Ординатура / Офтальмология / Учебные материалы / Clinical Diagnosis and Management of ocular trauma
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Clinical Diagnosis and Management of Ocular Trauma |
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Commotio Retinae |
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Commotio retinae is also known as Berlin’s edema or |
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concussion edema. It is caused by blunt trauma (a |
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contrecoup injury), with the force being transmitted |
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through the vitreous and finally onto the retina and |
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choroids. With this condition, there will be a confluent |
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area of retinal whitening due to outer photoreceptor |
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disruption and RPE damage, but not edema. Blood |
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vessels are seen distinctly and are undisturbed under |
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the retinal whitening. The retinal opacification gradually |
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subsides over several weeks and visual function usually |
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returns to its pretrauma level. However, a permanent |
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loss of vision is not unusual and can be associated with |
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changes in the retinal pigment epithelium. |
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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 |
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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
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Clinical Diagnosis and Management of Ocular Trauma |
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hemorrhage such as leukemia, accidental trauma, |
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Moreira CA Jr, Ribeiro MD, Belfort R Jr. Epidemiological |
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leukemia, thrombocytopenia, anemia, etc. should be |
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study of eye injuries in Brazilian children. Arch |
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ruled out. Severe visual morbidity with shaken baby |
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Ophthalmol 1988;106:781-84. |
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Rapoport I, Romem M, Kinek M, et al. Eye injuries in |
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syndrome may be due to retinal detachment, optic |
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children in Israel. A National Collaborative Study. Arch |
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nerve atrophy or cortical blindness. |
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Ophthalmol 1990;108:376-79. |
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Canavan VM, O’Flaherty MJ, Archer DB, et al. A ten year |
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Eye Injury Prevention |
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survey of eye injuries in Northern Ireland. Br J |
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Ophthalmol 1980;64:618-25. |
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7. |
Holden R, Morsman DG, Davidek GMB, O’Conner GM. |
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The vast majority of eye injuries are preventable. Key |
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External ocular trauma in instrumental and normal |
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components of prevention include parental |
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deliveries. Br J Obstet Gynecol 1992;99:132. |
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supervision, education of children and protective |
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Angell LK, Robb RM, Berson FG. Visual prognosis in |
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eyewear. Ophthalmologists and parents must reinforce |
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patients with ruptures in Descmet’s membrane due to |
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forceps injury. Arch Ophthalmol 1981;99:21-37. |
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the importance of not playing with objects like |
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9. |
Sezen F. Retinal hemorrhages in new born infants. Br J |
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gillidanda, fire-crackers and bow and arrow. Health |
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Ophthal 1970;55:248. |
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education on the preventive aspects of ocular trauma |
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Volpe NJ, Larrison WI, Hersh PS et al Secondary |
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in schools as well as through mass media like television |
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hemorrhage in traumatic hyphema. Am J Ophthalmol |
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can help in achieving this goal. |
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1991; 112: 507-13. |
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Protective eyewear is the most important measure |
11. Thomas MA, Parrish RK, Feuer WJ. Rebleeding after |
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to prevent eye injuries in children. Plano polycarbonate |
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traumatic hyphema. Arch Ophthalmol 1986 Feb; |
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104(2):206-10. |
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goggles with a 2-3 |
mm center thickness are |
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12. |
McGetrick JJ, Jampol LM, Goldberg MF, et al. |
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recommended for sports. |
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Aminocaproic acid decreases secondary hemorrhage |
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after traumatic hyphema. Arch Ophthalmol 1983 Jul; |
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Summary |
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101(7):1031-33. |
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Kutner B,Fourman S, Brein K Aminocaproic acid |
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reduces the risk of secondary hemorrhage in patients |
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Ocular trauma is an important cause of monocular |
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with traumatic hyphema. Arch Ophthalmol 1987 Feb; |
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blindness in children. Due to young age, inability to |
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105(2):206-08. |
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cooperate with examination and the potential for |
Stern WH, Monclal KM. Vitrectomy instrumentation for |
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surgical evacuation of total anterior chamber hyphema |
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development of amblyopia, children presenting with |
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and control of recurrent anterior chamber hemorrhage. |
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eye injuries are evaluated and treated slightly differently |
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Ophthalmol Surg 1979; 10: 34-37. |
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from adults. Proper communication should be |
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McCuen BW, Fung WE. The role of vitrectomy |
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maintained between the ophthalmologist and family |
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instrumentation in the treatment of severe traumatic |
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throughout the course of treatment. |
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hyphema. Am J Ophthalmol 1979;88:930-34. |
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Dass AB, Ferrone PJ, Chu RY etal. Senstivity of spiral |
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computed tomography scanning for detecting intraocular |
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References |
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foreign bodies. Ophthalmology 2001; 108: 2326-28. |
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17. |
Kuhn F, Morris R,Mester V, et al. Internal limiting |
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1. Jaison SG, Silas SE, Daniel R, Chopra SK.A review of |
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membrane removal for traumatic macular holes. |
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Ophthalmic Surg Lasers 2001 Jul-Aug;32(4):308-15. |
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childhood admission with perforating ocular injuries in |
18. |
Amari F, Ogino N, Matsumura M et al. Vitreous surgery |
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a hospital in north-west India. Indian journal of |
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for traumatic macular holes. Retina. 1999; 19(5):410-13. |
