Melvin D. Rabena,
Dante J. Pieramici,
Mark W. Balles
The retina, marvelous in its design and function, is a fragile tissue, easily injured and possessing only modest capabilities for repair. The mechanisms of traumatic injury of the retina are numerous and can be categorized into those associated with blunt force (contusion/rupture), those resulting from sharp or lacerating forces, those resulting from acceleration/deceleration forces, and other more complex mechanisms. The most common injuries of the retina involve contusion related trauma (closed globe) and to understand the diffuse nature of these injuries requires an appreciation of the mechanical changes the globe undergoes following blunt impact (Fig. 173.1).
Our ability to manage severe ocular injuries has certainly improved in the past 50 years; however, involvement of the retina continues to be an ominous sign, portending a poor visual prognosis.
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FIGURE 173.1 Closed globe injury. (a) Dimensional changes in the eye following contusion (blunt) injury. The anteroposterior dimension of the globe shortens (large arrow) as it expands equatorially (smaller arrows). (b) Forces generated at the lens-iris diaphragm and vitreous base attachment site at the point of maximum equatorial expansion. |
CONTUSION (BLUNT, CLOSED GLOBE)
When a blunt force strikes the eye, the eyeball is shortened in the anteroposterior dimension and elongated equatorially. As the lens-iris diaphragm and the anterior vitreous base are anchored to the eyewall, portions of these structures are forced posteriorly, while their sites of attachment to the eyewall move equatorially. This results in additional forces generated at the attachment sites leading to characteristic contusion injuries such as a retinal dialysis. More complex less well understood interactions between the movement of the eyewall and the vitreous gel lead to posteriorly located retinal injuries such as a traumatic macular hole or choroidal rupture.
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Key Features: Contusion (Closed Globe Injuries) |
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CHOROIDAL RUPTURE
A choroidal rupture is a tear in the choroid, Bruch's membrane, and retinal pigment epithelium (RPE)[1] and was first described by von Graefe in 1854.[2] Choroidal ruptures may occur anteriorly, where they are usually parallel to the ora serrata, or posteriorly, where they are usually crescentic and oriented around the optic nerve (Fig. 173.2). Anterior choroidal ruptures are thought to occur directly at the site of impact, while posterior pole choroidal ruptures result indirectly from the movements of the eyewall.
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FIGURE 173.2 Choroidal rupture. (a) Fundus photograph showing multiple concentric choroidal ruptures, one through the fovea. (b-d) Corresponding red-free fundus photograph, late-phase fluorescein angiogrpahy and ocular coherence tomography. |
Identification of a choroidal rupture acutely may be difficult because of co-existing anterior segment or vitreous opacities (i.e., hyphema). Even in cases of clear ocular media, posterior segment hemorrhage, which may be subretinal, retinal, or preretinal, is often present obscuring the rupture (Fig. 173.3). In such cases, one or more ruptures are almost always present, only to be identified with subsequent clearing of the blood or with fluorescein angiographic testing.
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FIGURE 173.3 Choroidal rupture. (a) Acutely after injury, retinal and subretinal hemorrhage and commotio retinae obscure the peripapillary choroidal rupture from view. (b) The same patient, 2 months later. After clearing of the hemorrhage, the peripapillary, concentric choroidal rupture can be seen. |
Most patients presenting with choroidal ruptures do not regain vision to the 20/40 level.[3] Visual outcome is often difficult to predict at presentation but poor fial vision is associated with foveal location of the rupture, multiple ruptures, and poor presenting visual acuity.[3] Choroidal ruptures heal with time through the process of fibrous and fibrovascular proliferation. Choroidal neovascularization may be a late complication of a choroidal rupture occurring months or years following the initial injury. The development of choroidal neovascularization is associated with more posteriorly located choroidal ruptures and older aged patients. Laser photocoagulation,[4] photodynamic therapy,[5] or anti-VEGF therapy of choroidal rupture-associated choroidal neovascularization can be beneficial in minimizing visual loss.
