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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Posterior Segment
Ocular Trauma
C H A P T E R
24Management of Traumatic
Hemorrhages to the
Posterior Segment
Javier A Montero, Jose M Ruiz-Moreno (Spain)
Introduction
Ocular trauma is a significant cause of visual impairment in the United States and the leading cause of unilateral blindness worldwide. Ocular trauma is more frequent among adult males mainly due to occupational reasons, though females and children may also present ocular damage secondary to trauma. Isolated damage to the anterior segment occurs in more than half of the cases and isolated damage to the posterior segment is uncommon.1
Approximately 2.5 million injuries occur annually, 40,000 of which cause serious visual loss. Vision is lost because of primary mechanical damage of vital ocular structures and secondary complications, such as infectious endophthalmitis and retinal detachment due to intraocular fibrous proliferation and contraction.1
The presence of marked vitreous hemorrhage is associated with poor visual prognosis in ocular trauma involving the posterior segment. Poor prognostic factors include presenting visual acuity of light perception or lower, hyphema, and traumatic cataract. Severe vitreous hemorrhages after closed-globe injury are frequently associated with various anterior and posterior segment pathologies, and early vitrectomy is considered to improve early visual rehabilitation and management of any potentially treatable posterior pathology.2
Ocular hemorrhage associated with trauma may occur after blunt and penetrating injuries. A careful and complete ophthalmic examination is required in every case since injuries causing minimal signs of damage to one part of the eye may cause a significant injury in another part of the eye with severe consequences for the patient and occasionally to the ophthalmologist who has misdiagnosed the trauma.
Blunt injuries are more common and cause more cases of visual impairment than penetrating injuries, although the frequency of severe damage, blindness, and loss of the globe itself is greater with ocular
penetration or rupture. Two types of injuries may disrupt the continuity of the sclera: penetration by relatively sharp objects, and rupture caused by massive blunt trauma.
The visual prognosis is more favorable when the primary mechanical damage caused by sharp penetration is limited to the anterior segment of the eye. Modern microsurgical techniques permit better wound closure and reconstruction of the anterior ocular structures. Penetrating injuries involving the posterior segment carry a less favorable prognosis. The primary mechanical damage of vital structures by such injuries may be so great that useful vision is instantly destroyed. However, the application of appropriate vitreoretinal surgery to prevent or treat secondary complications may result in the preservation of eyes that would otherwise be lost.
Both eyes should always be examined. Visual acuity determination should be performed in the first place; if standardized charts are not available we should at least be able to determine finger counting and reading abilities and the distance of these exams should be recorded. If none of these abilities can be reached, the light perception and projection abilities should be recorded. The evaluation of the direct and consensual pupillary reflexes is of great prognostic value. Decreased visual acuity is usually a sign of severity. Over 40% of the cases report marked visual acuity loss (lower than 20/200) associated with severe ocular trauma.
Anterior segment examination may disclose corneal lacerations, traumatic iritis, hyphema, damage to lens and vitreous opacities among others, which may limit the examination of the posterior segment (Fig. 24.1). Ocular examination should be extremely careful until the absence of ocular perforation has been established, avoiding pressure on the eye ball and administration of drops or ointments (Fig. 24.2).
In the presence of hyphema posterior segment examination should be gently performed in order to prevent further bleeding and scleral indentation should be avoided for 2-3 weeks.
