Berlin’s Edema (Commotio Retinae)
After a blunt contusion to the front of the eye, a patient may experience acute visual loss caused by Berlin’s edema (commotio retinae). In this condition the retina develops a gray-white color that affects primarily the outer retina that may be confined to the macular area ( Figure 8.01A and E ) or may involve extensive areas of the peripheral retina ( Figure 8.01B ). In some cases the whitening may be accompanied by retinal or preretinal hemorrhages ( Figure 8.02A and B ) or subretinal blood and choroidal rupture. The retinal whitening in the macular area may clear completely, and central vision may be restored ( Figure 8.01F ). In other instances, loss of central vision may be permanent and may be associated with no visible fundus change, mottling of the retinal pigment epithelium (RPE), migration of pigment into the overlying retina, or partial or full-thickness macular hole formation ( Figures 8.02D, E and F, and 8.05 ). The whitening in the peripheral retina may be followed initially by pigment mottling and later by atrophy of the RPE and migration of pigment into the overlying retina, producing a peripheral change that clinically and histopathologically simulates retinitis pigmentosa ( Figure 8.02E and F ).
Fluorescein angiography typically shows no evidence of retinal vascular or choroidal permeability alterations in the area of Berlin’s edema ( Figure 8.01C and D ). Angiography occasionally shows a transient leakage of dye from the retinal arterioles in the posterior pole or staining at the level of the RPE ( Figure 8.02C ). Following resolution of the outer retinal whitening, angiography may or may not show evidence of window defects in the RPE. Vitreous fluorophotometry usually shows no evidence of breakdown of the blood–retinal barrier. Optical coherence tomography (OCT) shows increased density of the photoreceptor layers initially ( Figure 8.01J–L ), followed by lucent areas if the receptors show cell death followed by thinning of the receptor layer. If the injury is mild the receptors recover and the OCT findings resolve. Multifocal electroretinogram (ERG) shows depression of the amplitudes in the affected area which recover if the outer segments regenerate or remain permanently affected if the receptors do not recover. Light and electron microscopic studies of Berlin’s edema in humans as well as that produced experimentally in animals have shown that the outer retinal whitening is caused by fragmentation of the photoreceptor outer segments and acute damage to the receptor cells ( Figure 8.01G and H ). OCT, if done during this stage, will show increased reflectivity of the photoreceptor layer and sometimes small clear spaces suggesting disruption of the photoreceptors. This loss of transparency is associated with no or minimal extracellular or intracellular edema in the retinal cells and with minimal damage to the choriocapillaris. Other changes may include breakdown of the outer blood–retinal barrier at the level of the RPE that is usually re-established between 7 and 14 days. If only the outer segments of the receptor cells are involved, these will regenerate rapidly and the retina may regain its normal appearance and function. The OCT findings also normalize. A more severe contusion may cause contusion necrosis and atrophy of the outer retina ( Figure 8.02G and H ) and a macular hole. The contusion damage to the retinal receptor cells is probably caused by mechanical distortion of the retina by deformation of the vitreous as well as hydraulic forces.
Subretinal hemorrhage caused by choroidal rupture may occasionally accompany Berlin’s edema (see Chapter 3 ). Trauma similar to that which causes Berlin’s edema may also cause acute damage to the RPE and serous detachment of the macula ( Figure 8.02C , and see Figure 8.03A–C ), as well as acute tears in the RPE.
Posterior Choroidal Rupture(Traumatic Choroidopathy)
Acute contusion necrosis of the RPE or, more frequently, a rupture in the inner choroid and RPE at the posterior pole may cause a serous and/or hemorrhagic detachment of the retina often in the macula or juxtapapillary region ( Figure 8.03 ). In the case of contusion necrosis a localized serous detachment of the retina occurs and angiography shows multiple focal areas of diffusion of fluorescein from the choroid across the damaged RPE into the subretinal fluid ( Figure 8.03A–C ). Following resolution of the detachment, varying degrees of RPE atrophy may develop. Tears in the RPE may be evident after a contusion injury. When there is a choroidal rupture, the localized subretinal hematoma typically overlies and obscures the rupture ( Figure 8.03D ). In some cases, outer retinal whitening (Berlin’s edema) accompanies the choroidal rupture ( Figure 8.02B ). (See discussion of contusion maculopathy, Chapter 8.) As the subretinal blood disappears, the rupture involving the choroid and RPE becomes visible as a curvilinear yellowish line with tapered ends concentric with, but often remotely located from, the optic disc ( Figure 8.03E, G, I, and J ). The rupture typically involves only the inner layers of the choroid but may be full thickness in some cases. In many patients the choroidal rupture is outside the foveolar area and visual acuity often returns to near normal. Occasionally a macular hole or evulsion of the optic nerve head may accompany an underlying choroidal rupture. Choroidal ruptures may occur after minor trauma in patients with angioid streaks (see Figure 3.38I ).