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Key Features: Choroidal Rupture |
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COMMOTIO RETINAE
First described in 1873,[6] commotio retinae (Berlin's edema) occurs after blunt injury to the eye and is characterized by decrease in central and/or peripheral vision and a transient gray-white patchy discoloration and opacification of the outer neurosensory retina (Fig. 173.4). The opacification may be accompanied by retinal, subretinal, or preretinal hemorrhage and choroidal rupture.[7] Central and peripheral vision tends to improve as the retinal whitening resolves; however, in other cases, central vision loss may be permanent, associated with RPE changes and pigment migration.[8] The peripheral pigmentary changes when present, can mimic retinitis pigmentosa.[9,10]
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FIGURE 173.4 Commotio retinae in the extramacular retina. The retinal whitening affects the outer retina and is seen in this patient in association with retinal hemorrhage. One month later, the retinal whitening had resolved with some pigment migration into the neurosensory retina. |
Fluorescein angiography typically shows no alteration in retinal vascular permeability.[11,12] Experimentally produced commotio retinae in owl monkeys has shown disruption of the photoreceptor outer segments and acute damage to the photoreceptor cells.[13] This was followed by pigment migration to the ganglion cell layer and, in severe injuries, thinning of the outer plexiform and outer nuclear layers with variable loss of the photoreceptor outer segments. No evidence of intracellular or extracellular retinal edema was seen in this model, which appears clinically identical to human patients with this condition.
The visual prognosis is good in extrafoveal or mild injuries and the vision tends to recover in a vast majority of cases (60%).[14] Permanent vision loss may occur if there is significant damage in the fovea or there are associated retinal injuries such as a choroidal rupture or macular hole formation. There is no treatment of proven benefit for this condition.
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Key Features: Commotio Retinae |
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TRAUMATIC MACULAR HOLE
Trauma is the mechanism of macular hole formation in ~10% of cases.[15] Macular holes may be present immediately following the contusion injury or may take days to weeks to form. The pathophysiologic mechanism(s) underlying traumatic macular hole formation are unclear but in most cases, traumatic holes probably result from similar, albeit more abrupt, tractional vitreofoveal interface changes similar to idiopathic macular holes.[16] Traumatic macular holes range in size from 0.2 to 0.5 disk diameters and may be round or oval in appearance (Fig. 173.5). Ocular coherence tomography reveals findings similar to nontraumatic holes, although at times, a more ragged/irregular appearance to the edges of the hole are present. Sometimes, traumatic macular holes may close spontaneously, particularly in younger patients, and a period of observation is reasonable before deciding on surgery in these cases. Vitrectomy with or without peeling of the internal limiting membrane (ILM) can result in hole closure in over 90% of the cases with visual improvement of two or more lines in more than three out of four patients and more than half of the patients achieving 20/50.[17] Eyes with associated macular RPE atrophy or choroidal injury have a poorer visual prognosis and may have only limited improvement after surgery.[18,19] Progression to retinal detachment rarely occurs as macular holes are usually stable lesions.[20]
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FIGURE 173.5 Traumatic macular hole. (a) Color fundus photograph and (b) ocular coherence tomography revealing small full-thickness macular hole less than 500 ?m in diameter caused by contusion injury to the eye. (c) Anterior segment photograph shows zonular fiber dialysis. |
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Key Features: Traumatic Macular Hole |
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CHORIORETINITIS SCLOPETARIA
Chorioretinitis sclopetaria is characterized by a rupture of the retina and choroid after nonpenetrating ocular trauma in which a high-velocity projectile usually a shotgun or BB pellet, strikes or passes tangential to the globe.[21] The first case caused by a shotgun, was described by Goldzeiher[22] in 1901. The concussive force of the injury causes full-thickness rupture of the retina, Bruch's membrane, and choroid with associated hemorrhage and is followed by retraction of these tissues to expose the bare sclera (Fig. 173.6).[21] It is relatively rare, especially during peacetime, as it is most often the result of gun related injuries.[23]
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FIGURE 173.6 Chorioretinitis sclopetaria. (a) This 16-year-old boy noted decreased vision after being shot with a BB gun from 4 ft away. Vision was 8/200. Note the entry wound in the left lower lid just above the inferior orbital rim. Subconjunctival hemorrhage is also visible. (b) Fundus photographs of the inferonasal quadrant in this patient show the acute appearance of choroidal and retinal rupture with preretinal hemorrhage typical in chorioretinitis sclopetaria. The sclera remains intact. (c) Computed tomography scan shows the location of the BB at the orbital apex. Note that the globe appears intact, without the 'flat tire' sign seen in perforating injuries of the globe. (d) Seven months later, the patient's vision has improved to 20/70. The retina has remained attached without surgical intervention, and a white scar with pigment proliferation and intraretinal pigment migration along its margins is present in the inferonasal quadrant. |
Both the posterior pole and the peripheral retina may be involved, with marked choroidal and retinal hemorrhages associated with tears in these layers. The sclera remains intact and may be visible on ophthalmoscopy but may be obstructed acutely by overlying vitreous hemorrhage and intraretinal and subretinal hemorrhage. Retinal detachment occurs only rarely, and with resolution of the hemorrhage the lesion typically heals and develops irregular border with the formation of white fibrous scars and associated pigment migration and proliferation.[24] The visual prognosis is usually poor owing to the initial severity of the injury, however cases of excellent visual return have been reported.[25] Vitrectomy may be used to remove nonclearing vitreous hemorrhage[26] or repair retinal detachment; however, surgery is not often required.
