage. Patients with this condition are at a greater risk for developing a choroidal neovascular membrane, so they should be followed every 3 to 6 months. They should also be instructed to monitor their vision daily with an Amsler grid and to report any significant changes.

Fig. 30.8: Foreign body impacted in retina temporal to fovea

modalities are necessary. CT scan has emerged as the imaging modality of choice to rule out IOFB. Modern spiral CT scanning with 1mm cuts is effective in detecting a 0.5 mm metallic, glass or stone in 100% of cases.16 MRI is contraindicated if a metallic foreign body is suspected.

Endophthalmitis occurs in up to 48% of eyes with an IOFB injury and only the timing of surgery (>24 hours) and the type of FB (e.g. wood) are associated with higher rates. The clinical findings include retinal periphlebitis, marked anterior chamber reaction or hypopyon, and severe vitreal inflammation.

Metallic IOFBs can cause toxic retinal metallosis, but even inert IOFBs can cause proliferative vitreoretinopathy and/or debilitating ocular inflammation. The treatment is prompt surgical removal via pars plana vitrectomy (with or without lensectomy) involving magnetic and/or forceps assisted IOFB removal.

Fig. 30.9: Post-traumatic choroidal rupture with macular hole

Retinitis Sclopeteria

Retinitis sclopeteria or chorioretinitis sclopeteria is a rare condition in which the patient sustains both a choroidal and retinal rupture. It is a concussive injury to the posterior segment and results from shock waves produced by orbital penetration of a high-velocity object. The object does not penetrate the sclera but

Management of Pediatric Ocular Trauma

187

ruptures the choroid and retina in the area adjacent to its path. The visual acuity is almost always poor. This condition occurs when a high-velocity object grazes the globe, but does not rupture the sclera. Patients with retinitis sclopeteria require a prompt retinal consult because surgical intervention may be necessary.

Traumatic Macular Hole

Traumatic macular hole (Fig. 30.10) is clinically similar to the idiopathic variety in appearance. It can follow commotio retinae, subretinal hemorrhages and cystoid macular edema. Postcontusion necrosis may result in macular edema and macular cyst formation. Over months to years, rupture of cyst layer/s can lead to formation of lamellar or full thickness macular hole. Acute lamellar or full thickness macular hole is usually caused by contrecoup vitreofoveal traction.

Fig. 30.10: Post-traumatic large macular hole

Pars plana vitrectomy with removal of internal limiting membrane (ILM) and gas/ silicon oil tamponade has been found to be successful (anatomical closure) in more than 90% of cases.17 Visual improvement has been reported in 69-94% of cases.17-19 Surgical adjuvant such as autologus plasmin enzyme may improve the rate of anatomic success20. However, because a significant number of cases of traumatic macular hole may close spontaneously, it may be wise to just follow up these patients for initial 3 months or so.

Traumatic Retinal Detachment

Traumatic retinal detachment (RD) (Fig. 30.11) is a rhegmatogenous detachment that can be caused by retinal dialysis or a retinal tear. B-scan ultrasonography is necessary to rule out an RD if media is hazy and one is unable to visualize fundus. When appropriate, utilize scleral depression after trauma to help rule out retinal dialysis.

Fig. 30.11: Post-traumatic retinal detachment with early macular pucker

A patient with a macula-on RD (i.e. the macular region of the retina is intact) should receive a retinal consultation and undergo surgery within 1 to 2 days of diagnosis. These patients should be confined to bed rest until surgery. A macula-off RD (i.e. the macular region has detached) is less urgent and these patients should have a retinal consultation and surgery within approximately one week.

Children’s lack of cooperation with postoperative positioning influences the surgeon’s decision during retinal detachment surgery. It’s very difficult to separate the nondetached posterior hyaloid in pediatric eye; nonetheless, vitreous removal should be as complete as possible as leaving behind the posterior hyaloid increases the risk of proliferative vitreoretinopathy. Plasmin may have a future role in these cases. Silicon oil is preferred over gases as tamponading agent as former requires minimal positioning and immobility.

Child Abuse

Child abuse must always be considered in a child younger than 3 years of age who presents with intraocular hemorrhages, cataract or subluxated lens, retinal detachment or retinischiasis, or periorbital ecchymosis. The ocular findings in shaken baby syndrome may occur without any obvious external injury. Retinal hemorrhages have been described in shaken baby syndrome in which repeated acceleration and deceleration is supposed to damage intraocular and intracranial blood vessels and thereby results in intraocular and intracranial hemorrhage. Typically the retinal hemorrhages are bilateral, but may be asymmetric or even unilateral. Other causes of retinal

188

 

 

Clinical Diagnosis and Management of Ocular Trauma

 

hemorrhage such as leukemia, accidental trauma,

4.