Intravenous fluorescein is helpful in detecting choroidal ruptures partly obscured by subretinal blood or in detecting small ruptures that may be difficult to visualize ophthalmoscopically ( Figure 8.03F ). If the rupture involves only the inner layers, angiography will show large choroidal vessels traversing the defect in the pigment epithelium, Bruch’s membrane, and choriocapillaris ( Figure 8.03K ). Angiography may demonstrate evidence of chorioretinal vascular anastomosis at the site of the rupture ( Figure 8.03L ).
Histologically, the choroidal rupture involves at least the choriocapillaris, Bruch’s membrane, and the RPE. ( Figure 8.03H ). The inner layers of the retina overlying the rupture may or may not be damaged.
Some patients may develop visual loss within several months or years after trauma because of spontaneous bleeding or serous exudation from choroidal neovascularization arising at the site of an old choroidal rupture ( Figure 8.03I and J ). This neovascularization is usually type II and often produces a pigment halo at the site of ingrowth of the vessels into the subsensory retinal space. Similar delayed neovascularization may occur at the site of a choroidal rupture caused by the impact of an intraocular foreign body, or at a surgically produced choroidal perforation made during the course of scleral buckling for retinal detachment. Extensive organization of subretinal blood may produce a variety of disciform scars, some of which may simulate a melanoma.
Gass has seen several patients who, following contusion injury to the head, have developed a typical ophthalmoscopic and angiographic picture of idiopathic central serous chorioretinopathy within several days of the accident. Probably these are patients predisposed to this disease who, as a result of the emotional stress rather than direct trauma to the eye, develop a detachment. The prognosis for spontaneous recovery is excellent.
Macular Complications of Peripheral Chorioretinal Contusion and Rupture (Sclopetaria)
Contusion and rupture of the peripheral choroid and retina caused by a high-velocity missile striking or passing close to but not penetrating the globe (sclopetaria) is an infrequent manifestation of nonpenetrating ocular trauma. A large, often ragged retinal and choroidal break associated with surrounding retinal whitening and varying amounts of blood are the cardinal fundoscopic features ( Figure 8.04A–F ). The white sclera may be visible within the break. In spite of the break in the retina, rhegmatogenous detachment occurs infrequently. Loss of macular function may occur acutely because of extension of the damage posteriorly ( Figure 8.04A ), associated macular hole, or it may develop many months after the injury as a result of vascular proliferative and exudative changes occurring within the peripheral scar ( Figure 8.04G–L ). Late fundus appearance is characterized by plaque-like fibrous proliferation with variable amount of pigment with scalloped margins. The pathogenesis of the loss of tissue seems to be partially from dissolution and partly from retraction of the retinal and choroidal tissue. Retinal detachment is uncommon due to scarring and fibrous proliferation that follow the injury.
Posttraumatic Macular Hole and Foveolar Pit
The foveolar part of the retina is extremely thin, and blunt trauma may cause a full-thickness macular hole by either one or a combination of mechanisms: (1) contusion necrosis; (2) subfoveal hemorrhage; and (3) vitreous traction. A macular hole may accompany or soon develop in patients with severe Berlin’s edema, with a subretinal hemorrhage caused by choroidal rupture ( Figure 8.05 ), or in a whiplash separation of the vitreous from the retina (see Chapter 7 for additional discussion of the pathogenesis of macular hole).