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Key Features: Chorioretinitis Sclopetaria |
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TRAUMATIC RETINAL TEARS, DIALYSIS, AND DETACHMENT
As mentioned above movement of the eyewall relative to the vitreous following blunt trauma creates tractional forces at the vitreous base and pars plana. Blunt trauma to the eye can cause retinal tears, dialysis, and retinal detachment. Traumatic retinal detachments account for ~15% of all detachments and tend to occur in a much younger patient population than do nontraumatic detachments. Traumatic detachment is four times more common in males than in females, compared with a similar incidence between the sexes for nontraumatic detachments.[27,28]
Retinal dialysis is the most common type of retinal break associated with traumatic retinal detachment. It occurs most commonly in the inferotemporal quadrant (66% of detachments) followed by the superonasal quadrant (14% of detachments). A retinal dialysis is characterized by a break or separation at the anterior edge of the ora serrata and it differs from a retinal tear as the vitreous remains attached to the posterior edge of the dialysis.[29,30] In the same series, giant retinal tears accounted for 16% of detachments, retinal flap tears accounted for 11%, and tears in an area of lattice accounted for 8% of detachments.[28] Avulsion of the anterior vitreous base in association with detachment always indicates a history of significant ocular trauma. Retinal detachments associated with retinal dialysis and other traumatic retinal breaks tend to progress slowly and may not present for months or years following the injury.
Retinal tears associated with ocular trauma may be treated with cryoretinopexy or laser retinopexy. Traumatic retinal detachments can be treated using scleral buckling or vitrectomy techniques. Proliferative vitreoretinopathy (PVR) is the most common reason for surgical failure in the management of trauma related retinal detachment. Cases of retinal detachment associated with PVR generally require more advanced vitreoretinal surgical techniques including; vitrectomy, membrane dissection, retinectomy, and use of long-active intraocular gases or silicone.
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Key Features: Traumatic Retinal Tears, Dialysis, and Detachment |
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ACCELERATION/DECELERATION INJURY
OPTIC NERVE EVULSION
Evulsion of the optic nerve is the rarest form of traumatic optic neuropathy. The optic nerve may be partially or completely separated from the globe. In total evulsion the vitreous and retina separate from the optic disk and the lamina cribosa is detached from the choroid and sclera. Partial evulsion involves partial disruptions of laminar-scleral connections. Cases can involve severe orbital trauma;[31,32] however, other cases of partial evulsion have been reported after seemingly minor trauma.[33,34] Fundus examination shows total or partial absence of the optic disk however immediately after injury the disk is often obscured by overlying vitreous hemorrhage. Partial evulsion may mimic an optic nerve pit in appearance. Serous macular detachment has been reported after partial evulsion injury.[33]
Fluorescein angiography may demonstrate either normal, partial, or absent retinal vascular filling. Anterior segment neovascularization may develop in rare cases as a result of posterior segment ischemia. Computed tomography or magnetic resonance imaging usually demonstrates an intact nerve sheath.[26]
Presumed mechanisms of injury include extreme rotation and anterior globe displacement, sudden marked increase in intraocular pressure after traumatic compression in which the optic nerve is pneumatically disinserted and sudden elevation of intraorbital pressure stretches optic nerve until it is evulsed from its scleral insertion.[35]
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Key Features: Optic Nerve Evulsion |
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SHAKEN BABY SYNDROME