Moreira CA Jr, Ribeiro MD, Belfort R Jr. Epidemiological

 

 

 

 

leukemia, thrombocytopenia, anemia, etc. should be

 

study of eye injuries in Brazilian children. Arch

 

 

ruled out. Severe visual morbidity with shaken baby

 

Ophthalmol 1988;106:781-84.

 

 

5.

Rapoport I, Romem M, Kinek M, et al. Eye injuries in

 

 

syndrome may be due to retinal detachment, optic

 

 

 

children in Israel. A National Collaborative Study. Arch

 

 

nerve atrophy or cortical blindness.

 

 

 

 

Ophthalmol 1990;108:376-79.

 

 

 

 

 

 

 

 

 

 

 

6.

Canavan VM, O’Flaherty MJ, Archer DB, et al. A ten year

 

 

Eye Injury Prevention

 

survey of eye injuries in Northern Ireland. Br J

 

 

 

Ophthalmol 1980;64:618-25.

 

 

 

 

 

 

 

 

 

 

 

7.

Holden R, Morsman DG, Davidek GMB, O’Conner GM.

 

 

The vast majority of eye injuries are preventable. Key

 

 

 

External ocular trauma in instrumental and normal

 

 

components of prevention include parental

 

deliveries. Br J Obstet Gynecol 1992;99:132.

 

 

supervision, education of children and protective

8.

Angell LK, Robb RM, Berson FG. Visual prognosis in

 

 

eyewear. Ophthalmologists and parents must reinforce

 

patients with ruptures in Descmet’s membrane due to

 

 

 

forceps injury. Arch Ophthalmol 1981;99:21-37.

 

 

the importance of not playing with objects like

 

 

 

9.

Sezen F. Retinal hemorrhages in new born infants. Br J

 

 

gillidanda, fire-crackers and bow and arrow. Health

 

 

 

Ophthal 1970;55:248.

 

 

education on the preventive aspects of ocular trauma

10.

Volpe NJ, Larrison WI, Hersh PS et al Secondary

 

 

in schools as well as through mass media like television

 

hemorrhage in traumatic hyphema. Am J Ophthalmol

 

 

can help in achieving this goal.

 

1991; 112: 507-13.

 

 

Protective eyewear is the most important measure

11. Thomas MA, Parrish RK, Feuer WJ. Rebleeding after

 

 

to prevent eye injuries in children. Plano polycarbonate

 

traumatic hyphema. Arch Ophthalmol 1986 Feb;

 

 

 

104(2):206-10.

 

 

goggles with a 2-3

mm center thickness are

 

 

 

12.

McGetrick JJ, Jampol LM, Goldberg MF, et al.

 

 

recommended for sports.

 

 

 

Aminocaproic acid decreases secondary hemorrhage

 

 

 

 

 

 

after traumatic hyphema. Arch Ophthalmol 1983 Jul;

 

 

Summary

 

 

 

101(7):1031-33.

 

 

 

 

13.

Kutner B,Fourman S, Brein K Aminocaproic acid

 

 

 

 

 

 

 

 

 

 

 

reduces the risk of secondary hemorrhage in patients

 

 

Ocular trauma is an important cause of monocular

 

 

 

 

with traumatic hyphema. Arch Ophthalmol 1987 Feb;

 

 

blindness in children. Due to young age, inability to

14.

105(2):206-08.

 

 

cooperate with examination and the potential for

Stern WH, Monclal KM. Vitrectomy instrumentation for

 

 

 

surgical evacuation of total anterior chamber hyphema

 

 

development of amblyopia, children presenting with

 

 

 

 

and control of recurrent anterior chamber hemorrhage.

 

 

eye injuries are evaluated and treated slightly differently

 

 

 

 

Ophthalmol Surg 1979; 10: 34-37.

 

 

from adults. Proper communication should be

15.

McCuen BW, Fung WE. The role of vitrectomy

 

 

maintained between the ophthalmologist and family

 

instrumentation in the treatment of severe traumatic

 

 

throughout the course of treatment.

16.

hyphema. Am J Ophthalmol 1979;88:930-34.

 

 

 

 

 

Dass AB, Ferrone PJ, Chu RY etal. Senstivity of spiral

 

 

 

 

 

 

computed tomography scanning for detecting intraocular

 

 

References

 

 

 

foreign bodies. Ophthalmology 2001; 108: 2326-28.

 

 

 

 

17.

Kuhn F, Morris R,Mester V, et al. Internal limiting

 

 

1. Jaison SG, Silas SE, Daniel R, Chopra SK.A review of

 

membrane removal for traumatic macular holes.

 

 

 

Ophthalmic Surg Lasers 2001 Jul-Aug;32(4):308-15.

 

 

childhood admission with perforating ocular injuries in

18.

Amari F, Ogino N, Matsumura M et al. Vitreous surgery

 

 

a hospital in north-west India. Indian journal of

 

for traumatic macular holes. Retina. 1999; 19(5):410-13.

