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TRAUMATIC RETINOPATHIES

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Commotio Retinae  
 

Commotio retinae is characterized by gray-white discoloration of the outer retina due to photoreceptor outer segment disruption following blunt eye...

Commotio retinae is characterized by gray-white discoloration of the outer retina due to photoreceptor outer segment disruption following blunt eye trauma. It may be accompanied by hemorrhages or choroidal rupture.

It can occur centrally or peripherally, and when it involves the macula, it is called Berlin´s edema.

Prognosis is usually excellent except in cases with associated subfoveolar choroidal rupture and/or subfoveolar hemorrhage.

These changes gradually resolve spontaneously.

Choroidal Rupture  
 

Choroidal ruptures are breaks in the choroid, Bruch´s membrane, and retinal pigment epithelium (RPE) that result from blunt ocular trauma.

...

Choroidal ruptures are breaks in the choroid, Bruch´s membrane, and retinal pigment epithelium (RPE) that result from blunt ocular trauma.

Anterior ruptures are usually parallel to the ora serrata, while posterior ruptures have a crescent shape and are concentric to the optic disc.

Patient may have decreased vision if there is commotion retinae or subretinal hemorrhage, or if the rupture is located in the macula.

During the healing phase choroidal neovascularization is a common finding.

Purtscher Retinopathy  
 

Purtscher’s retinopathy is a hemorrhagic and vaso-occlusive vasculopathy. It usually follows severe compression injury to the head or trunk.

It...

Purtscher’s retinopathy is a hemorrhagic and vaso-occlusive vasculopathy. It usually follows severe compression injury to the head or trunk.

It is characterized by the presence of multiple patches of superficial retinal whitening and retinal hemorrhages surrounding the optic nerve head that are associated with severe loss of vision.

The pathogenesis of Purtscher’s syndrome is unclear but it is possibly due to complement induced leukocyte aggregation and leukoembolism.

Purtscher-like retinopathy is seen in diverse conditions, including acute pancreatitis, fat embolization, amniotic fluid embolization, preeclampsia, HELLP (hemolysis, elevated liver enzymes and low platelets) syndrome, and vasculitic diseases such as lupus.

Traumatic Macular Hole  
 

Traumatic macular hole is an anatomical opening or dehiscence of the fovea, resulting from a blunt trauma that causes changes...

Traumatic macular hole is an anatomical opening or dehiscence of the fovea, resulting from a blunt trauma that causes changes in the vitreoretinal interface, leading to loss of central vision.

This type of injury occurs in 6% of patients who have sustained blunt ocular trauma, and its pathogenesis is not fully understood. However, it is known that the formation of epiretinal membranes, atrophy of the photoreceptors of the fovea and hydraulic forces have an important role. It may be a sequel of Berlin’s edema.

Symptoms depend on the stage of the disease and include progressive loss of central vision and metamorphopsia. A large macular hole can produce a scotoma in central vision.

Chorioretinitis Sclopetaria  
 

Chorioretinitis sclopetaria is a full-thickness disruption of the choroid and retina secondary to the concussive forces generated by the deceleration...

Chorioretinitis sclopetaria is a full-thickness disruption of the choroid and retina secondary to the concussive forces generated by the deceleration of a high-velocity projectile near the sclera, without entering the eye.

The projectile creates shock waves that can rupture the choroid and retina, but leave the sclera intact. Vitreous hemorrhages are common. Lesions heal with a white fibrous scar and retinal pigment epithelium changes and are usually located in the peripheral retina.

Differential Diagnosis

  • Choroidal rupture
Intraocular Foreign Bodies  
 

When faced with a trauma patient with a opening eye injury, the possibility of an intraocular foreign body (IOFB) should...

When faced with a trauma patient with a opening eye injury, the possibility of an intraocular foreign body (IOFB) should always be either confirmed or discarded. CT scan is the most reliable exam to find an IOFB. Whenever there is a contradiction between the medical history and images obtained, it is wiser to assume the presence of an IOFB and act accordingly.

Generally an IOFB should be removed. It carries a risk of endophthalmitis, especially in a rural setting, when there is a possibility of soil contamination. Timing of intervention should be based on the chemical constitution of the IOFB, as well as the ophthalmological findings and systemic status of the patient.