140 |
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Clinical Diagnosis and Management of Ocular Trauma |
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The size, location and characteristics of hemorrhages |
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should be recorded. Vitreous hemorrhages may vary |
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in size, location and density. Initially they are usually |
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close to the damaged area, though they may later |
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spread and occupy the whole vitreous cavity precluding |
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examination of posterior segment structures. If |
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posterior segment examination is not satisfactory due |
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to the presence of anterior segment or vitreous hemor- |
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rhages contact A-scan and B-scan ultrasonography are |
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helpful for detecting posterior vitreous detachment and |
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differentiating it from retinal detachment (Fig. 24.3). |
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The symptoms associated with posterior hemor- |
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Fig. 24.1: Subconjunctival hemorrhage after severe blunt |
rhages will depend on the locations and size of the |
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hemorrhage. Peripheral retinal hemorrhages may be |
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trauma masking scleral rupture. The patient presented |
asymptomatic; retinal, choroidal or retrohyaloidal |
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vitreous hemorrhage with choroidal rupture |
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hemorrhages affecting the posterior pole will present |
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as central scotomata (Fig. 24.4); and patients with |
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vitreous hemorrhages will complain of floaters, blurred |
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vision or even light perception vision, depending on |
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the amount of blood present. |
Fig. 24.2: Retroequatorial intraocular foreign body which penetrated through the lower lid
A careful examination of the vitreous, posterior pole and peripheral retina under pharmacologic mydriasis is mandatory, since anterior or posterior hemorrhage may later mask damage to the posterior segment. Indirect ophthalmoscopy is a useful tool to evaluate damage to the posterior segment allowing a fast binocular examination of the vitreous and the retina and verification of the presence of intraocular foreign bodies (IOFB). Posterior pole biomicroscopy using contact and non contact lenses will improve the detailed examination of the macula, though non contact lenses are more useful reducing the risk of squeezing an injured eye. Scleral depression may increase the risk of intraocular bleeding and should only be performed once ocular rupture has been discarded.
Anterior, central and posterior vitreous examination should be performed and the presence of any hemorrhage or vitreous opacity recorded. The location and size of the opacities should be recorded, as well as the presence of posterior vitreous detachment. Pigment clusters may appear floating in the peripheral or anterior vitreous following detachment of the vitreous base from the pars plana.
Fig. 24.3: Ultrasonography A and B scan reveals a marked choroidal hemorrhage with vitreous blood
Fig. 24.4: Grade I vitreous hemorrhage
Management of Traumatic Hemorrhages to the Posterior Segment |
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141 |
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Pathogenesis |
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penetration may cause visual impairment. They include |
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the toxic effects of IOFB, such as copper and iron, |
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Blunt trauma may cause damage to the eye by three |
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and the introduction of bacteria and fungi with |
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different mechanisms: coup, contrecoup and ocular |
consequent infectious endophthalmitis. Retained lens |
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compression. Coup refers to local damage at the site |
material and blood and the incarceration of vitreous |
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of impact, whereas contrecoup refers to injuries at the |
and uvea causes chronic inflammation that may play |
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opposite side of the eye caused by shock waves that |
an important role in the stimulation of intraocular |
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traverse the eyeball with foci of tissue damage along |
fibrocellular proliferation. At a later stage, blood and |
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the path of the shock waves, especially at interfaces |
lens material in the presence of large scleral wounds |
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of tissues of different density. |
may induce formation of fibrocellular proliferation |
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The ocular compression mechanism is determined |
which, upon contraction may cause traction retinal |
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by the inextensibility of the eyeball and the |
detachment, retinal breaks, rhegmatogenous retinal |
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incompressibility of intraocular fluids so that when the |
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detachments, proliferative vitreoretinopathy, cyclitic |
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eye is compressed along its anterior-posterior axis, it |
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membranes, ciliary body detachments, hypotony, and |
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expands in its equatorial plane causing severe traction |
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phthisis bulbi. |
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at the vitreous base. Ocular compression may cause |
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scleral rupture even in eyes which have not undergone |
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previous surgery. In these cases the two most common |
Classification |
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locations for scleral rupture are at the limbus and |
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parallel to the muscle insertions between the insertion |
Even though these lesions seldom appear isolated, |
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and the equator. The hallmarks of scleral rupture are |
hemorrhages to the posterior segment may be classi- |