 

 

ophthalmology 1994;42(4):199-201.

19.

Chow DR, Williams GA, Trese MT et al. Successful closure

 

 

2. Sarda RP, Mehrotra AS, Ratnawat PS, et al. Ocular injuries

 

of traumatic macular holes. Retina 1999;19(5):405-09.

 

 

in childhood. Indian J Ophthalmol 1971;19:67-70.

20.

Margherio AR, Margherio RR, Hartzer M et al Plasmin

 

 

3. Niiranen M, Raivio I. Eye injuries in children. Br J

 

enzyme-assisted vitrectomy in traumatic pediatric macular

 

 

Ophthalmol 1981;65:436-38.

 

holes. Ophthalmology 1998 Sep;105(9):1617-20.

 

 

 

 

 

 

 

C H A P T E R

31Management of Blunt

Retinal Trauma

Arturo Pérez-Arteaga, Yuri Flores (Mexico)

Introduction

As part of the ocular traumatology, the damage caused by an impact directly or indirectly to the retina, can be smooth, and with total visual recovery, or in some other cases, can cause a severe visual impairment, with tremendous consequences for the life of the patient.

The visual prognosis after ocular trauma depends on a number of factors; a large proportion of eyes with severe and irreversible visual loss due to trauma almost always exhibit posterior segment injuries. These injuries lead to vitreoretinal complications that may occur immediately, days, weeks, or even years after the initial trauma. Recent advances in microsurgical techniques, as well as an improved understanding of the pathophysiology of these vitreoretinal complications, may minimize the visual loss, even in the more severely affected eyes. Therefore, although prevention remains the ultimate goal, the adequate diagnosis and “state of the art” management of posterior segment injuries are important factors in reducing the magnitude of visual loss in injured eyes.

If well the traumatic lesions to the posterior segment of the eye too often are not alone, it means that an ocular trauma is able to cause damage in many other structures of the globe, we will try in this chapter, to establish didactic classifications in order to cover the broad spectrum of possible lesions, and so improve the clinical evaluation, allowing the physician, to decide an adequate option of treatment for each particular patient.

We have also to remember, that very often the impact to the retina, in particular in cases of blunt, trauma is not frequently a direct impact, it is a result of the transmission of forces inside the eye, and the wave of impact goes frequently from the anterior segment, to the posterior segment of the eye; the implications of this physical concept are that sometimes the damage caused in the retina not always correlate with the force of the impact and the mechanism of trauma; this can lead to underestimate the damage

in cases of minor trauma. Maybe this is the first concept that the attending surgeon must keep in mind when observing and evaluating a traumatized eye.

In this order of ideas, the possibilities are enormous; blunt ocular trauma, orbital trauma and systemic trauma may cause a variety of posterior segment abnormalities (our matter in this chapter); trauma may cause damage to the retina (commotio retinae), retinal pigment epithelium (retinal pigment epithelial edema), choroid (choroidal rupture) and optic nerve (optic nerve evulsion) alone or in combination; traumatic macular holes and retinal detachment or dialysis; trauma to the orbital tissues adjacent to the globe can cause concussive forces with damage to multiple structures within the eye (chorioretinitis sclopetaria); systemic trauma may result in diffuse retinopathy (Purtscher’s retinopathy, shaken baby syndrome) or localized retinal abnormalities (whiplash retinopathy, fat embolism syndrome). Alterations in intravascular (Valsalva retinopathy) or intracranial pressure (Terson’s syndrome) due to a variety of causes may result in preretinal or vitreous hemorrhage and associated visual loss.

The purpose of this chapter is to review the mechanism of posterior segment injury in blunt trauma, the initial evaluation and a perspective of some of the most important entities involved in the trauma to the posterior segment.

Mechanism of Damage in

Blunt Trauma

The transfer of blunt forces to the globe is the mechanism seen in the majority of ocular injuries. Even in high-speed projectile injuries, in which the mechanism of injury is primarily due to penetrating or sharp forces, associated blunt forces are involved.

Blunt forces involve the posterior segment in several ways:

190

 

Clinical Diagnosis and Management of Ocular Trauma

 

 

First there is direct contusion tissue damage at the

globe status is obvious, careful documentation of these

 

 

 

 

site of impact. This is known as a coup injury, and

circumstances, as well as the use and type of safety

 

 

includes retinal edema, necrotic changes, and

glasses or other protective devices, has medical and

 

 

choroidal hemorrhage at the site of impact.

legal relevance. The history should determine the

 

 

Second, injury can occur distant from the impact

preinjury ocular status and the possibility of extraocular

 

 

site as the force is transferred through the globe

trauma; the ocular baseline should include preinjury

 

 

to a contralateral site. This is called the contracoup

vision, refractive status (myopic eyes are affected with

 

 

injury; examples of it include retinal edema and

more severity with minor traumas), preexisting ocular

 

