Traumatic Retinopathies PDF

Commotio Retinae ​ AKA as Berlin’s edema ​ Traumatic retinopathy secondary to direct trauma to the globe ○​ High impact sports ○​ Violence ○​ Motor vehicle accidents ​ Damage to the outer retinal layers caused by shock waves that traverse the eye from the site o...

Commotio Retinae ​ AKA as Berlin’s edema ​ Traumatic retinopathy secondary to direct trauma to the globe ○​ High impact sports ○​ Violence ○​ Motor vehicle accidents ​ Damage to the outer retinal layers caused by shock waves that traverse the eye from the site of impact following blunt trauma ​ A sheen-like retinal whitening appears some hours following injury ​ The most commonly seen in the posterior pole but may occur peripherally as well ​ In some cases, visual recovery is limited if associated w/ ○​ Macular pigment epitheliopathy ○​ Choroidal rupture ○​ Cystoid macular edema ○​ Macular hole (most common due to vitreous detachment) ​ Signs and symptoms ○​ Gray-white opacification of the neurosensory retina w/ or w/o internal hemorrhages ○​ Blurry vision or vision loss immediately following the trauma ○​ May decrease VA as low as 20/200 ​ ​ ​ ​ Complete Commotio Retinae affecting periphery ○​ Swelling will disappear and VA will return to 20/20 becasue no fibrovascular tissue ​ ○​ Annular opacification surrounding the macula of commotio retinae after blunt trauma ​ Management and prognosis ○​ Fortunately, the prognosis for visual recovery is good, as the condition clears in 3-4 weeks ○​ There is no acute treatment ○​ IV steroids have been used ​ Complications ○​ Late choroidal atrophy  ​ ○​ A hockey player sustained a hockey stick injury to his left eye w/ resultant acute retinal whitening and scattered intraretinal hemorrhages. 2 months later, significant reactive hyperplastic pigmentary change developed, which resulted in permanent vision loss. Chorioretinitis Sclopetaria ​ AKA traumatic chorioretinal rupture, chorioretinitis proliferans ​ Rare ​ Rupture of the choroid and overlying neurosensory retina secondary to high-velocity projectile object passing adjacent to or through the orbit without penetrating the globe (bullet, BB gun, explosions) ​ This injury causes a full-thickness chorioretinal defect and visual loss ​ ○​ Extensive vitreous and retinal hemorrhage developed in a patient who sustained a gunshot wound to the left orbit (left). Four months later, pigment atrophy was seen in the macular region, along with fibrotic scarring further temporally. Vision was counting fingers ​ ○​ This patient developed chorioretinitis sclopetaria from a bullet injury to the left orbit. Hemorrhage involved all layers of the choroid and retina (left). After three months, the hemorrhages cleared, though the involved areas developed fibrotic  scarring and atrophy. While the globe remained intact, the vision only improved to hand motions ​ Simultaneous retraction of the choroids and retina at the site of the break reveals bare sclera ​ 2 mechanisms have been considered here: ○​ Damage adjacent to the pathway of the missile is responsible for the direct injury ○​ Indirect injury is caused by the shock waves transmitted to the globe ​ “Split and retract” ​ Bruch’s membrane and RPE are inelastic making rupture more likely ​ Sclera is elastic maintains intact ​ ​ Risk factors ○​ Young males ○​ Pellets (BB gun, shotgun) ○​ Bullets (rifle, foam) ○​ Paintball ○​ Cork ○​ Tree branch ​ Signs and symptoms ○​ VA is often limited due to the mechanism and severity of the injury NLP to 20/1000 ○​ Vitreous Hemorrhage or Subhyaloid or intra-retinal hemorrhage of the posterior pole ○​ Relative Afferent pupillary defect ○​ There is often surrounding commotio present ○​ As the hemorrhage clears, claw-like breaks in Bruch membrane and the choriocapillaris become visible ○​ late-onset widespread pigmentary disturbances and varying degrees of glial or fibrovascular tissue proliferation ​ The force of a bullet likely caused rupture of the choroid, hemorrhage and ultimately a whitish reactive fibroglial proliferation  ○​ ​ This patient sustained a BB gun injury, which entered the orbit, though did not cause rupture of the globe. The missile produced substantial intraretinal hemorrhage inferiorly, along with disorganization of the retina. Eventually, pigmentary degeneration ensued, along with widespread fibrotic scarring throughout the retina (right). ​ Diagnostic procedures ○​ CT / Sonogram to evaluate vitreous heme extent to R/O RD ​ Foreign body ​ Fractures ○​ OCT ​ Rupture through the choroid, RPE and outer retina ​ Management ○​ Observation ○​ Therapy is limited ○​ Commotio retinae can be observed as retinal edema and resolves