Central macular pits identical to those seen in patients following sun gazing have been described following blunt trauma to the eye and whiplash injuries ( Figure 8.05H ). Loss of visual function occurs infrequently as the result of whiplash. The syndrome of whiplash maculopathy consists of a history of flexion–extension of the head and neck trauma without direct eye injury, immediate mild reduction in acuity of no worse than 20/30 in one or both eyes, gray swelling of the foveal zone, and the development of a 50–100-μm-diameter foveolar pit. The retinal opacity disappears, and the acuity usually returns to 20/20, but the pit and its whitish borders remain. There may be a slight posterior vitreous detachment, and there may be a micro-operculum. Fluorescein angiography either is normal or may show a tiny focal area of early hyperfluorescence. Grey described a similar pit developing in three patients who experienced direct trauma to the eye and postulated that any agent, either physical or toxic, that causes selective central photoreceptor loss will give rise to the appearance of a central foveolar pit. Small prefoveal vitreous wisps, opercula, and full-thickness macular holes are other changes that may be caused by trauma-induced alterations at the vitreous–macular interface. The mechanism of traumatic macular hole could be a primary concussive break or dissolution of cells resulting in a cystoid change that broke down leaving a defect. Spontaneous closure of traumatic macular holes is well documented and hence waiting 4–6 months for this may prevent unnecessary surgery.
Patients with trauma-induced macular holes not associated with a large rim of retinal detachment, or if accompanied by pigment epithelial atrophy, are probably not good candidates for macular hole surgery because of contusion damage to the retina surrounding the hole (see discussion of macular hole in Chapter 7 ).
Purtscher’s Retinopathy
Following severe compression injury to the head or trunk, the patient may experience visual loss associated with a peculiar retinopathy in one or both eyes. The characteristic ophthalmoscopic findings in Purtscher’s retinopathy include multiple patches of superficial retinal whitening and retinal hemorrhages surrounding the optic nerve head, which usually appears normal ( Figure 8.06A, B, G, H and L ). The white patches are located mainly in the area surrounding the optic disc and often do not extend into the center of the macula. Part of the retinal whitening appears to lie anterior to the retinal vessels. In some cases there may be confluence of the white patches ( Figure 8.06G ). Fluorescein angiography in milder cases may show leakage of dye from the retinal arterioles, capillaries, and venules in the area of the white retinal lesions and, in more severe cases, may show evidence of arteriolar obstruction and leakage in the region of the white patches ( Figure 8.06C and D ). These patches and hemorrhages disappear, but the patient may be left with some loss of central vision and optic atrophy ( Figure 8.06E and F ).
The pathogenesis of Purtscher’s retinopathy is controversial. The white patches that are often referred to as exudates are probably focal areas of ischemic retinal whitening. Angiographic findings of retinal arteriolar leakage in some cases of Berlin’s edema as well as in some cases of Purtscher’s retinopathy suggest that acute endothelial damage related to trauma may predispose the retinal vascular tree to intravascular coagulopathy or granulocytic aggregation that may be the cause of multiple arteriolar obstructions. Air embolism in patients with chest compression and fat embolism in patients with long-bone fractures have been implicated as causative factors in some cases of Purtscher’s retinopathy. The white retinal infarcts, however, in fat embolism are usually smaller and are often situated more peripherally in the retina.
The characteristic restriction of the retinal lesions in Purtscher’s retinopathy to the posterior retina may be related to the unique anatomy of the blood supply of the peripapillary and macular areas. Most of the retinal vessels lie within the nerve fiber layer except for two capillary layers, one lying in the ganglion cell layer and the second in the inner nuclear layer with anastomosis between them. A third capillary layer exists in the macula, lying between these two layers, and a fourth layer of capillaries exists within the most superficial aspect of the nerve fiber layer around the disc. This fourth layer of peripapillary capillaries extends for two disc diameters nasal to the disc and for four disc diameters temporal to the disc, although for only one disc diameter along the horizontal meridian. Unlike the other capillaries in the retina, the peripapillary capillaries have fewer feeding arterioles and fewer anastamoses. As a result they may be more susceptible to embolic occlusion. Histopathologic examination of an eye 34 months after development of Purtscher’s retinopathy has demonstrated inner retinal atrophy compatible with retinal arterial occlusion.
A fundoscopic picture virtually identical to that of Purtscher’s retinopathy may occur in patients with central retinal artery obstruction, acute pancreatitis, lupus erythematosus, dermatomyositis, scleroderma, and amniotic fluid embolism (see discussion in Chapter 6 ).