Shaken baby syndrome presents as retinal hemorrhages and cotton-wool spots in an abused infant who may have sustained violent shaking; direct eye, head, or chest trauma; or choking.[6,36] Papilledema and vitreous hemorrhage may occur in association, along with subdural or subarachnoid hemorrhage or cerebral contusion. Ocular injury may be present in up to 30-40% of abused children.[36-38] Retinal manifestations are most common (Fig. 173.7) and may appear similar to Terson's syndrome, Purtscher's retinopathy, or central retinal vein occlusion.[6] Other rare retinal manifestations include; subhyaloidal hemorrhage (hemorrhagic macular cyst) and circular perimacular folds. The prognosis is poor, with children suffering from the sequelae of their intracranial injuries as well as ocular visual loss, which may be secondary to macular scarring, vitreous hemorrhage, retinal detachment,[39] or from amblyopia. Retinal reattachment surgery or vitrectomy for nonclearing vitreous hemorrhage may be beneficial.[26]
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FIGURE 173.7 Shaken baby syndrome. This 1-month-old child was hospitalized in the neonatal intensive care unit with subarachnoid and subdural hemorrhages due to child abuse. The fundus photograph of the right eye taken at that time demonstrates a large, bean-shaped macular subinternal limiting membrane hemorrhage. A glistening light reflex is present on its surface, and white, intraretinal patches are seen in the macula temporal to the hemorrhage. Similar findings were present in the fellow eye. |
Intraretinal, subretinal, pretinal, and vitreous hemorrhages may occur following either vaginal or caesarean birth in over one-third of newborns (Fig. 173.8). These hemorrhages tend to resolve quickly and are generally gone by 1 month following birth.[40] They can mimic retinal hemorrhages seen in the shaken baby syndrome and should be considered in the differential diagnosis.
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FIGURE 173.8 Intraretinal hemorrhages following birth. Fundus photograph of newborn with multiple intraretinal hemorrhages some with white centers. |
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Key Features: Shaken Baby Syndrome |
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RETINAL TRAUMA ASSOCIATED WITH OPEN GLOBE INJURIES
Open globe injuries (full-thickness eyewall defect present) are classified as lacerating if they are the result of sharp force (i.e., nail injury) or rupture if the eyewall opens as a result of blunt force.[41]
A ruptured globe occurs when a blunt object of significant force strikes the eyewall. This causes typical deformation changes in the eyewall and marked increase in the intraocular pressure. When significant blunt force is applied, or in cases of inherent or acquired eyewall weakness and lesser forces, the eyewall will rupture or burst at its weakest points. The most common locations are just posterior to the rectus muscle insertions where the sclera is thinnest, at the equator, at the site of previous surgical incisions, or at the limbus. Ruptured globes carry a poor prognosis as the injuries typically result in diffuse ocular trauma with posteriorly located wounds.[42]
Lacerating open globe trauma is sub-classified into penetrating, perforating, and intraocular foreign body (IOFB) injuries. Penetrating wounds are the result of sharp forces that result in full-thickness defect entrance wounds. They tend to carry a favorable prognosis unless the wounds are large and extend posteriorly. IOFB injuries are essentially penetrating injuries in which the lacerating object remains lodged into the eye. They also may carry a favorable prognosis if the foreign body is small and sharp in nature. IOFB injuries must be identified acutely as they carry a higher risk of traumatic endophthalmitis, particularly if the IOFB is not removed urgently. CT scan and/or B-scan testing should be performed in all cases of open globe injury when one cannot visualize the posterior segment. Perforating injuries are through-and-through injuries of the eye (Fig. 173.9). They are often the result of missile injuries and the perforating object generally comes to rest in the orbit. The exit site for perforating injuries is often the posterior segment of the eye, and these injuries carry a very poor prognosis.