 

choroidal contusions in the posterior pole; in these

diseases (e.g. retinal diseases, pseudoexfoliation,

 

 

lesions the posterior pole was not impacted directly,

glaucoma), and previous ocular surgery (e.g. cataract,

 

 

but the transmission of forces affect it in different

retinal surgery). The note of circumstances that should

 

 

degree.

raise suspicions of open globe injuries is mandatory,

 

 

Finally, there are injuries caused by the globe

high-speed projectile injuries, use of power tools, high-

 

 

deformation; some authors have documented by

speed grinding of metal, leak from high-pressure

 

 

high-speed cinematography, globe deformation

hydraulic system, metal-on-metal impact, sharp

 

 

following the application of blunt forces to the

penetrating injuries and severe blunt injury (racquetball

 

 

cornea. In these movies we can see initially how

or golf ball, stick or bat injury to orbit).

 

 

the anteroposterior axis is compressed; then the

 

 

 

 

anteroposterior axis is decompresses and so a

Individual Pathologies Description

 

 

 

rebound expansion occurs. Then the equatorial

 

 

 

axis begins to expand as the anteroposterior axis

COMMOTIO RETINAE

 

 

compresses but doesn’t reach maximum expansion

 

 

 

 

 

 

until after the anteroposterior axis begin its rebound

Definition and Clinical Findings

 

 

decompression. This tremendous change of intra-

Commotio retinae is also known as Berlin’s edema, but

 

 

ocular forces of compression and decompression

the latter term is not completely appropriate. The clinical

 

 

within different axis of the globe, creates shearing

 

 

characteristic of this condition is a confluent area of

 

 

forces within the eye at tissue interfaces that are

 

 

retinal whitening due to outer photoreceptor disruption

 

 

especially concentrated at the vitreous base.

 

 

and RPE damage, but not edema. Blood vessels are seen

 

 

Choroidal rupture, vitreous base avulsion, iris root

 

 

distinctly and are undisturbed under the retinal

 

 

disinsertion, retinal dialysis and tears, and posterior

 

 

whitening. Commotio retinae results in retinal

 

 

vitreous separation are examples of injuries caused

 

 

opacification following blunt trauma. Mild commotio

 

 

by these shearing forces.

 

 

retinae usually settles spontaneously with minimal

 

 

After reading this, the clinical comprehends that

 

 

sequelaebutmoreseverecasesareassociatedwithvisual

 

 

he must be aware of damage caused by ocular blunt

 

 

loss. Commotio retinae can occur anywhere in the

 

 

trauma at any site of the eye; so a complete evaluation

 

 

retina, but it is usually maximal in the area opposite to

 

 

of all structures is mandatory, even in case of an

 

 

the blow (countracoup injury). So, explaining the

 

 

“pretended minor trauma”.

 

 

pathophysiology of the condition, the retinal changes

 

 

 

 

 

 

Initial Evaluation

are caused by a contrecoup that is created by blunt

 

 

trauma, with the force being transmitted through the

 

 

 

 

vitreous and finally onto the retina and choroid

 

 

Proper identification and management of patients with

 

 

(Figs 31.1 and 31.2).

 

 

posterior segment injury begin with a systematic

 

 

 

 

 

 

approach to obtaining a complete history and conduc-

Histopathology

 

 

ting a thorough ophthalmic examination. The reader

 

 

will be able to see more details in some other chapters

Immediately after injury, the only abnormality is

 

 

of this book, but some important points will be

disruption of the receptor outer segments. From one

 

 

featured regarding the posterior segment blunt trauma;

to six days after trauma, many receptor cells undergo

 

 

because open and closed globe injuries are approached

degeneration. The retinal pigment epithelium phago-

 

 

differently it is important for the ophthalmologist to

cytoses the degenerating outer segments, occasionally

 

 

make this determination as soon as possible.

migrating into the retina. There is no extracellular retinal

 

 

The circumstances surrounding the trauma are

edema. The opacity of commotio retinae seems to

 

 

important and should be obtained directly from the

represent disrupted receptor cells. Visual loss may result

 

 

patient and/or an eyewitness in particular if the patient

from permanent loss of receptors. The pigment

 

 

is unable to communicate. Even in cases in which the

epithelial response to traumatic receptor damage is

 

 

 

 

 

 

Management of Blunt Retinal Trauma

191

spontaneously. However, they should also be adverted that in some instances visual acuity remains disabled. Concurrent treatment of any resultant uveitis should include a topical cycloplegic and, when appropriate, a topical corticosteroid. Cystoid macular edema (CME) is a classical complication of ocular inflammation. CME can result from a rupture of the inner or outer bloodocular barrier, and it responds poorly to topical and surgical modalities. Topical nonsteroidal and steroidal preparations along with oral carbonic anhydrase inhibitors and injected steroidal depots have been used, but with varied results; sometimes these medication makes a placebo effect in the patient but also in the physician.

