- •Preface
- •1: Anatomy and Physiology of the Retina
- •Pars Plana
- •Ora Serrata
- •Macula
- •Fovea, Foveola, and Umbo
- •Neurosensory Retina
- •Photoreceptors
- •Retinal Pigment Epithelium
- •Retinal Blood Flow
- •Choroid
- •Vitreous
- •Normal Retinal Adhesion
- •Blood-Retinal Barrier
- •Physiology of the Retina
- •Clinical Correlation: Retina
- •Clinical Correlation: Retinal Pigment Epithelium
- •Clinical Correlation: Vitreous, Retinal Adhesion, and Blood-Retinal Barrier
- •2: Ancillary Testing for Retinal and Choroidal Diseases
- •Fluorescein Angiography
- •Fluorescein Angiography: Hyperfluorescence
- •Fluorescein Angiography: Hypofluorescence
- •Indocyanine Green Angiography
- •Electroretinography
- •Electro-Oculography
- •Echography
- •Scanning Laser Ophthalmoscopy
- •Optical Coherence Tomography
- •3: Clinical Features of Retinal Disease
- •Cherry Red Spot
- •Chorioretinal Folds
- •Choroidal Neovascularization
- •Cotton Wool Spot
- •Cystoid Macular Edema
- •Drusen
- •Flecked Retina Syndromes
- •Foveal Yellow Spot
- •Intraretinal Hemorrhages
- •Lipid Exudates
- •Macular Atrophy
- •Optic Disc Edema With Macular Star
- •Peripheral Pigmentation
- •Pigmented Lesions
- •Preretinal Hemorrhage
- •Retinal Crystals
- •Retinal Neovascularization
- •Retinitis
- •Rubeosis
- •Tumors
- •Vasculitis
- •Vitelliform Lesions
- •Vitreous Hemorrhage
- •Vitreous Opacity
- •White Dot Syndromes
- •White-Centered Retinal Hemorrhages
- •4: Macular Diseases
- •Age-Related Macular Degeneration: Nonexudative
- •Age-Related Macular Degeneration: Exudative
- •Angioid Streaks
- •Central Serous Chorioretinopathy
- •Cystoid Macular Edema
- •Macular Hole
- •Myopic Degeneration
- •Pattern Dystrophy
- •Photic Retinopathy
- •5: Retinal Vascular Diseases
- •Branch Retinal Artery Occlusion
- •Branch Retinal Vein Occlusion
- •Central Retinal Artery Occlusion
- •Central Retinal Vein Occlusion
- •Hypertensive Retinopathy
- •Idiopathic Juxtafoveolar Retinal Telangiectasis
- •Leukemic Retinopathy
- •Ocular Ischemic Syndrome
- •Pregnancy-Related Retinal Disease
- •Radiation Retinopathy
- •Retinal Arterial Macroaneurysms
- •Retinopathy of Prematurity
- •Sickle Cell Retinopathy
- •6: Hereditary Retinal Disorders
- •Albinism
- •Choroideremia
- •Cone Dystrophies/Cone-Rod Dystrophies
- •Congenital Stationary Night Blindness
- •Dominant Drusen
- •North Carolina Macular Dystrophy
- •Retinitis Pigmentosa (Rod-Cone Dystrophies)
- •Stargardt Disease
- •7: Drug Toxicities
- •Aminoglycoside Toxicity
- •Crystalline Retinopathies
- •Iron Toxicity
- •Phenothiazine Toxicity
- •8: Intraocular Tumors
- •Choroidal Hemangioma
- •Choroidal Melanoma
- •Choroidal Metastasis
- •Choroidal Nevus
- •Choroidal Osteoma
- •Congenital Hypertrophy of the Retinal Pigment Epithelium
- •Intraocular Lymphoma
- •Melanocytoma
- •Phakomatoses: Neurofibromatosis
- •Phakomatoses: Sturge-Weber Syndrome
- •Phakomatoses: Tuberous Sclerosis
- •Phakomatoses: Von Hippel-Lindau Disease
- •Phakomatoses: Wyburn-Mason Syndrome
- •Retinoblastoma
- •9: Inflammatory Diseases
- •Acute Posterior Multifocal Placoid Pigment Epitheliopathy
- •Acute Retinal Necrosis
- •Cytomegalovirus Retinitis
- •Diffuse Unilateral Subacute Neuroretinitis
- •Endophthalmitis
- •Intermediate Uveitis
- •Multifocal Choroiditis and Panuveitis
- •Multiple Evanescent White Dot Syndrome
- •Neuroretinitis
- •Posterior Scleritis
- •Presumed Ocular Histoplasmosis Syndrome
- •Sarcoidosis
- •Syphilis
- •Systemic Lupus Erythematosus
- •Toxocariasis
- •Toxoplasmosis
- •Tuberculosis
- •Vogt-Koyanagi-Harada Syndrome
- •10: Trauma
- •Choroidal Rupture