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ophthalmology 1994;42(4):199-201. |
19. |
Chow DR, Williams GA, Trese MT et al. Successful closure |
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2. Sarda RP, Mehrotra AS, Ratnawat PS, et al. Ocular injuries |
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of traumatic macular holes. Retina 1999;19(5):405-09. |
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in childhood. Indian J Ophthalmol 1971;19:67-70. |
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Margherio AR, Margherio RR, Hartzer M et al Plasmin |
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3. Niiranen M, Raivio I. Eye injuries in children. Br J |
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enzyme-assisted vitrectomy in traumatic pediatric macular |
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Ophthalmol 1981;65:436-38. |
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holes. Ophthalmology 1998 Sep;105(9):1617-20. |
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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:
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Clinical Diagnosis and Management of Ocular Trauma |
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First there is direct contusion tissue damage at the |
globe status is obvious, careful documentation of these |
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site of impact. This is known as a coup injury, and |
circumstances, as well as the use and type of safety |
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includes retinal edema, necrotic changes, and |
glasses or other protective devices, has medical and |
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choroidal hemorrhage at the site of impact. |
legal relevance. The history should determine the |
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Second, injury can occur distant from the impact |
preinjury ocular status and the possibility of extraocular |
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site as the force is transferred through the globe |
trauma; the ocular baseline should include preinjury |
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to a contralateral site. This is called the contracoup |
vision, refractive status (myopic eyes are affected with |
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injury; examples of it include retinal edema and |
more severity with minor traumas), preexisting ocular |
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choroidal contusions in the posterior pole; in these |
diseases (e.g. retinal diseases, pseudoexfoliation, |
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lesions the posterior pole was not impacted directly, |
glaucoma), and previous ocular surgery (e.g. cataract, |
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but the transmission of forces affect it in different |
retinal surgery). The note of circumstances that should |
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degree. |
raise suspicions of open globe injuries is mandatory, |
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Finally, there are injuries caused by the globe |
high-speed projectile injuries, use of power tools, high- |
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deformation; some authors have documented by |
speed grinding of metal, leak from high-pressure |
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high-speed cinematography, globe deformation |
hydraulic system, metal-on-metal impact, sharp |
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following the application of blunt forces to the |
penetrating injuries and severe blunt injury (racquetball |
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cornea. In these movies we can see initially how |
or golf ball, stick or bat injury to orbit). |
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the anteroposterior axis is compressed; then the |
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anteroposterior axis is decompresses and so a |
Individual Pathologies Description |
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rebound expansion occurs. Then the equatorial |
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axis begins to expand as the anteroposterior axis |
COMMOTIO RETINAE |
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compresses but doesn’t reach maximum expansion |
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until after the anteroposterior axis begin its rebound |
Definition and Clinical Findings |
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decompression. This tremendous change of intra- |
Commotio retinae is also known as Berlin’s edema, but |
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ocular forces of compression and decompression |
the latter term is not completely appropriate. The clinical |
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within different axis of the globe, creates shearing |
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characteristic of this condition is a confluent area of |
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forces within the eye at tissue interfaces that are |
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retinal whitening due to outer photoreceptor disruption |
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especially concentrated at the vitreous base. |
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and RPE damage, but not edema. Blood vessels are seen |
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Choroidal rupture, vitreous base avulsion, iris root |
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distinctly and are undisturbed under the retinal |
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disinsertion, retinal dialysis and tears, and posterior |
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whitening. Commotio retinae results in retinal |
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vitreous separation are examples of injuries caused |
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opacification following blunt trauma. Mild commotio |
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by these shearing forces. |
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retinae usually settles spontaneously with minimal |
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After reading this, the clinical comprehends that |
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sequelaebutmoreseverecasesareassociatedwithvisual |
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he must be aware of damage caused by ocular blunt |
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loss. Commotio retinae can occur anywhere in the |
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trauma at any site of the eye; so a complete evaluation |
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retina, but it is usually maximal in the area opposite to |
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of all structures is mandatory, even in case of an |
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the blow (countracoup injury). So, explaining the |
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“pretended minor trauma”. |
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pathophysiology of the condition, the retinal changes |
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Initial Evaluation |
are caused by a contrecoup that is created by blunt |
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trauma, with the force being transmitted through the |
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vitreous and finally onto the retina and choroid |
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Proper identification and management of patients with |
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(Figs 31.1 and 31.2). |
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posterior segment injury begin with a systematic |
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approach to obtaining a complete history and conduc- |
Histopathology |
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ting a thorough ophthalmic examination. The reader |
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will be able to see more details in some other chapters |
Immediately after injury, the only abnormality is |
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of this book, but some important points will be |
disruption of the receptor outer segments. From one |
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featured regarding the posterior segment blunt trauma; |
to six days after trauma, many receptor cells undergo |
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because open and closed globe injuries are approached |
degeneration. The retinal pigment epithelium phago- |
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differently it is important for the ophthalmologist to |
cytoses the degenerating outer segments, occasionally |
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make this determination as soon as possible. |
migrating into the retina. There is no extracellular retinal |
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The circumstances surrounding the trauma are |
edema. The opacity of commotio retinae seems to |
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important and should be obtained directly from the |
represent disrupted receptor cells. Visual loss may result |
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patient and/or an eyewitness in particular if the patient |