A metallic IOFB can be associated with specific toxicity. A copper IOFB may cause an acute intraocular inflammation, endophthalmitis-like, that can lead to visual loss. Therefore it should be removed as soon as possible. Chronic copper body retention leads to a clinical picture named chalcosis. It is characterized by chronic uveitis, glaucoma, greenish discoloration of the iris, Kayser-Fleischer ring and sunflower cataract. A ferrous IOFB is also associated with toxicity. Manifestations are rare in an acute phase. Chronic retention can lead to brownish endothelial deposits, brownish discoloration of the iris, cataract, glaucoma, pigmentary degeneration of the retina and optic disc edema, collectively known as siderosis.

Retinal Detachment  
 

Ocular trauma cases are typically complex. Correct management demands a thorough structuring and adequate planning. Decisions such as the number...

Ocular trauma cases are typically complex. Correct management demands a thorough structuring and adequate planning. Decisions such as the number of surgeries planned, what issues should be addressed in each and the timing between them should be pondered ahead in order to maximize potential gains in visual function and decrease the risk of complications.

Traumatic retinal detachment is a serious complication of ocular trauma. Typically these are complex cases that should only be approached by an experienced vitreoretinal surgeon.

Several types of retinal detachment can occur after trauma. Rhegmatogenous retinal detachment is caused by a retinal break. The time between ocular trauma and the development of retinal detachment varies from hours to years. Several factors can influence this time window, such as the type of breaks, their location, presence of vitreous hemorrhage, status of the vitreous, and the presence of vitreo-retinal traction. Traction is a fundamental mechanism in the initiation and perpetuation of the retinal detachment, and should be addressed specifically

Two main surgical options are available for dealing with traction. Scleral buckling, relieves traction by shortening the distance between the end points of the traction force. In trauma cases the vectors of vitreoretinal traction are generally multidirectional and therefore a circumferential buckle should be favored. Pars plana vitrectomy (PPV) addresses the traction at its origin – the vitreous. Furthermore, PPV simultaneously addresses both dynamic and stationary traction. It also allows the approach of other co-existing intra-ocular pathologies. PPV should be as thorough as possible.

Tractional retinal detachment is caused by vitreo-retinal traction, when no retinal break is present. Usually the progression is insidious. The preferred surgical approach should be PPV, because it allows the elimination of traction at its origin, addresses both stationary and dynamical traction, and is able to release anterior (peripheral), posterior and subretinal traction.

Terson Syndrome  
 

Terson´s syndrome is defined by the occurrence of intraocular hemorrhage secondary to subarachnoid (the most common cause) or subdural hemorrhage....

Terson´s syndrome is defined by the occurrence of intraocular hemorrhage secondary to subarachnoid (the most common cause) or subdural hemorrhage. There are several hypotheses to explain this phenomenon. Generally it is accepted that the presence of fluid in the intracranial extravascular compartment, causes a rise of intracranial pressure that consequently leads to an increase of the intraluminal pressure in the venous channels draining the globe. This in turn leads to rupture of the intraocular veins with subsequent hemorrhage.

Hemorrhage can be subretinal, intraretinal, preretinal (subhyaloid) or intravitreal. One particular entity, which can result from the hemorrhage, is a hemorrhagic macular cyst (HMC). HMC is present in up to 40% of patients with Terson syndrome. Two types of HMC have been described. Submembranous HMC with blood collected under the ILM and preretinal HMC with blood located between the ILM and the posterior hyaloid. The cyst can have diverse appearances according to its age. Initially it is red, becoming white when blood breakdown has started and transparent when blood breakdown is complete.

Intraocular hemorrhage in the context of intracranial bleeding has prognostic implications. In patients with subarachnoid hemorrhage and Terson syndrome, mortality is two to four times higher than in patients with no intraocular bleeding. Also, the risk of coma in a patient with intracranial bleeding and Terson syndrome doubles when compared with a patient with no intraocular bleeding.  Therefore, screening of patients with subarachnoid or subdural hemorrhage under mydriasis should be mandatory.

Ophthalmic complications in Terson syndrome include: epiretinal membrane formation, amblyopia, proliferative vitreoretinopathy and retinal detachment.

Even with no intervention the visual prognosis is usually good. Intervention should be pondered taking into consideration the particular characteristics of the patient, visual acuity and fundus findings. Pars plana vitrectomy is the standard approach in non-clearing hemorrhages. If an HMC is present and according to its characteristics, PVD should be induced and an eventual ILM peel is warranted in preretinal HMC.