Fig. 31.1: Commotio retinae

Fig. 31.2: Berlin`s edema

similar to that observed in experimental retinal detachment and light-induced retinal damage.

Management

There is usually no treatment required because commotio retinae tends to resolve without sequela. The management consists of repairing the traumatic collateral damage and emotionally supporting of the patient, especially if vision is poor. Visual acuity monitoring, Amsler grid testing, and measurement of retinal thickness can provide data indicating the progress of recovery; however, no known topical, oral or surgical solution has been offered as a treatment for the commotion it self. If patients initially have decreased acuity, they should be informed that, in the majority of cases, improvement takes place

TRAUMATIC MACULAR HOLE

Initial Concepts

The first macular holes reported by Knapp, in 1869, and Noyes, in 1878, were traumatic in nature. Traumatic macular holes are reported to occur in about 6% of eyes with blunt trauma. The mechanism of traumatic macular hole formation may not be singular. Idiopathic macular holes are believed to be caused by tangential vitreoretinal traction at the fovea; so, traumatic macular holes may be caused by a similar mechanism. In fact, surgical repair of traumatic macular holes is identical to that for idiopathic macular holes, with removal of the posterior hyaloid and peeling of epiretinal or internal limiting membranes, and yields similar anatomic and visual results. There is no doubt that some of these traumatic macular holes may be caused by cystoid degeneration following postcontusion commotio and RPE edema. Under these circumstances the visual prognosis would be more guarded and surgical repair may not be as effective.

Pathogenesis

Macular holes have become the focus of much interest and controversy in ophthalmology. Much of this renewed interest stems from new theories of pathogenesisand the development of a possiblesurgical treatment for macular holes. Despite the numerous proposed theories, the pathogenesis of these lesions is still not well understood. Most current investigators believe that tangential vitreous traction plays an important role in their pathogenesis, as we described in the section of mechanism of blunt trauma. However, there are several mechanisms by which this tangential traction may be produced. Gass mentioned that condensation and contraction of the prefoveal cortical vitreous with glial cell proliferation in this condensed vitreous may generate tangential traction. Guyer and

192

 

Clinical Diagnosis and Management of Ocular Trauma

 

Green suggested that fluid movements of the liquefied

macular holes. This sudden traction exerted on the

 

 

 

 

vitreous in an enlarged premacular bursa can exert

anatomically thin fovea results in an immediate

 

 

traction on the remaining formed cortical vitreous, with

formation of a macular hole in most cases (Fig. 31.3).

 

 

that traction transmitted tangentially to the fovea.

 

 

 

These finding suggests that the named mechanisms

Treatment

 

are important in the generation of tangential traction

Vitrectomy surgery for idiopathic macular holes has

 

 

leading to the macular hole formation, and cellular

 

 

been shown to improve vision in some eyes. Current

 

 

proliferation may not play a major role in their

 

 

techniques include removal of the posterior hyaloids

 

 

pathogenesis. Studies also found that retinal fragments

 

 

and all epiretinal membranes from the macular area

 

 

are a rare feature of the vitreous in these patients; they

 

 

and prolonged postoperative macular gas tamponade.

 

 

are thus unlikely to be a constituent of macular hole

 

 

However, the role of vitrectomy surgery for a macular

 

 

opercula. Opercula are therefore better termed

 

 

hole caused by blunt ocular trauma is not still well

 

 

pseudo-opercula, as has been previously suggested.

 

 

established.

 

 

A mild chronic inflammatory infiltrate (lymphocytes)

 

 

The results of different series are encouraging.

 

 

is present in some cases of macular holes. Inflammation

 

 

Despite significant blunt trauma of different types,

 

 

and cellular or fibrocellular membrane fragments are

 

 

vitrectomy surgery for macular holes can result in a

 

 

more frequent in traumatic holes than in idiopathic

 

 

high likelihood of improved vision and a risk of comp-

 

 

holes. The significance of this difference is unclear, but

 

 

lications, that seems no greater than with vitrectomy

 

 

it is likely a direct result of the initial trauma.

 

 

surgery for idiopathic macular holes. Further, studies

 

 

 

 

 

Studies of Mechanical Forces

of different approaches with posterior vitrectomy are

 

 

needed to establish a consistent result for this condition;

 

 

Evidence from animal studies and biomicroscopic and

meanwhile different approaches are being performing

 

 

surgical observations of patients with a traumatic

according the case, the criteria and the resources

 

 

macular hole strongly suggest that vitreous traction is

worldwide.

 

 

important in their pathogenesis. Experimental

 

 

 

observation shows that sudden compression of the

TRAUMATIC RETINAL TEARS

 

 

globe produces an immediate stress on the retina at

(RETINAL BREAKS)

 

 

points of vitreous attachment. High-speed photography

Despite the surgical management (enough material to

 

 

of blunt trauma reveals indentation of the cornea

 

 

fill an entire book), we will describe in this stage some

 

 

followed by expansion of the globe at the equator.

