Treatment and Management of Posterior Segment Trauma. Ocular Trauma 09/01/2015. Mary Beth Yackey, OD Cincinnati Eye Institute

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1 Treatment and Management of Posterior Segment Trauma Mary Beth Yackey, OD Cincinnati Eye Institute Ocular Trauma Significant cause of vision loss 2.5 million eye injuries per year in the USA 40 thousand cause serious loss of vision 75% are monocularly blind Vision loss is due to primary mechanical damage of vital structures and secondary complications Secondary complications include Endophthalmitis Tractional Retinal Detachment (TRD) due to intraocular fibrosis, proliferation and contracture 1

2 Sequale of Blunt Ocular Trauma Angle recession Hyphema Vitreous hemorrhage Retinal tears or Retinal detachment Subluxed or dislocated lens Commotio Retinae Choroidal rupture Macular hole Avulsed optic nerve Scleral rupture Importance of Complete Ophthalmological Exam An eye with no anterior damage may present with a severe posterior injury Also, a patient with iritis or hyphema may have posterior segment damage Retinal tear Choroidal rupture Blowout fracture Vitreous Hemorrhage Occurs secondary to damage to blood vessels of iris, ciliary body, retina or choroid, and retinal tear 2

3 Mechanisms of Vitreous Hemorrhage Abnormal Vessels Diabetic retinopathy (31 54 percent) of vitreous hemorrhages are caused by diabetes Neovascularization from branch or central retinal vein occlusion (4 16 percent) Sickle cell retinopathy (0.2 6 percent) Rupture of Normal Vessels Retinal tear (11 44 percent) Trauma (12-19 percent) Posterior vitreous detachment with retinal vascular tear (4 12 percent) Retinal detachment (7 10 percent) Terson s syndrome (0.5 1 percent) Blood From Adjacent Source Macroaneurysm (0.6 7 percent) Age-related macular degeneration (0.6 4 percent) Source: Spraul, C. W. and H. E. Grossniklaus, Surv Ophthalmol 1997;42(1):3 39. Assume retinal tear until proven otherwise ASAP!! Indirect Ophthalmoscopy RD, PVD B scan sonography If view is obstructed, must perform B scan to rule out Retinal tears/ Retinal detachment Management If no apparent retinal detachment on B scan, have patient sleep with head of bed elevated Treatment 3

4 Treatment of traumatic vitreous heme Once the retina can be visualized, treatment is aimed at the underlying etiology as soon as possible. Vitrectomy is also indicated for nonclearing vitreous hemorrhage, neovascularization of the iris and/or angle, or ghost cell glaucoma. Timing of vitrectomy depends on the underlying etiology. New therapies, such as intravitreal injection of hyaluronidase, are currently being studied and may provide additional treatment options in the future. Commotio Retinae The damage to the outer retinal layers caused by shock waves that traverse the eye from the site of impact following blunt trauma Seen in the posterior pole and occasionally peripherally Berlin edema= Commotio retinae in the posterior pole 20/200 VA Good prognosis for visual recovery Clears in 3-4 weeks Visual recovery is limited by Associated macular pigment epithelopathy Choroidal rupture Macular hole formation NO ACUTE TREATMENT Commotio Retinae Several mechanisms for the retinal opacification have been proposed, including extracellular edema, glial swelling, and photoreceptor outer segment disruption. With foveal involvement, a cherry-red spot may appear, because the cells involved in the whitening are not present in the fovea. 4

5 Choroidal Rupture Eye is compressed along its anterior-posterior axis Eye becomes stretched in horizontal axis because of hydraulic displacement of the vitreous Bruch s membrane-has little elasticity and may tear along with overlying RPE and underlying choriocapillaris Associated subretinal heme (SRH) is common Occasionally CNVM develops as a late complication in response to damage in Bruch s membrane Amsler Grid testing is necessary CNVM may require treatments Multiple anti-vegf, PDT vs submacular surgery CNVM may reoccur despite treatment Choroidal Rupture May be single or multiple Commonly seen in periphery May be eccentric to the disc Through central macula-likley causes permanent visual loss NO IMMEDIATE TREATMENT Choroidal Rupture 5

6 Post-traumatic Macular Hole Fovea is thin Blunt trauma may lead to FTMH by contusion or vitreous contraction Macular Hole Treatment Foveal detachments (Stage I) Without treatment, about half of Stage I macular holes will progress. Partial-thickness holes (Stage II) Without treatment, about 70 percent of Stage II macular holes will progress. Full-thickness holes (Stage III) The size of the hole and its location on the retina determine how much it will affect a person s visual acuity. When a Stage III macular hole develops, most central and detailed vision can be lost. If left untreated, a macular hole can lead to a detached retina, that should receive immediate medical attention. 6

7 Retinitis Sclopetaria High speed missile injury to orbit Large areas of choroidal-retinal rupture and necrosis Extensive subretinal and retinal heme may be found in 2 quadrants Widespread scaring occurs as blood absorbs Macula is almost always involved Therefore, significant vision loss Retinitis Sclopetaria Treatment of Retinitis Scleropetaria The pathogenesis of sclopetaria appears to be mechanical disruption and retraction of tissue rather than acute tissue dissolution. The risk of acute retinal detachment is low. Recommendation is nonsurgical management for the initial treatment of these patients, with continued observation for complications that may later occur. Such as RD 7