in few days ○​ Choroidal rupture monitor closely could develop secondary choroidal neovascularization membranes ○​ Significant vision loss or vitreous hemorrhage or a retinal detachment surgery with vitrectomy and/or scleral buckling ○​ The prognosis is poor in cases that involve the macular area Purtscher Retinopathy ​ 1910 Purtshcer described multiple patches of superficial retinal whitening, intraretinal hemorrhages, and papillitis following severe head trauma ​ Caused by microvascular damage with occlusion and ischemia – especially chest compressive injury – also the head trauma ​ Patients presents with sudden visual loss may range from 20/20 to CF ​ Signs ○​ Multiple, unilateral or bilateral ○​ Superficial ○​ White retinal patches, resembling large cotton-wool spots associated with superficial peripapillary hemorrhages ​ ○​ These two patients experienced Purtscher retinopathy with scattered areas of cotton-wool spots or accumulation of axoplasmic debris from crush injuries ​ Signs ○​ Cotton-wool spots ○​ Retinal hemorrhages ○​ Putcher flecken ​ Pathognomonic finding ​ Polygonal area of retinal whitening a clear demarcating line b/w the affected retina and contagious normal retinal vessels ​ 50% patients ○​ ​ Left eye demonstrating peripapillary cotton wool spots and pathognomonic Purtscher flecken (arrow macular retinal whitening, which spares the retina immediately adjacent to the arterioles ○​ ​ Purtscher retinopathy. (A) Right eye demonstrating patches of superficial retinal whitening throughout the posterior pole in a 30-year-old man 2  days after he was assaulted and suffered head trauma. Visual acuity is 20/100 in both eyes. (B) Left eye shows symmetric involvement ​ The fundus changes may be seen immediately and may progress for 1–2 days following trauma ○​ ​ Color photograph (left) and a fluorescein angiogram (right) in a patient with Purtscher retinopathy confirms the alteration in vascular permeability, which demonstrates variable degrees of late leakage ​ FA ○​ findings are variable and include normal choroidal filling, focal areas of retinal arteriolar obstruction, patches of capillary nonperfusion, venous staining, and disc leakage ​ Prognosis is guarded ○​ acute fundus changes usually resolve within a few weeks ○​ but permanent variable visual impairment occurs in approximately 50% of cases as a result of macular or optic nerve damage ​ OCT ○​ Hyperreflectivity in the inner retinal layer corresponding to cotton-wool spots ○​ Variable degree of macular edema ○​ Chronic cases outer retinal atrophy and photoreceptor loss ○​ ​ This patient with metastatic pancreatic cancer presented with bilateral Purtscher-like retinopathy. CWS indicating superficial capillary ischemia are seen along the arcades and in a peripapillary distribution. Adjacent to the fovea is a deeper polygonal zone of whitening referred to as Purtscher flecken. These Purtscher flecken correspond to a band-like zone of hyper-reflectivity at the level of the inner nuclear layer on spectral domain OCT referred to as PAMM or paracentral acute middle maculopathy. PAMM can be associated with a wide spectrum of retinal vascular diseases ​ Case not associated w/ trauma are sometimes referred to as “Purtscher-like retinopathy” ​ Purtscher-like retinopathy is seen in diverse condition  ○​ Acute pancreatitis ○​ Fat embolization ○​ Amniotic fluid embolization ○​ Preeclampsia ○​ Hemolysis, elevated liver enzyme, and low platelets (HELLP) syndrome ○​ Vasculitic disease, such as Lupus ​ ​ Traumatic ○​ Head trauma ○​ Chest compression ○​ Long bone fracture ○​ Orthopedic surgery ○​ Weightlifting ○​ Battered baby syndrome ○​ Barotrauma ​ Non-traumatic ○​ Acute pancreatitis ○​ Pancreatic adenocarcinoma ○​ Chronic renal failure ○​ Connective tissue disorders ( SLE, Dermatomyositis, Scleroderma) ○​ Hemolytic uremic syndrome ○​ Orbital injection ○​ Thrombotic thrombocytopenic purpura ○​ Embolism (fat, air, amniotic fluid) ​ Treatment ○​ 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 ​ High doses of IV steroids ​ Efficacy not been established is still controversial  ​ ○​ This patient with severe alcoholic pancreatitis presented with acute Purtscher retinopathy. Note the CWS, the retinal hemorrhages, and the severe ischemia and non-perfusion on the FA. Indirect Ocular Injuries ​ Valsalva retinopathy ○​ Pre-retinal and subhyaloidal hemorrhage ○​ Secondary to a sudden increase in intrathoracic and/or intrabdominal pressure ○​ Sudden rise in intraocular venous pressure causes retinal capillaries to spontaneously rupture and bleed ○​ Clinically present an hemorrhagic detachment of the ILM ○​ VA variably affected ○​ ​ These are