- •Commotio Retinae
- •Optic Nerve Avulsion
- •Shaken Baby Syndrome
- •Valsalva Retinopathy
- •11: Peripheral Retinal Diseases
- •Cystic Retinal Tufts
- •Lattice Degeneration
- •Retinal Breaks
- •Retinal Detachment
- •Senile (Adult-Onset) Retinoschisis
- •12: Diseases of the Vitreous
- •Amyloidosis
- •Asteroid Hyalosis
- •Idiopathic Vitritis
- •Persistent Hyperplastic Primary Vitreous
- •Posterior Vitreous Detachment
- •Proliferative Vitreoretinopathy
- •Vitreous Hemorrhage
- •13: Histopathology of Retinal Diseases
- •Macular Diseases
- •Retinal Vascular Diseases
- •Intraocular Tumors
- •Inflammatory Diseases
- •Trauma
- •Peripheral Retinal Diseases
- •14: Clinical Trials in Retina
- •The Diabetic Retinopathy Study
- •The Early Treatment Diabetic Retinopathy Study
- •The Diabetic Retinopathy Vitrectomy Study
- •The Diabetes Control and Complications Trial
- •The Branch Vein Occlusion Study
- •The Central Vein Occlusion Study
- •The Multicenter Trial of Cryotherapy for Retinopathy of Prematurity
- •The Macular Photocoagulation Study
- •The Treatment of Age-Related Macular Degeneration With Photodynamic Therapy (TAP) Study
- •Branch Retinal Vein Occlusion: Macular Edema
- •Branch Retinal Vein Occlusion: Neovascularization
- •Central Serous Chorioretinopathy
- •Central Retinal Vein Occlusion
- •Choroidal Neovascularization
- •Diabetic Retinopathy: Clinically Significant Macular Edema
- •Diabetic Retinopathy: High-Risk Proliferative Diabetic Retinopathy
- •Peripheral Retinal Neovascularization
- •Retinal Arterial Macroaneurysm
- •Retinal Tears and Retinal Detachment
- •Retinal Telangiectasis and Retinal Angiomas
- •Photodynamic Therapy with Verteporfin
- •Index
c h a p t e r 10
Trauma
Timothy W. Olsen, MD
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C H A P T E R 10 Trauma |
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CHOROIDAL RUPTURE
A choroidal rupture occurs following blunt trauma to the globe. The term choroidal rupture is a misnomer in that the abnormality is a break in Bruch’s membrane and the apposing retinal pigment epithelium. Choroidal ruptures have been reported in a variety of blunt injuries to the eye, including those involving contact with hands or fists, soccer balls, tennis balls, paint balls, or bungee cords; airbag deployment; and forceps delivery.
Symptoms
The location of the choroidal rupture determines the initial symptoms. If the rupture is outside of the central macula, the patient is likely to be asymptomatic. Ruptures that are juxtafoveal or subfoveal cause central visual loss or scotoma.
Clinical Features
Choroidal ruptures are commonly crescent shaped or circumlinear and typically form around the optic nerve. When multiple ruptures occur temporal to the disc, they may appear as a series of concentric lines, with the optic disc as its center. Choroidal ruptures that occur nasal to the disc have a less regular pattern.
Choroidal ruptures may be difficult to diagnose initially due to subretinal blood or commotio retinae. As the view clears, the rupture appears as a yellow-white streak, with large choroidal vessels visible. Visual acuity from the choroidal rupture alone may range from 20/20 to counting fingers.
With time, scar tissue fills in the choroidal rupture and may change its color or appearance to a shade of gray. The most common complication of choroidal rupture is a choroidal neovascular membrane. These membranes can occur from 1 month to several years after the injury. The choroidal neovascular membrane originates adjacent to the scar tissue and may bleed or grow into the subfoveal space.