8 Ruptured Globe Globe rupture occurs when the integrity of the outer membranes of the eye is disrupted by blunt or penetrating trauma. Any full-thickness injury to the cornea, sclera, or both is considered an open globe injury and is approached in the same manner in the acute setting. Suspect Ruptured Globe if: Teardrop shape pupil Decrease in ocular ductions Deepened or flattened anterior chamber Obvious aqueous humor leakage Severe vitreous heme IOP may be reduced, elevated, or normal Confirmed by Seidel test Ruptured globe Commonly caused by penetrating trauma, but can also occur by blunt mechanisms Suspect when a large FB protrudes from near the globe Such objects should be left in place Avoid any manipulation of the globe, apply a rigid shield if possible 8

9 Traumatic retinal breaks Vitreous traction can cause dialysis or RD Fibrocellular proliferation may lead to VRT or RD Direct contusive injury to the globe: coup versus countercoup Often multiple Commonly found inferotemporal and supranasal Contusion injury may cause large equatorial breaks, dialysis, or MH Traumatic retinal tears Examination: In most patients with tears, retinal pigment epithelial cells, released through the tear, will be visible in the anterior vitreous (Shafer s sign). This is highly predictive of a retinal tear (approximately 90%). The granules are relatively large, pigmented, and are seen in the anterior vitreous, especially inferiorly. Therefore, the patient should be examined during eye movements, allowing inferior vitreous to present itself through the pupil. Although less suggestive than pigment cells, red blood cells may also be seen and should raise suspicion of a retinal tear. Red blood cells are smaller than pigment cells. Symptoms: Patients often present with new onset floaters (from vitreous hemorrhage or vitreous detachment) and photopsia (from vitreoretinal traction). A retinal tear at the ora serrata Most commonly from blunt trauma If the trauma is intense there may also be a retinal break at the optic disc but the most frequent location is in the lower temporal quadrant. The condition is most typically asymptomatic Retinal Dialysis 9

10 Horseshoe Tear Horseshoe tears also occur at sites of strong vitreoretinal adhesion, most commonly at the irregular posterior margin of the vitreous base during PVD. They are more common in the superior temporal quadrant followed by the superior nasal quadrant. U-tears consist of a flap in which its apex is pulled anteriorly by the vitreous while the base remains attached to the retina. Maybe caused from penetrating or blunt trauma Direct blow to the eye may cause the retina to tear away from its attachment. Retinal Holes Treatment of Retinal Tear Laser photocoagulation, in which an intense beam of light travels through the eye and makes tiny burns around the tear in the retina. The burns form scars that prevent fluid from getting under the retina. Cryopexy (freezing), probe freezes and seals the retina around the tear. 10

11 Treatment of Retinal Detachment Pneumatic retinopexy. In this procedure, a gas bubble is injected into the middle of the eyeball. The gas bubble floats to the detached area and lightly presses the detached retina to the wall of the eye. Then a freezing probe (cryopexy) or laser beam (photocoagulation) is used to seal the tear in the retina. Scleral buckling surgery. A piece of silicone sponge, rubber, or semihard plastic is placed on the outer layer of the eye and sewn in place. This relieves pulling (traction) on the retina, preventing tears from getting worse, and it supports the layers of the retina. Vitrectomy. This is the removal of the vitreous gel from the eye. Vitrectomy allows for better access to the retina and other tissues. Scar tissue can be peeled off the retina, holes can be repaired, very large tears closed, and retinal detachments can be directly flattened. 11

12 Traumatic RD in Young patients Young patients have higher incidence of injury Rarely develop an acute RRD following blunt trauma because their vitreous has not yet undergone synerisis or liquefaction Vitreous provides and internal tamponade of retinal tears or dialysis Over time, the vitreous may liquefy over a tear Fluid pass through the break and detaches the retina Traumatic RD in Young Patients 1-12% of RD are found immediately 2-30% are found within 1 month 3-50% are found within 8 months 4-80% are found within 24 months Traumatic RD s in young patients may be shallow and chronic Multiple demarcation lines Subretinal deposits Intraretinal cysts Optic Disc Avulsion The optic nerve is forcibly disinserted from the retina, choroid, and vitreous, and the lamina cribrosa is retracted from the scleral rim. Both complete and partial avulsions have been described. Optic nerve avulsion usually results when an object intrudes between the globe and the orbit wall and displaces the eye. Several mechanisms have been postulated; sudden extreme rotation of the globe, sudden rise in intraocular pressure leading to the expulsion of nerve out of scleral canal or sudden anterior displacement of the globe. 12

13 Optic disc avulsion Rare presentation of ocular trauma Often difficult to diagnose secondary to vitreous heme precluding view of optic nerve excavation Multiple hemorrhage around the nerve head and edema of the papillary retina B-scan ultrasonography may need to be performed It is essential to confirm the diagnosis so that the patient may not be subjected to unnecessary treatment such as optic nerve decompression or high-dose steroids. Optic Disc Avulsion Purtscher Retinopathy Hemorrhagic and vasoocclusive vasculopathy Compression injuries to the thorax or head leads to vision loss due to Cotton wool spots (CWS) Heme Retinal edema Commonly found around the disc Purtscher-like retinopathy is seen in diverse conditions, including acute pancreatitis; fat embolization; amniotic fluid embolization; preeclampsia; hemolysis, elevated liver enzymes, and low platelets (HELLP) syndrome; and vasculitic diseases, such as lupus. 13

14 Purtscher Retinopathy Treatment of Purtscher Retinopathy No proven treatment exists for Purtscher retinopathy that occurs after traumatic injury. In patients with retinopathy due to systemic vasculitis, steroid therapy is theoretically beneficial. Control of the underlying disease with other medications may be indicated. Prognosis varies from blindness to total recovery of vision. Thank you! 14