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severe reduction in visual acuity, an afferent pupillary |
fied for a didactic purpose as: |
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defect, hypotony, abnormally deep anterior chamber, |
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Vitreous hemorrhages |
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decreased ocular ductions, severe subconjunctival |
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Retrohyaloidal hemorrhages |
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edema, hyphema, and vitreous hemorrhage. Scleral |
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Retinal hemorrhages |
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rupture can rarely be confirmed by ophthalmoscopy |
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Choroidal hemorrhages |
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because severe vitreous hemorrhage and/or hyphema |
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Papillary and peripapillary hemorrhages |
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nearly always accompany scleral rupture. Ultrasono- |
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Hemorrhages associated with indirect trauma |
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graphy and computed tomographic scanning may |
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show a shrunken globe, retinal detachment, partial or |
VITREOUS HEMORRHAGES |
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complete posterior vitreous detachment and |
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The presence of vitreous hemorrhage has been |
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vitreoretinal adherences. The visual prognosis of |
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associated with retinal detachment and surgical removal |
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ruptured globes is usually very poor. |
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of the blood seems to reduce the frequency of retinal |
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The aetiologies and the mechanisms of damage of |
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detachment.3 The role of the presence and manage- |
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penetrating injuries are highly variable and cause a |
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ment of vitreous hemorrhage has been reported by |
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wide spectrum of acute structural alterations and |
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several series,4, 5 as well as the role of the quantification |
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secondary complications. |
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Penetration of the eye by relatively blunt objects |
of the hemorrhage. Brinton et al reported functional |
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causes compression of the globe resulting in |
recovery in 48% of the eyes presenting moderate to |
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iridodialysis, subluxation and dislocation of the lens, |
severe vitreous hemorrhage vs 67% of the eyes with |
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traumatic cataract, choroidal rupture, retinal breaks |
mild or no vitreous hemorrhage.6 |
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at the vitreous base borders and vitreous detachment. |
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Blood proteins may be involved in vitreous proli- |
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Ruptures of the uvea produce anterior chamber, |
feration mediated by hemorrhages. Fibronectin is a |
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choroidal, subretinal, and vitreous hemorrhage. |
high molecular weight glycoprotein with a chemotactic |
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Massive blunt trauma causes corneal and scleral |
action on retinal pigment epithelium (RPE), fibroblasts |
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ruptures and may avulse the optic nerve. |
and giant cells and mediates in the interaction between |
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Penetrating objects cause lacerations of the cornea, |
collagen and the RPE. Fibronectin has been detected |
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iris, lens, sclera, ciliary body, choroid, retina, and optic |
in epiretinal membranes in human eyes following |
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nerve, usually combined with anterior chamber, |
retinal detachment repair after ocular trauma.7, 8 Platelet |
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choroidal, subretinal, and vitreous hemorrhages and |
derived growth factor (PDGF), complement and |
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occasional prolapse and incarceration of the lens, uvea, |
interleukins also induce intravitreal fibrosis. |
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retina, and vitreous. Cleary and Ryan reported on the |
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It is necessary to quantify the amount of vitreous |
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increased frequency of retinal detachment following |
hemorrhage. One accepted classification for this |
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penetrating ocular trauma associated with vitreous |
quantification was proposed at the Vitrase for Vitreous |
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hemorrhage.3 The secondary complications of ocular |
Hemorrhage study9 as Grade I when retinal detail is |
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142 |
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Clinical Diagnosis and Management of Ocular Trauma |
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Fig. 24.5: Grade 3 vitreous hemorrhage
visible with some hemorrhage present and laser photocoagulations is possible; Grade 2 with large retinal vessels visible but central retinal is not visible enough to perform adequate posterior laser treatment; Grade 3 with red reflex and no retinal vessels are seen behind the equator; and Grade 4 with no red reflex.
The symptoms of vitreous hemorrhage are visual acuity loss, perception of mobile dark spots in the visual field. Associated signs are visualization of erythrocytes floating in the anterior vitreous behind the lens with dilated pupil. Intense vitreous hemorrhage may lead to loss of pupillary reflex and blurring of retinal details (Fig. 24.5). Retinal tear and detachment should be disclosed in all cases of traumatic vitreous hemorrhage. B scan ultrasonography is a useful tool to perform examination of vitreoretinal adherences.
Vitreous hemorrhages may appear secondary to blunt trauma following scleral rupture, vitreous detachment, tears in the iris, ciliary body, choroid, or retina. We should assume that a retinal break is present until proved otherwise. Blood from choroidal ruptures accumulates beneath the neurosensory retina passing through the retina into the vitreous cavity.