 

 

features that can differentiate a Traumatic retinal Tear

 

 

This outward expansion of the equator is followed by

 

 

from those Non-Traumatic and the clinical features to

 

 

flattening of the posterior pole and then posterior

 

 

evaluate during the initial examination.

 

 

displacement of the posterior pole of the eye. It seems

 

 

Peripheral retinal breaks occur at sites of strong

 

 

likely that with this trampoline-like movement of the

 

 

vitreoretinal adhesions. During blunt trauma vitreo-

 

 

posterior pole, traction forces may in fact be along

 

 

retinal traction may occur by the forceful displacement

 

 

the surface of the retina, that is tangential, not unlike

 

 

or separation of the vitreous. Globe deformation also

 

 

what occurs in a more gradual manner with idiopathic

 

 

causes various shearing forces that further amplify the

 

 

 

 

 

 

vitreoretinal traction (coup and countercoup).

 

 

 

Retinal breaks resulting from trauma can be

 

 

 

horseshoe-shaped flap tears or operculated holes.

 

 

 

Formed vitreous is often attached to the elevated flap

 

 

 

of a horseshoe tear and the free-floating operculum

 

 

 

of the hole. These tears can occur along the vitreous

 

 

 

base or at the edge of lattice degeneration or

 

 

 

chorioretinal adhesions. If a retinal vessel is involved

 

 

 

in the tear, a dense vitreous hemorrhage can occur;

 

 

 

the attending surgeon must always remember that a

 

 

 

vitreous hemorrhage can advice about a retinal rupture,

 

 

 

that sometimes is covered by the blood at the initial

 

 

 

examination.

 

 

 

Giant retinal tears are retinal breaks that extend

 

 

 

3 or more clock hours. They occur at the edge of the

 

 

Fig. 31.3: Traumatic macular hole

vitreous base, which remains attached to the anterior

 

 

 

 

Management of Blunt Retinal Trauma

 

193

flap; their formation will depend upon the transmission

true in traumatic detachments associated with

 

of forces inside the globe, but also upon some previous

subretinal or vitreous hemorrhage, giant retinal tears,

 

retinal damage (e.g. high myopia).

or severe ocular contusions in which there has been

 

A retinal dialysis is a discontinuity or separation

an opportunity for RPE and other fibroglial cells to

 

of the retina from the pars plana at the ora. It is most

gain access to the vitreous cavity. Even a condition

 

frequently traumatic in nature and is characterized

like vitreitis can lead to retinal detachment because

 

by attachment of the vitreous to the posterior retinal

of its inflammatory condition.

 

flap. This is in contradistinction to retinal tears, in

Some studies conducted to study phakic retinal

 

 

which the vitreous usually adheres to the anterior

detachments have characterized some of the implied

 

flap; anyhow, vitreo-retinal traction is present in almost

features and have helped to establish improved

 

all the times. Traumatic retinal dialysis occurs most

guidelines for medicolegal determinations. Myopes

 

often in either the inferotemporal or superotemporal

typically developed giant tears and nasal dialyses;

 

quadrant. The risk of progression to retinal

emmetropes frequently developed inferotemporal

 

detachment is significant.

dialyses. It also has been noticed that lattice degene-

 

Therefore, all traumatic retinal tears and dialyses

ration did not increase post-traumatic detachments risk.

 

are treated prophylactically with photocoagulation or

Dialyses and giant tears caused 69% of traumatic

 

cryotherapy. Giant retinal tears that continue to tear

detachments in comparison with 6% of the cause of

 

despite photocoagulation also can be treated with

nontraumatic detachments. Experience has shown that

 

scleral buckling.

the overwhelming majority of traumatic retinal

 

 

detachments are rhegmatogenous in origin. Retinal

 

TRAUMATIC RETINAL DETACHMENT

breaks are predominantly located within the vitreous

 

base region but may occur at sites of focal scleral impact

 

Like in the previous section, the retinal detachment

 

or from posterior vitreous avulsion.

 

can include entire books; we will describe only some

 

 

 

features regarding the traumatic etiology of this

Management

 

condition.

 

Although the use of scleral buckling techniques alone

 

 

 

Mechanism of Pathology

may be sufficient, closed microsurgery may be required

 

in some cases to relieve retinal traction and to facilitate

 

Traumatic retinal detachments occur primarily as the

 

the identification and permanent closure of the retinal

 

result of retinal changes at the vitreous base. Goffstein

breaks. Prophylactic measures including the use of

 

and Burton, reported that 53% of traumatic retinal

closed microsurgery, play a vital role in the manage-

 

detachments were caused by retinal dialyses, 16% by

ment of traumatic retinal breaks and prevention of

 

giant retinal tears, 11% by horseshoe flap tears, and

complex retinal detachment.