Retinal and Vitreous Hemorrhage Associated with Subarachnoid and Subdural Hemorrhage (Terson’s Syndrome)
Terson described vitreous hemorrhage occurring in patients with subarachnoid hemorrhage and attributed it to a sudden increase in venous pressure that ruptures epipapillary and peripapillary capillaries. Others have attributed the intraocular hemorrhages to a rapid increase in intracranial pressure causing compression of the central retinal vein and its choroidal anastomotic channels. Approximately 20% of patients suffering either spontaneous or posttraumatic subarachnoid or subdural hemorrhages develop intraocular hemorrhages that in most cases are confined to the juxtapapillary and macular areas ( Figure 8.07A–D ). Intraretinal and subretinal bleeding occurs primarily from the optic disc and retinal blood vessels. The intraretinal hemorrhages can be superficial or deep, blot or flame-shaped. Often some of the deep intraretinal hemorrhages appear petalloid with feathery margins due to dissection of blood into the outer plexiform layer ( Figure 8.07G–I ). Intraretinal and subretinal bleeding occurs primarily from the optic disc and retinal blood vessels. Elevated mounds of blood either beneath the internal limiting membrane of the retina or in the subhyaloid space may occur ( Figure 8.06K ). In most cases these hemorrhages clear spontaneously and visual function is unaffected. Occasionally the vitreous hemorrhage fails to clear and vitrectomy may be necessary to restore vision. The surgeon may find some evidence of retinal blood vessel and RPE damage ( Figure 8.07E and F ). The amount of blood in the eye is not necessarily related to the severity of the subarachnoid hemorrhage. A perimacular retinal fold may develop after resolution of the subinternal limiting membrane hematoma in some patients. Epiretinal membrane in the macula is the most common sequela of Terson’s syndrome but is not associated with visual morbidity. Because severe proliferative vitreoretinopathy occasionally develops, patients should be monitored periodically with ultrasonography while awaiting clearance of the blood, and prompt vitrectomy carried out if needed.
Terson’s syndrome is seen with ruptured aneurysms ( Figure 8.07G–J ), arteriovenous malformations, head trauma, including gunshot injuries, post epidural injections, and post endoscopic ventricular colloid cyst removal and dissecting aneurysms of the vertebrobasilar system. Children with subarachnoid hemorrhage are less likely to develop vitreous and retinal hemorrhages compared to adults. This may be due to better resilience of the vessels in children compared to adults.
Hemorrhagic Maculopathy Caused by Subarachnoid and Epidural Injections
Patients may develop multiple scotomas caused by retinal hemorrhages in one or both eyes immediately after the injection of oxygen into the subarachnoid space during the course of myelography, or following epidural injection of corticosteroids for relief of back pain. These hemorrhages often occur as the result of bleeding from the deep retinal capillary plexus and cause a petalloid pattern of blood with tapered edges centrally surrounding the center of the macula. Sudden elevation of the cerebrospinal fluid pressure and elevation of retinal venous pressure are the most likely explanations for the hemorrhages, some of which may occur from the superficial as well as the deep retinal capillaries in a pattern similar to that seen in Terson’s syndrome. The prognosis for the spontaneous return of normal visual function is good.
Postcontusion Neuroretinopathy
Blunt trauma to the eye or periorbital region may cause acute visual loss associated with a swollen optic disc, and optic disc and retinal hemorrhages that are usually confined to the posterior fundus ( Figure 8.08A–C ). Some of the blood is derived from the deep plexus of retinal blood vessels and may extend into the outer plexiform layer of Henle to form a radiating pattern centrally. The fundus picture may simulate that seen in patients with papillophlebitis, with Terson’s syndrome (see Figure 8.07H–J ), and following epidural injections. A sudden elevation in the central retinal venous pressure caused by the trauma is presumed to be important in the pathogenesis of the optic disc and retinal hemorrhages. A similar pattern of inner and outer retinal hemorrhages occasionally occurs unilaterally in healthy patients, with no explanation for them (see Figure 8.07K and L ).
Shaken-Baby Syndrome
Shaken-baby syndrome results from severe shaking of infants, often as a form of punishment. The signs and symptoms are nonspecific and may mimic infection, intoxication, or metabolic abnormalities. These include (1) bradycardia, apnea, and hypothermia; (2) lethargy, irritability, seizures, hypotonia, full or bulging fontanelle, and increased head size; (3) scattered superficial retinal hemorrhages, dome-shaped subinternal limiting membrane or subhyaloid hematomas, and cotton-wool patches; and (4) skin bruises. A history of a recent minor accident or shaking in an effort to resuscitate may be obtained in some cases. The retinopathy may simulate that seen in Terson’s syndrome, Purtscher’s retinopathy, or central retinal vein occlusion ( Figure 8.08D–L ). Late fundoscopic changes include a circular retinal fold that may create a crater-like depression in the macula and traumatic retinoschisis. The circular retinal fold may be a product of abrupt vitreoretinal traction associated with shaking, vitreous traction after partial separation of the vitreous in the central macular region, or contraction of the internal limiting membrane or the posterior hyaloid membrane after resolution of a subinternal limiting membrane or subhyaloid hematoma. Laboratory findings include bloody cerebrospinal fluid and subdural tap and, in almost all cases, computed tomographic evidence of at least one of the following: subdural hemorrhage, subarachnoid hemorrhage, or cerebral contusion. The prognosis is poor, and many children are left with severe neurologic and developmental defects, including visual deficits and in some cases blindness.