Vitrectomy is indicated for vitreous hemorrhage caused by ocular contusion when a retinal detachment is suspected because of sudden additional loss of vision, when a retinal detachment is detected through a window in the hemorrhage, when a large retinal break or retinal detachment is diagnosed by ultrasound, or when there is no improvement after a reasonable period of observation.10-13
RETROHYALOIDAL HEMORRHAGES
Retrohyaloidal hemorrhages usually appear following incomplete posterior vitreous detachment as a result
Fig. 24.6: Retrohyaloidal hemorrhage
of vitreoretinal traction or transit of subretinal blood (Fig. 24.6). Retrohyaloidal or preretinal hemorrhages are usually thick, masking retinal vessels and may show a characteristic boat-shape with a superior horizontal level. Even though retrohyaloidal blood tends to disappear spontaneously, treatment has been proposed in order to reduce the contact of blood with the retina and decrease its toxic effect.14-16
INTRARETINAL HEMORRHAGES
Intraretinal hemorrhages may appear under different circumstances associated with ocular or distant trauma. The location of the blood will determine the presence of symptoms. Extrafoveal blood is usually asymptomatic. Juxtafoveal and subfoveal blood may present as paracentral or central scotomata.
Subretinal blood is toxic for the retina and the RPE17 and thick hemorrhages worsen visual prognosis. Additionally, it is considered that the presence of hemorrhage limits the closure of the retinal or choroidal tear.
The image of retinal hemorrhages may vary depending on how deep the retina is affected. Blood affecting the retinal nerve fibre layer appears as flame shaped hemorrhages, whereas hemorrhages affecting the nuclear layers appear as irregular shaped spots (Figs 24.7 to 24.9). Retinal hemorrhages usually do not mask retinal vessels.
CHOROIDAL HEMORRHAGES
Posterior choroidal ruptures are probably caused by anterior-posterior compression and equatorial expansion. Blunt trauma may produce hemorrhage into the choroid secondary to Bruch’s membrane rupture and tear of the overlying RPE and underlying choriocapillaris. Patients with angioid streaks and other conditions known to be associated with an inelastic and fragile Bruch’s membrane are especially vulnerable to choroidal rupture.
Management of Traumatic Hemorrhages to the Posterior Segment |
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143 |
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Choroidal hemorrhages may vary in intensity from |
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small subretinal hemorrhages associated with Bruch’s |
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membrane ruptures to huge suprachoroidal |
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hemorrhages that may complicate corneal or scleral |
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lacerations leading to expulsive hemorrhages. |
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Choroidal hemorrhages may be massive leading |
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to ocular hypotony and choroidal detachment, usually |
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associated with vitreous hemorrhage or mask subretinal |
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hemorrhages.18 |
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Direct choroidal ruptures are uncommon and |
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usually anterior and oriented parallel to the ora. Indirect |
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ruptures are more common and tend to occur away |
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from the site of impact. A choroidal rupture may be |
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initially obscured by a subretinal hemorrhage caused |
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Fig. 24.7: Submacular hemorrhage |
by tearing of the choriocapillaris. Later, after the blood |
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has resorbed, a white curvilinear streak concentric to |
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causing central scotoma |
the optic disc is seen. Only rarely is a rupture oriented |
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radially with respect to the optic disc. Most are temporal |
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to the disc and single, although nasal and multiple |
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ruptures can also occur (Fig. 24.10). Typical small |
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choroidal hemorrhages are rounded, dark red-blue |
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and frequently take many weeks to resorb and may |
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leave areas of pigment alteration. |
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Visual prognosis is generally good unless the |
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choroidal rupture is under the foveola, or an associated |