from permanent loss of receptors. The pigment |
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is unable to communicate. Even in cases in which the |
epithelial response to traumatic receptor damage is |
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Management of Blunt Retinal Trauma |
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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
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Clinical Diagnosis and Management of Ocular Trauma |
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Green suggested that fluid movements of the liquefied |
macular holes. This sudden traction exerted on the |
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vitreous in an enlarged premacular bursa can exert |
anatomically thin fovea results in an immediate |
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traction on the remaining formed cortical vitreous, with |
formation of a macular hole in most cases (Fig. 31.3). |
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that traction transmitted tangentially to the fovea. |
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These finding suggests that the named mechanisms |
Treatment |
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are important in the generation of tangential traction |
Vitrectomy surgery for idiopathic macular holes has |
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leading to the macular hole formation, and cellular |
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been shown to improve vision in some eyes. Current |
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proliferation may not play a major role in their |
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techniques include removal of the posterior hyaloids |
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pathogenesis. Studies also found that retinal fragments |
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and all epiretinal membranes from the macular area |
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are a rare feature of the vitreous in these patients; they |
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and prolonged postoperative macular gas tamponade. |
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are thus unlikely to be a constituent of macular hole |
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However, the role of vitrectomy surgery for a macular |
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opercula. Opercula are therefore better termed |
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hole caused by blunt ocular trauma is not still well |
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pseudo-opercula, as has been previously suggested. |
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established. |
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A mild chronic inflammatory infiltrate (lymphocytes) |
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The results of different series are encouraging. |
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is present in some cases of macular holes. Inflammation |
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Despite significant blunt trauma of different types, |
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and cellular or fibrocellular membrane fragments are |
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vitrectomy surgery for macular holes can result in a |
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more frequent in traumatic holes than in idiopathic |
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high likelihood of improved vision and a risk of comp- |
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holes. The significance of this difference is unclear, but |
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lications, that seems no greater than with vitrectomy |
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it is likely a direct result of the initial trauma. |
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surgery for idiopathic macular holes. Further, studies |
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Studies of Mechanical Forces |
of different approaches with posterior vitrectomy are |
|
|
needed to establish a consistent result for this condition; |
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|
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. |
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|
important in their pathogenesis. Experimental |
|
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|
observation shows that sudden compression of the |
TRAUMATIC RETINAL TEARS |
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|
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 |
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|
of blunt trauma reveals indentation of the cornea |
|
|
|
fill an entire book), we will describe in this stage some |
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|
followed by expansion of the globe at the equator. |
|
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|
features that can differentiate a Traumatic retinal Tear |
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|
This outward expansion of the equator is followed by |
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from those Non-Traumatic and the clinical features to |
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|
flattening of the posterior pole and then posterior |
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|
evaluate during the initial examination. |
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|
displacement of the posterior pole of the eye. It seems |
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Peripheral retinal breaks occur at sites of strong |
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likely that with this trampoline-like movement of the |
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|
vitreoretinal adhesions. During blunt trauma vitreo- |
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posterior pole, traction forces may in fact be along |
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|
retinal traction may occur by the forceful displacement |
|
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|
the surface of the retina, that is tangential, not unlike |
|
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|
or separation of the vitreous. Globe deformation also |
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what occurs in a more gradual manner with idiopathic |
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causes various shearing forces that further amplify the |
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vitreoretinal traction (coup and countercoup). |
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Retinal breaks resulting from trauma can be |
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|
horseshoe-shaped flap tears or operculated holes. |
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|
Formed vitreous is often attached to the elevated flap |
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|
of a horseshoe tear and the free-floating operculum |
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|
of the hole. These tears can occur along the vitreous |
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|
base or at the edge of lattice degeneration or |
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|
chorioretinal adhesions. If a retinal vessel is involved |
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in the tear, a dense vitreous hemorrhage can occur; |
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the attending surgeon must always remember that a |
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vitreous hemorrhage can advice about a retinal rupture, |
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that sometimes is covered by the blood at the initial |
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|
examination. |
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Giant retinal tears are retinal breaks that extend |
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|
3 or more clock hours. They occur at the edge of the |
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|
Fig. 31.3: Traumatic macular hole |
vitreous base, which remains attached to the anterior |
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|
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 |
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|||
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 |
|
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|
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 |
|
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|
features regarding the traumatic etiology of this |
Management |
|
|
condition. |
|
||
Although the use of scleral buckling techniques alone |
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||
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||
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 |
|
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|
194 |
|
Clinical Diagnosis and Management of Ocular Trauma |
|
|
surgeon according the case, the experience and the |
VITREOUS BASEAVULSION |
|
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||
|
|
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 |
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|
|
associated with a dialysis or giant tear in 26% of |
|
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|
|
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