 

8% by tears at the edge of lattice. Retinal detachments

Traumatic retinal detachments are treated primarily

 

can also happen secondary to traumatic tears of the

by scleral buckling. The results and visual outcomes

 

ciliary epithelium. Sometimes during the clinical evalua-

are quite favorable. As previously mentioned, most

 

tion is difficult to identify the specific cause.

of these patients (young patients) have well-formed

 

vitreous with posterior hyaloid attachment. Sometimes

 

The majority of these traumatic tears and detach-

 

during a pars plana vitrectomy a posterior vitreous

 

ments occur in younger individuals. The vitreous often

 

detachment may be difficult to create and the

 

is quite well formed and has not yet undergone a

 

morbidity associated with the vitrectomy may be

 

posterior vitreous detachment (PVD). This well-formed

 

greater than that seen with scleral buckling.

 

vitreous often limits the progression of retinal detach-

 

Because of these reasons, some authors attempt

 

ment, especially if it is caused by an inferior dialysis.

 

to avoid an intraocular approach in the repair of these

 

As time progresses and the vitreous becomes more

 

detachments. However, there are several well known

 

liquid or separates further, the detachment can then

 

indications for a primary repair of retinal detachment

 

progress more rapidly. This explains why many

 

by pars plana vitrectomy; vitreous hemorrhage

 

traumatic detachments do not present until several

 

obscuring visualization, posteriorly dislocated crystalline

 

months or even years after the original trauma. At this

lens, giant retinal tear with everted flap, proliferative

 

point the physician must remember that after an initial

vitreoretinopathy, subretinal hemorrhage and a large

 

trauma, the patient must be educated to follow

irregular posterior retinal tear.

 

multiple evaluations, even without symptoms; this

In these traumatic cases it is useful sometimes to

 

condition can imply even some legal issues.

combine the vitrectomy with an encircling element to

 

Detachments also can be associated with

support the vitreous base on a broad, shallow buckle.

 

proliferative vitreoretinopathy (PVR). This is especially

The final decisions must be taken by the attending

 

 

 

 

 

194

 

Clinical Diagnosis and Management of Ocular Trauma

 

surgeon according the case, the experience and the

VITREOUS BASEAVULSION

 

 

 

 

available resources.

The vitreous base represents the region of strongest

 

 

VITREOUS HEMORRHAGE

adhesion between the retina and vitreous. The vitreous

 

 

base’s strong adhesion continues anteriorly beyond

 

 

Vitreous hemorrhage can occur through a variety of

the ora into the pars plana and ciliary epithelium.These

 

 

adhesions are stronger in the young eye.

 

 

different mechanisms and sometimes is not becoming

 

 

Avulsion of the vitreous base is characteristic of

 

 

the main trouble; in fact many times it is only the advice

 

 

blunt ocular trauma. It is the result of ocular

 

 

of some other disturbances occurring in the posterior

 

 

deformation and shearing forces caused by the blunt

 

 

segment because of the blunt trauma. It can be the

 

 

trauma mentioned previously in this chapter.

 

 

clinical manifestation of iridodialysis, ciliary body

 

 

Frequently the avulsed vitreous base may be

 

 

trauma, avulsion or tear of a retinal vessel, and

 

 

associated with a retinal dialysis or giant retinal tear

 

 

breakthrough of subretinal blood from a choroidal

 

 

because the same shearing forces (coup and counter-

 

 

rupture between the most important.

 

 

coup).Therefore, the presence of an avulsed vitreous

 

 

Visually significant vitreous hemorrhages should be

 

 

base should alert the examiner to the possibility of

 

 

followed closely; within the days after the trauma, the

 

 

associated retinal or ocular injuries. These injuries can

 

 

hemorrhage can change, but also can change the

 

 

occur later in time than the initial trauma. In fact, some

 

 

circumstances of the posterior segment it self. There

 

 

studies reported that an avulsed vitreous base was

 

 

may be peripheral retinal pathology and eyes with

 

 

associated with a dialysis or giant tear in 26% of

 

 

 

 

 

 

traumatic retinal detachments, a particular high

 

 

 

percentage; this condition should aware the surgeon

 

 

 

to observe frequently the retina for days and weeks,

 

 

 

in particular in younger patients.

 

 

 

CHOROIDAL RUPTURE

 

 

 

Definition and Cinical Findings

Fig. 31.4: Vitreous and pre-retinal hemorrhage

retinal tears and vitreous hemorrhage are at increased risk for detachment due to fibroglial proliferation. Sometimes the changes in the retina can not be seen through the blood, so frequent ultrasonography is recommended to rule out the development of retinal detachment and to follow up the vitreous hemorrhage it self (Fig. 31.4).