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subretinal hemorrhage extends under the foveola). |
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The overlying nerve fiber layer is almost never torn. |
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Therefore, a rupture can be located between the disc |
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and the macula and yet not affect the visual acuity. |
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Choroidal ruptures can, months to years later, be |
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complicated by the development of a choroidal |
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neovascular membrane, with serous or hemorrhagic |
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retinal detachment and loss of central vision.19 In these |
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Fig. 24.8: Spontaneous resorption of |
cases photodynamic therapy20 and more recently |
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intravitreal antiangiogenic therapy may be useful. |
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||
submacular hemorrhage |
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PAPILLARYAND PERIPAPILLARY |
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HEMORRHAGES |
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Papillary and peripapillary hemorrhages may appear |
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following optic nerve damage by blunt trauma. Possible |
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Fig. 24.9: Complete spontaneous resorption of macular |
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hemorrhage. Visual acuity was 20/20 |
Fig. 24.10: Choroidal ruptures |
144 |
|
Clinical Diagnosis and Management of Ocular Trauma |
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|
mechanisms include compression by intrasheath |
and venules. The aetiology of the white retinal |
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||
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|
hemorrhage and oedema and direct shock-wave |
lesions resulted is controversial. Extravasated lymph |
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|
trauma to the nerve fibers. The management involves |
from retinal vessels, reflux venous shock waves, |
|
|
high-dose intravenous steroids, especially if they can |
arteriolar and fat emboli and blood product emboli |
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|
be started within 8 hours, surgical decompression of |
formed after complement activation have been |
|
|
optic nerve sheath hematoma and neurosurgical |
proposed. Clinically, the retinal lesions resolve over |
|
|
decompression of the optic canal. Avulsion of the optic |
a period of weeks to a few months followed |
|
|
nerve may be accompanied by severe damage to other |
occasionally by pigment migration and optic |
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|||
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|
ocular tissues or be the sole manifestation of apparently |
atrophy. Visual acuity may return to normal or near |
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|
minor direct trauma. |
normal. |
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|
• Valsalva retinopathy is characterized by preretinal |
|
|
HEMORRHAGE ASSOCIATED WITH |
(retrohyaloidal) hemorrhages in the macular area, |
|
|
INDIRECT TRAUMA |
and is secondary to Valsalva manoeuvres associated |
|
|
• Shaken baby syndrome may be associated in one |
with vomiting, coughing. Visual function usually |
|
|
returns to normal spontaneously. Hemorrhages |
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|
third of the cases with ocular manifestations, above |
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|
located on the macula may present as decreased |
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|
all subconjunctival and retinal hemorrhages. |
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visual acuity, but the syndrome is usually |
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|
Intraocular hemorrhages are considered to be a |
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|
asymptomatic. |
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|
predictive of intracranial bleeding and the severity |
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|
• Retinitis sclopetaria is defined by the rupture of the |
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of the latter is related to that of the neurological |
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choroid or retina caused by shock waves generated |
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lesion. Funduscopic examination usually reveals |
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|
by passage of a high-velocity missile through the |
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retinal hemorrhages, perimacular folds, cotton |