patients who experienced Valsalva retinopathy after activities ranging from straining during a bowel movement to an acrobat who was suspended by his legs on a trapeze. The subhyaloidal hemorrhage usually clears spontaneously ○​ Etiologies ​ Ocular massage ​ CPR ​ Sexual activity  ​ Heavy exercise ​ Coughing ​ Vomiting ​ Lifting ​ Labor ​ Straining for a bowel movement ​ Blowing musical instruments ​ Compression injuries ○​ ​ In cases of nonclearing subhyaloidal hemorrhages, accelerated resolution can be carried out with a focal laser to the lower part of the pocket of hemorrhage, which permits it to diffuse or leak into the vitreous cavity (left). Focal laser treatment was performed on this patient, who had a nonresolving hemorrhage that had been monitored for a period of six weeks. Diffusion of the hemorrhage into the vitreous cavity after YAG laser treatment is demonstrated at 5 and 10 minutes (upper right and lower left). Two weeks post-treatment, the hemorrhage has completely resolved (right), though significant retinal striae did remain. ○​ OCT ​ Determine the location of the hemorrhage ​ Sub-ILM ​ Subhyaloid ​ Cough-induced valsalva retinopathy ○​ Treatment  ​ Observation/Conservative ​ Spontaneous resolution within weeks to months ​ Avoid anticoagulant drugs ​ Avoid strenuous physical activity ​ Some reports of laser treatment to release the hemorrhage ​ YAG laser or krypton lasers ​ Laser membranotomy disrupts the ILM or posterior hyaloid leading to drainage of the blood into the vitreous for faster resolution ​ Terson Syndrome ○​ Intraocular hemorrhage associated with ​ subarachnoid hemorrhage ​ intracerebral hemorrhage ​ traumatic brain injury ○​ Hemorrhage may be located in ​ Vitreous ​ Sub-hyaloid space ​ Sub-ILM space ○​ ​ This patient developed Terson syndrome as a result of a traumatic subarachnoid hemorrhage. He developed multiple sub-hyaloid and sub-ILM hemorrhages throughout the macula (left) and peripapillary areas (right). Note the presence of optic nerve edema likely indicative of elevated intracranial pressure. Fluorescein angiography generally does not show significant early leakage in these cases. Observation was recommended, and the patient did well with resolution of the hemorrhages and restoration of visual function ○​ Pathogenesis ○​ Possible pathophysiologic mechanisms ​ Subarachnoid blood may be directly transmitted forward through the optic nerve sheath ​ More commonly, a sudden increase in intracranial pressure leads to rapid effusion of CSF into the optic nerve sheath ​ Then dilation of the retrobulbar optic nerve mechanically compresses the central retinal vein and venous hypertension results in rupture of thin retinal vessels  ○​ ​ Multiple intraretinal and pretinal hemorrhages in a patient w/ Terson Syndrome ○​ Treatment ​ Hemorrhage can spontaneously clear – vision return to normal ​ For up to 3 months ​ 50% of vitreous hemorrhages do not resolve after 19 months ​ Pars Plana Vitrectomy is required in extended hemorrhages ​ ​ Bilateral Terson syndrome before treatment (top images) and after bilateral pars plana vitrectomy with resolution of hemorrhage (bottom images) ​ Shaken Baby Syndrome ○​ Infants and children who are subjected to abuse ○​ Multiple ocular findings could be find ○​ 30-40% of the victims present posterior segment abnormalities ○​ Causes: ​ Violent shaking ​ Direct ocular or head trauma ​ Chest injuries ​ Choking ○​ ○​ Clincial presentation ​ Diffuse retinal hemorrhages ​ Cotton wool spots ​ Papilledema ​ Vitreous hemorrhage ​ Perimacular folds ​ Hemorrhagic macular retinoschisis ○​ ○​ ○​ Treatment ​ Pars plana vitrectomy surgery required in non-clearing vitreous opacities or repair a RD ○​ IF suspected child abuse, should reported to local authorities ○​ Prognosis ​ Poor ​ Cortical blindness occurs in up to 15% ​ High-Altitude Retinopathy ○​ Clinical presentation: ​ Intraretinal hemorrhages and cotton-wool spots, along w/ optic nerve edema ​ Rare pre-retinal hemorrhages w/ extension to the vitreous may occur ○​ Cause: ​ Patients who exervise vigorously at high altititudes or are at a very high altitude for an extended period of time ​ Mountain climbers ○​ ​ These two patients experienced high-altitude retinopathy, with one patient exhibiting an occasional retinal and pre-retinal hemorrhage (left), while the other patient had more widespread superficial retinal hemorrhages throughout the fundus (right ○​ Mechanism: ​ Autoregulation in response to hypoxia increase in venous pressure secondary to raise intracranial pressure ​ Changes in retinal perfusion due Leads to retinal hemorrhages ○​ Treatment ​ Observation ​ Self-limiting condition ○​