It is preferable to treat vitreous hemorrhages expectantly; a conservative behavior should be the initial rule. Delayed clearing of the vitreous hemorrhage without the presence of other retinal abnormalities, presence of retinal tears that cannot be adequately visualized for treatment (corroborated with ultrasonography and sometimes even the clinical suspect), development of retinal detachment, and erythroclastic glaucoma are some indications for the surgical removal of the vitreous hemorrhage.

Choroidal ruptures are breaks in the choroid, the Bruch membrane, and the retinal pigment epithelium (RPE) that result from blunt ocular trauma and can be secondary to indirect or direct trauma. Cases secondary to direct trauma tend to be located more anteriorly and at the site of impact and parallel to the ora serrata, whereas those secondary to indirect trauma occur more posteriorly (countercoup). These ruptures have a crescent shape and are concentric to the optic disc. Indirect choroidal ruptures are almost 4 times more common than direct ruptures.

Histopathology

After blunt trauma, the ocular globe undergoes mechanical compression and then sudden hyperextension. Because of its tensile strength, the sclera can resist this insult; the retina is also protected because of its elasticity. The Bruch membrane does not have enough elasticity or tensile strength; therefore, it breaks! Concurrently, the small capillaries in the choriocapillaris are damaged, leading to subretinal or sub-RPE hemorrhage. Hemorrhage in conjunction with retinal edema may obscure the choroidal rupture during the acute phases, so frequently observation of retinal hemorrhages is mandatory.

As the blood clears, a white, curvilinear, crescentshaped streak concentric to the optic nerve is seen.

Management of Blunt Retinal Trauma

 

195

Direct choroidal ruptures are characterized by a

angiography may be a useful adjunct to detect CNV;

 

complete absence of choroid and RPE. The overlying

if CNV is absent, hypofluorescence occurs during the

 

retina is intact but atrophic because the lack of nutrition.

early phase of the angiogram due to disruption of the

 

In indirect choroidal ruptures, choroidal neovasculari-

choriocapillaris. During later stages, hyperfluorescence

 

zation (CNV) is a common finding during the early

occurs from the adjacent healthy choriocapillaris; if

 

healing phases. Most CNV is in the subretinal space.

CNV is present, early hyperfluorescence followed by

 

With time, most CNV involutes spontaneously. In a

late leakage is present on the angiogram.

 

small number of cases, a disciform scar or fibrous tissue

 

 

 

 

 

 

may grow into the retina and vitreous cavity. During

Management

 

the healing phase, choroidal neovascularization

Conservative treatment is recommended for most

 

occurs, but in most cases, it involutes spontaneously;

 

choroidal ruptures. During the healing phase of

 

a good, and long-term follow-up is mandatory in these

 

virtually all choroidal ruptures, CNV is present, with

 

lesions.

 

spontaneous resolution in the majority of the cases.

 

 

 

Diagnosis

In 15-30% of patients, CNV may recur and lead to

 

a hemorrhagic or serous macular detachment with

 

The physical findings are retinal edema (Berlin‘s

concomitant visual loss.

 

disease), hemorrhagic detachment of the macula,

The treatment of CNV will depend upon the locali-

 

serous detachment of the macula, subretinal hemor-

zation; if CNV is extrafoveal, it may be treated success-

 

rhage and a white curvilinear crescent-shaped streak

fully with laser photocoagulation; if CNV is subfoveal

 

concentric to the optic nerve (Figs 31.5 and 31.6).

or juxtafoveal, consider pars plana vitrectomy with

 

The imagines studies helping the diagnostic of

membrane extraction, with all the implicating risks

 

choroid hemorrhage and associated lesions; fluorescein

because of working near the fovea.

 

 

Most patients with choroidal ruptures do not reach

 

 

a final visual acuity of 20/40 or better; poor visual

 

 

acuity is associated with macular involvement. If the

 

 

rupture does not involve the fovea, good vision is

 

 

expected.

 

 

Most CNV occurs within the first year. However,

 

 

CNV has been reported to occur as late as 35 years

 

 

after the choroidal rupture. For legal reasons the

 

 

surgeon must always remember that choroidal

 

 

neovascularization can occur again, and so periodic

 

 

examinations are necessary.

 

 

Prognosis

 

Fig. 31.5: Choroid fracture

Fig. 31.6: Choroidal rupture

If the rupture does not involve the fovea, good vision is expected. In 15-30% of patients, CNV may arise again and lead to a hemorrhagic or serous macular detachment with concomitant visual loss. This usually occurs during the first year but can also occur decades later. Older age and macular rupture, the length of the rupture, and the distance of the rupture to the center of the fovea may be risk factors for CNV and so important factors in the long term prognosis.

OPTIC NERVE AVULSION

Definition and Clinical Findings

Traumatic optic neuropathy (TON) refers to an acute injury of the optic nerve secondary to trauma. The optic nerve axons may be damaged either directly or indirectly and the visual loss may be partial or complete. An indirect injury to the optic nerve typically occurs from the transmission of forces to the optic canal from