The histopathologic findings in the eyes of these patients reveal evidence of intraretinal blood, subhyaloid and subinternal limiting membrane hematomas, as well as blood in the subdural and subarachnoid spaces around the optic nerve ( Figure 8.08F–J ). The subdural and subarachnoid hemorrhage in the optic nerve may be subtle and the only manifestation of the shaken-baby syndrome. Special stains for iron may be helpful in detecting evidence of previous blood in these areas occurring many months before the eyes are obtained at autopsy.
The finding of retinal hemorrhages in a child with suspected injury is more likely to be caused by shaking than by blunt trauma, and it is an important predictor of neurologic injury.
Retinal Vessel Rupture Associated with Physical Exertion (Valsalva Retinopathy)
A sudden rise in intrathoracic or intra-abdominal pressure, particularly against a closed glottis (Valsalva’s maneuver) during lifting, bowel movement, coughing, or vomiting, may cause a rapid rise of intravenous pressure within the eye and spontaneous rupture of superficial retinal capillaries in otherwise normal eyes or in eyes associated with acquired retinal vascular abnormalities (diabetic or hypertensive retinal angiopathy) or congenital retinal vascular disease (retinal telangiectasis and congenital retinal artery tortuosity) ( Figure 8.09 ). Sudden loss of vision may result from hemorrhagic detachment of the internal limiting membrane, vitreous hemorrhage, or, if bleeding occurs near the foveal region, dissection of blood beneath the retina. The author has seen one moderate myope develop extensive choroidal hemorrhage following violent incessant vomiting ( Figure 8.09A and B ). These patients typically have a circumscribed, round or dumbbell-shaped, bright red mound of blood beneath the internal limiting membrane in or near the central macular area ( Figure 8.09D, F, H, and J ). A glistening light reflex is present on the surface. A few fine striae indicative of wrinkling of the internal limiting membrane may be present on the surface of the hematoma. Part of the blood turns yellow after several days. The shape and color of these lesions may suggest an intraocular parasite ( Figure 8.09D and E ). A fluid level caused by settling of the formed blood elements may develop soon after the hemorrhage ( Figure 8.09H and J ). As the blood resolves, the serous detachment of the internal limiting membrane may persist for several days or weeks ( Figure 8.09I ). Spontaneous reattachment occurs, and the appearance of the macula and visual acuity usually return to normal.
Occasionally, a small (less than one disc diameter), round, preretinal hemorrhage centered in the foveal area occurs. The surface may show multiple yellow-white dots simulating that of a strawberry (see Figure 8.09D ). Its surface usually does not show a reflex suggestive of the presence of an internal limiting membrane. It may represent a small amount of blood lying between the internal limiting membrane and the posterior hyaloid interface. In addition, patients with these small central lesions often have a thin layer of blood lying beneath the retina in the paramacular area. Complete recovery of vision usually occurs spontaneously. In unusual circumstances where a subinternal limiting membrane hematoma is responsible for visual loss in the patient’s only normally functioning eye, neodymium-YAG laser disruption of the internal limiting membrane allowing the blood to gravitate into the inferior vitreous cavity may restore central vision more promptly ( Figure 8.09K and L ). Subinternal limiting membrane hemorrhage and preretinal hemorrhage identical to that just described occasionally occur in the normal individual in the absence of a clear-cut history of unusual exertion or Valsalva’s maneuver. Some patients may have evidence of retinal vascular disease, for example, diabetes or hypertension ( Figure 6.26G ). Other apparently healthy patients may give a history of multiple previous episodes of loss of central or paracentral vision secondary to spontaneous retinal hemorrhages. Their family members may give a similar history. Tortuosity of the second- and third-order retinal arterioles may or may not be present in these patients with a familial history ( Figure 6.01A–C ). No specific hematologic disorder has been described in this condition, which is probably inherited as an autosomal-dominant trait. Recovery of vision is the rule.