Ancillary Testing
The initial fluorescein angiogram may demonstrate hypofluorescence as a result of subretinal hemorrhage overlying the choroidal rupture. The choroidal rupture itself usually exhibits a hyperfluorescent streak corresponding to the break in the Bruch’s membrane-retinal pigment epithelial complex. A fluorescein angiogram is indicated if there is a suggestion of a choroidal neovascular membrane. Indocyanine green (ICG) angiography reveals hypofluorescence in the region of the choroidal rupture; ICG angiography may demonstrate more hypofluorescent streaks than expected clinically or by fluorescein angiography.
Pathology/Pathogenesis
Choroidal rupture is the indirect result of blunt trauma to the globe. When the globe is compressed in an anterior to posterior direction at the time of blunt injury, the sclera and retina may be elastic enough to resist injury, but the inelasticity of Bruch’s membrane makes it susceptible to tearing.
Treatment/Prognosis
There is no treatment for the choroidal rupture itself. Occasionally, bleeding (vitreous or subretinal hemorrhage) associated with choroidal rupture will require pars plana vitrectomy. Treatment options for a choroidal neovascular membrane include laser photocoagulation or surgical excision. The role of photodynamic therapy
is unclear.
Systemic Evaluation
No systemic evaluation is required for a choroidal rupture.
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Acute choroidal rupture following a bungee-cord injury to the right eye. The choroidal rupture appears as a yellow-white streak concentric to the optic disc.
Multiple choroidal ruptures in a 15-year-old boy who was struck in the right eye with a rock 6 weeks earlier. He developed a subfoveal choroidal neovascular membrane.
Fluorescein angiogram of the same patient reveals hyperfluorescence of the choroidal rupture and hypofluorescence corresponding to the surrounding subretinal hemorrhage.
Fluorescein angiogram of the same patient reveals a classic subfoveal choroidal neovascular membrane. Note the visibility of the larger choroidal vessels within the temporal choroidal rupture.
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C H A P T E R 10 Trauma |
COMMOTIO RETINAE
Commotio retinae, caused by an acute contusion of the neurosensory retina, is a condition of one or more graywhite patches of outer retina. This traumatic opacification of the outer retina is also known as Berlin’s edema.
Symptoms
If the commotio retinae (or commotio) affects the center of the macula, the patient will notice a central scotoma and decreased central vision. Commotio outside the macula is generally asymptomatic.
Clinical Features
The color change to gray-white appears in the outer retina several hours after the injury. The optic disc and retinal vessels are uninvolved. In milder cases of commotio, the color change is subtle and less opaque than in more severe injuries. Milder injuries are accompanied by a return of central vision and a restoration of normal retinal color and function within days to weeks. In more severe cases, the commotio appears dense gray, often with associated retinal or preretinal hemorrhage. Severe commotio, or retinal contusion, can lead to permanent vision loss, if centered in the macula. The long-term clinical features of severe commotio include pigmentary derangement of the underlying retinal pigment epithelium (RPE) and a loss of the foveal reflex.
Ancillary Testing
The fluorescein angiographic findings of mild commotio are typically normal. In severe cases, due to damage to the RPE, hyperfluorescence may be seen in the area of commotio.
Pathology/Pathogenesis
Histologic data from animal studies have shown immediate fragmentation of photoreceptor outer segments and intracellular retinal edema in areas of commotio. This intracellular edema is thought to account for the gray color of the outer retina. Histopathologic examination of a human eye with commotio that was enucleated 24 hours after injury revealed damage to the photoreceptors similar to that seen in animals. The extent of damage to the photoreceptors may be the primary factor in the reversibility of visual loss.
Treatment/Prognosis
There is no treatment for commotio retinae. Patients may have complete recovery of visual loss or may be left with central visual deficits.
Systemic Evaluation
No systemic evaluation is required for commotio retinae. Ruptured globe, retinal detachment, and other ocular injuries must be excluded.
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Commotio retinae in an 8-year-old boy who was struck in the right eye while wrestling. His vision was 20/200. There is prominent whitening of the outer retina throughout the macula.
This patient has a prominent patch of commotio retinae. The borders are well defined.
The borders between the normal and abnormal retina are fairly well defined. Note that the optic disc and retinal vessels are normal.
Although many individuals regain normal vision, retinal pigment epithelial alterations may limit visual recovery. Retinal pigment epithelial abnormalities include stippled hyperpigmentation and atrophy.