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FIGURE 173.9 Perforating intraocular foreign body injury. This patient suffered perforating pellet injury to the left eye. An intraocular foreign body (pellet) lodged in the orbit resulting after passing through the globe causing diffuse injury. Note the intraocular air (closed arrow) and foreign body (open arrow). |
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Key Features: Open Globe Injuries |
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MISCELANEOUS MECHANISM OF RETINAL INJURY
PURTSCHER'S RETINOPATHY
Purtscher described patches of superficial retinal whitening, intraretinal hemorrhages, and disk edema in five patients after severe compression injury to the head in 1910.[43] The characteristic fundus changes may be seen immediately and may continue to progress for 1-2 day following trauma.[21] Presenting visual acuity may range from 20/20 to count figers and findings typically are bilateral although unilateral cases have been described.[21]
The characteristic retinal findings in Purtscher's retinopathy are multiple patches of superficial retinal whitening and retinal hemorrhages surrounding the optic nerve. The disk may appear normal initially, but an afferent pupillary defect may be present, and later optic disk edema followed by atrophy may develop. Fluorescein angiography may show leakage of dye in the region of the white retinal patches, retinal and disk edema, venous staining, and areas of capillary nonperfusion. The retinal hemorrhages and white patches resolve over several months, although the patient may be left with some loss of vision secondary to pigmentary macular changes and optic atrophy.[44]
Several theories have been advanced to explain the pathogenesis of Purtscher's retinopathy. Retinal vascular injury with endothelial damage,[44,45] complement-induced granulocyte aggregation,[46] air embolism associated with crushing chest injuries,[44] and fat embolism associated with long bone fractures[47] have all been proposed as possible mechanisms. Patients with acute pancreatitis may have associated fat emboli and present with a Purtscher-like retinopathy.[48] The complement system is also activated in acute pancreatitis, as well as in severe trauma,[26] which lends support to the theory of retinal intravascular clotting as the mechanism of Purtscher's retinopathy.
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Key Features: Purtscher's Retinopathy |
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TERSON'S SYNDROME
Terson's syndrome is the term used to describe the association of retinal and vitreous hemorrhage with subarachnoid and subdural hemorrhage, first described by Terson in 1900.[49] Approximately 20% of patients with spontaneous or posttraumatic subarachnoid hemorrhage will present with intraocular hemorrhage.[50] These hemorrhages are typically located between the ILM and the rest of the neurosensory retina and may occasionally break into the vitreous cavity. The blood usually clears spontaneously; however, in cases of nonclearing vitreous hemorrhage, vitrectomy may be beneficial.[51]
The mechanism of intraocular hemorrhage in Terson's syndrome is thought to be due to significant hemorrhage from epipapillary and peripapillary capillaries that rupture after a sudden increase in venous pressure resulting from acute elevation of intracranial pressure after intracranial hemorrhage.[49] The hemorrhage may spread to the subretinal space, within the retina, the subretinal limiting membrane space, the subhyaloid space, or vitreous cavity.[52-55]
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Key Features: Terson's Syndrome |
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VALSALVA RETINOPATHY
Duane first used the term Valsalva hemorrhagic retinopathy in 1972[56] to describe the retinal hemorrhages observed in association with heavy lifting, coughing, vomiting, vigorous sexual activity or straining during bowel movement.[57]
Patients may note a sudden decrease in vision associated with these activities resulting in Valsalva retinopathy. Typical fundus findings include a well-circumscribed, round or dumbbell-shaped red elevation beneath the ILM or intraretinal hemorrhage in or near the fovea. There may be associated vitreous hemorrhage or dissection of blood beneath the retina. The blood is initially bright red with a prominent light reflex on the surface, but it may turn yellow after several days or weeks (Fig. 173.10). A fluid level may develop early with settling of red blood cells.[6] The visual prognosis is good, with most patients returning to normal vision.
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FIGURE 173.10 Valsalva maculopathy. This 22-year-old man noted decreased vision and a central scotoma immediately after a coughing episode 3 weeks before presentation. Visual acuity was 20/50. Note the bilobed appearance of the preretinal hemorrhage, now yellow because of hemolysis. Along the inferior margin of the hemorrhage, blood can be seen breaking through the internal limiting membrane and extending into the vitreous cavity inferiorly. One month later, the hemorrhage had almost completely resolved, and vision improved to 20/20. |
The presumed mechanism of retinal hemorrhage is rupture of superficial retinal capillaries owing to a sudden increase in retinal venous pressure after the rapid increase in intrathoracic or intraabdominal pressure associated with a Valsalva maneuver, such as coughing or vomiting.
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Key Features: Valsalva Retinopathy |
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