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orbit without directly striking the eye. Initial clinical |
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wool spots, optic disk edema, and venous stasis. |
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manifestations may be a subretinal or vitreous |
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Less frequently, vitreous hemorrhages, retinal |
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hemorrhage with decreased visual acuity. As the |
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detachment, retinoschisis and chorioretinal atrophy |
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blood clears, breaks in the Bruch’s membrane and |
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are seen. |
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|
in the choriocapillaris are frequently seen as well |
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• Terson syndrome is characterised by a preretinal |
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|
as fibrous tissue proliferation into the eye. Retinal |
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hemorrhage associated with subarachnoidal |
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detachment rarely occurs because of fibrous tissue |
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hemorrhage. The intraocular hemorrhage has been |
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proliferation binding the retina to the choroid. |
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classically attributed to transit of blood through the |
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optic nerve sheaths. Presently, intraocular blood |
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|
is considered to be secondary to rupture of |
Medical Management |
|
|
peripapillary and epipapillary capillaries caused by |
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|
Intravitreal ovine hyaluronidase has been used to |
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|
increased intracranial pressure. Ophthalmoscopy |
|
|
|
usually reveals a preretinal hemorrhage in the |
promote resorption of intravitreous blood. 1125 |
|
|
peripapillary and macular area located exterior to |
patients with vitreous hemorrhage and visual acuity |
|
|
the inner limiting membrane (ILM). However, blood |
worse than 20/200 during more than one month were |
|
|
may go through the ILM and appear as a vitreous |
randomized 55 IU or 75 IU ovine hyaluronidase or |
|
|
hemorrhage. The most frequent complication of |
saline. Clearance of blood was achieved at months |
|
|
Terson syndrome is the appearance of epiretinal |
1, 2 and 3 in 13%, 26%, and 33% of patients injected |
|
|
membranes. |
with 55 IU compared with 6%, 16%, and 26% of |
|
|
• Purtscher retinopathy is a haemorrhagic vasculo- |
saline-treated patients.9 |
|
|
pathy characterized by multiple retinal |
Tissueplasminogen activator has been used in |
|
|
hemorrhages, areas of retinal pallor around the |
combination with surgery,21 with intravitreal injection |
|
|
optic disk and decreased visual acuity. A serous |
of gas (in patients with traumatic choroidal rupture)22 |
|
|
macular detachment may appear associated with |
or as isolated therapy23 with favorable results, |
|
|
vascular dilation and tortuosity and optic disk |
improving vision and occasionally deferring the need |
|
|
oedema. Purtscher retinopathy is secondary to |
for vitrectomy. These procedures have been used in |
|
|
blunt head trauma and thoracic compression. This |
cases of subfoveal21, 22, 24 and retrohyaloidal23 thick |
|
|
syndrome is usually bilateral and the symptoms |
hemorrhages. After a mean follow-up of 10.5 months |
|
|
usually appear 48 hours after the trauma. The |
final visual acuity improved by 2 lines or greater in |
|
|
peripheral retina is commonly spared. Fluorescein |
10 (67%) of 15 eyes and measured 20/80 or better |
|
|
angiography can reveal focal areas of arteriolar |
in 6 (40%) of 15 eyes in on series with complications |
|
|
obstruction, capillary nonperfusion, disc edema, |
including breakthrough vitreous hemorrhage in three |
|
|
and dye leakage from retinal arterioles, capillaries, |
eyes and endophthalmitis in one eye.24 However the |
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|
|
|
Management of Traumatic Hemorrhages to the Posterior Segment |
|
145 |
|
reported series were short and randomized clinical trials |
because of the removal of nonclearing vitreous |
|
|
are missing. |
hemorrhage. Vitreoretinal surgery is also of great value |
|
|
Krypton, Argon and Nd-YAG laser treatment have |
in the repair of penetrating injuries with retained |
|
|
been performed in patients with intraocular |
nonmagnetic foreign bodies and selected cases of |
|
|
hemorrhages to improve visual acuity by removing |
magnetic IOFB that are difficult or dangerous to extract |
|
|
preretinal blood permitting its transit to the vitreous |
with an electromagnet and in the management of eyes |
|
|
cavity. Dellaporta reported on the use of argon laser |