Evulsion of the Optic Disc
A forceful backward dislocation of the optic nerve from the scleral canal can occur under several circumstances, including: (1) extreme rotation and forward displacement of the globe; (2) penetrating orbital injury causing a backward pull on the optic nerve; or (3) sudden increase in intraocular pressure causing a rupture of the lamina cribrosa. This latter mechanism might be more appropriately termed “expulsion” rather than “evulsion.” In all cases a tear in the lamina cribrosa and nerve fibers at the disc margin occurs. This tear may be partial or complete and may be associated with massive intraocular hemorrhage ( Figure 8.10G and H ) or only minimal bleeding ( Figure 8.10A–C, E, and F ). In the latter case the dark, pit-like deformity caused by a partial evulsion may simulate an optic pit ( Figure 8.10A ). Visual loss from these injuries is usually great. Over a period of weeks or months, fibroglial proliferation obliterates the cavity caused by the evulsion ( Figure 8.10D ).
A penetrating injury of the optic nerve head may simulate a partial evulsion ( Figure 8.10I ).
Ocular Decompression Retinopathy
Some patients following glaucoma surgery will develop superficial and deep retinal hemorrhages as a result of the pressure lowering ( Figure 8.10J and L ). Most often, even though there is an increase in the retinal and choroidal blood flow due to the sudden low intraocular pressure; retinal bleeding is not seen. However, if the increased blood flow is excessive, autoregulation of retinal vessels cannot tolerate the volume, which overwhelms the capacitance of the capillary bed and retinal veins, resulting in retinal bleeding. A sudden decrease in intraocular pressure also induces forward shifting of the lamina cribrosa and acute blockage of axonal transport. This indirectly compresses the central retinal vein and precipitates hemorrhagic retinopathy resembling a retinal vein occlusion ( Figure 8.10J and L ).
Some of the hemorrhages may be white-centered. The visual acuity is typically unaffected by these changes, unless a significant central retinal vein occlusion occurs.
Intraocular Foreign Bodies
A great variety of foreign bodies may penetrate the ocular wall and become lodged within the choroid and retina. In most instances their identity is known and measures for removal are often undertaken promptly. In some cases, however, the invasion of the foreign body may not be recognized until months or years later, when the patient experiences signs or symptoms related to breakdown of the foreign body (e.g., siderosis or chalcosis; Figure 8.11B, C, I, and J ) or when a mass lesion in the fundus is discovered on routine eye examination ( Figure 8.11B–E ). Occasionally it may simulate a melanoma and result in removal of the eye ( Figure 8.11B–E ). The use of ultrasonography, radiography, and electroretinography in mass lesions of uncertain etiology can reduce the chances of this mistake ( Figure 8.11B ). The late development of subretinal neovascularization occurring at a foreign-body impact site may occur (see Chapter 9 ).
Chorioretinopathy and Optic Neuropathy Associated with Retrobulbar Injections
Acute visual loss may be associated with retrobulbar local anesthetic injections. There are a variety of mechanisms causing visual loss. These include penetration of the eye wall, penetration of the optic nerve, compression of the optic nerve, intra-arterial injection of anesthesia, and spasm of the central retinal artery ( Figure 8.12 ). In cases of perforation of the eye the site of exit is often visible in the posterior pole and is associated with variable amounts of intraretinal, subretinal, and vitreous blood ( Figure 8.12A and B ). Retinal detachment, vitreous traction, and subretinal neovascularization may occur as late complications ( Figure 8.12A–D ). Penetration of the optic nerve sheaths may be associated with intrasheath injection, brainstem anesthesia, respiratory arrest, and anterior extension of the anesthetic into the subretinal space. Intrasheath injection as well as injection into the optic nerve may cause occlusion of the central retinal artery and vein, or severe ischemic optic neuropathy ( Figure 8.12E–L ). Risk factors include: sharp needles, needles longer than 1.25 inches (3.17 cm), axial myopia, multiple injections, injections by nonophthalmologists, enophthalmos, previous scleral buckling procedure, traditional superonasal gaze position during the injection, and poor patient cooperation. Use of blunted retrobulbar needles 1.25 inches (3.17 cm) or less in length and injection with the eye in the straight-ahead position may be helpful in preventing visual loss.
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