with posttraumatic endophthalmitis. Secondary |
|
|
retinotomies to the posterior pole of one patient with |
complications, including traction and rhegmatogenous |
|
|
|
|||
thick submacular hemorrhage permitting escape of |
retinal detachments, are minimized by the timely |
|
|
subretinal blood into the vitreous.25 A less aggressive |
removal of hemorrhage, disrupted lens, and damaged |
|
|
approach using Nd-YAG laser was tried on patients |
vitreous. |
|
|
with retrohyaloidal hemorrhages.14 Visual acuity in all |
Additionally, the presence of vitreous hemorrhage, |
|
|
cases before laser treatment was hand movement. |
as well as delay in IOFB removal, preoperative retinal |
|
|
After laser treatment, the hemorrhage instantly drained |
detachment and primary surgical repair combined with |
|
|
into the vitreous cavity, resulting in rapid improvement |
the IOFB removal have been significantly associated |
|
|
of vision. After a mean follow-up of 26.3 months no |
with the postoperative retinal detachment and a poorer |
|
|
retinal damage or rebleeding occurred due to the laser |
visual outcome.27 |
|
|
treatment, and vitrectomy was not required in any |
The aim of vitrectomy is to remove vitreous |
|
|
eye. However most of the reports lack long term |
opacities. A standard three-port 25 or 23 G vitrectomy |
|
|
follow-up. Ulbig et al reported on the the effects of |
technique is preferred for nonclearing vitreous |
|
|
drainage of premacular subhyaloid hemorrhage into |
hemorrhage. Initially, a central core of opaque vitreous |
|
|
the vitreous with an Nd-YAG laser in a large series of |
is removed, beginning sufficiently close to the lens that |
|
|
21 patients with a circumscribed premacular subhyaloid |
the tips of the cutter and endoilluminator can be |
|
|
hemorrhage of various causes with long-term follow- |
visualized, while maintaining the cutting orifice of the |
|
|
up. Even though in 16 eyes visual acuity improved |
probe under visual control in order to be able to |
|
|
within 1 month, four eyes had persistent, dense, |
examine the aspirated material. The excision is |
|
|
nonclearing vitreous opacity for at least 3 months and |
progressively carried posteriorly until the anticipated |
|
|
finally required vitrectomy. One case with clotted |
plane of the posterior hyaloid is approached. A small |
|
|
hemorrhage did not drain into the vitreous. Final visual |
opening is made in the detached posterior hyaloid, |
|
|
outcome was determined by the underlying diagnosis, |
through which unclotted blood is aspirated by use of |
|
|
such as Valsalva retinopathy (7 eyes), diabetic |
active suction from a soft-tipped cannula. Once the |
|
|
retinopathy (7 eyes), branch retinal vein occlusion (4 |
retina has been visualized, it is best to remove as much |
|
|
eyes), and retinal macroaneurysm, Terson syndrome, |
retrohyaloidal blood as possible to prevent dispersion |
|
|
or blood dyscrasia (1 eye each). Eyes with Valsalva |
into the vitreous cavity with consequent loss of visual |
|
|
retinopathy fared the best. Complications included a |
control. |
|
|
macular hole in 1 eye and a retinal detachment from |
Recently opacified vitreous may be red, yellow or |
|
|
a retinal break in a myopic patient. The authors |
mild green whereas old blood looks brown and dirty. |
|
|
concluded that drainage of premacular subhyaloid |
While removing dense haemorrhagic vitreous we may |
|
|
hemorrhage into the vitreous with an Nd-YAG laser |
find areas with old liquefied blood that may obscure |
|
|
is a viable treatment alternative for eyes with recent |
visualization of the retina. In such cases we should bring |
|
|
bleeding, but the risks and benefits have to be weighed |
the probe forward in order to be able to visualize its |
|
|
in a randomized trial and compared with those of |
tip until visualization of the vitreous cavity has become |
|
|
deferral of treatment or primary vitrectomy. |
clearer. Actively bleeding foci in the iris, ciliary body |
|
|
Nd-YAG laser has been reported to complete |
or retina are treated by raising the intraocular pressure |
|
|
vitreous hemorrhages in order to achieve vitreolysis |
and using endodiathermy if necessary. If visualization |
|
|
and permit spontaneous resorption of the vitreous |
of the bleeding foci is not possible, a fluid-air |
|
|
blood.26 |
interchange can be performed to permit |
|
|
SURGICAL MANAGEMENT |
endodiathermy and the eye is refilled with liquid in |
|
|
order to proceed with vitrectomy. Fresh blood tends |
|
||
Vitreoretinal surgery is helpful in the management of |
to clot and firmly adhere to the retina, whereas old |
|
|
subluxation or dislocation of the lens, vitreous |
blood liquefies in a few days and is more easily |
|
|
hemorrhage, and retinal detachment caused by ocular |
aspirated. |
|
|
trauma, permitting identification and treatment of |
Significant vitreous hemorrhages occurring weeks |
|
|
retinal breaks created at the time of blunt injuries |
before surgery are usually associated with sponta- |
|
|
|
|
|
|
