Purtscher Retinopathy (Purtscher Syndrome )..Dr. Sajid Mumtaz Sodhar

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Source : The Lancet 2011; 378:1653 (DOI:10.1016/S0140-6736(11)60474-1 ) Cotton-wool spots and intraretinal haemorrhages. (A) right eye; (B) left eye. The Lancet, Volume 378, Issue 9803, Page 1653, 5 November 2011 Dr. Sajid Mumtaz Sodhar S O D H A R C O U R T E S Y “ Oh!!!!MUSLIM You are not a true believer if you harm your neighbor.”

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Common Causes and Treatments of Sudden Loss of Vision Central Retinal Artery Occlusion : (CRAO) Occlusion of the retinal artery causes sudden profound loss of vision in one eye. It is usually due to an embolus from a plaque in the internal carotid artery. If the vision loss lasts less than 24 hours this is called "amaurosis fugax" and the embolus is assumed to have passed through the retinal circulation with on irreversible consequences. If only a branch of the artery is occluded then the visual defect will be in the upper or lower half of the visual field. If symptoms have been present only 6 to 12 hours then an attempt to dislodge or dissolve the embolus should be made. Treatment to prevent further occurrences may involve treating heart arrhythmias, hypertension, carotid stenosis, and high cholesterol.

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Central Retinal Vein Occlusion: Occlusion of the central retinal vein causes visual loss that is not pas rofound as that which occurs with retinal artery occlusion. Loss of visual acuity with central retinal vein occlusion is sudden but generalized, unless only a branch is affected. If a branch is affected only the corresponding part of the visual field is affected. Treatment of Central Retinal Vein Occlusion: Any risk factors that may have precipitated the vein occlusion need to be identified and treated. These may include hypertension, diabetes and hyperviscosity syndromes. Laser treatment is sometimes helpful for central retinal vein occlusion

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Optic Neuritis: Optic neuritis is inflammation of the optic nerve. Demyelination of the optic nerve causes painful, unilateral vision loss often with partial resolution of sight. Visual acuity is at its worst within one week. Other symptoms of optic neuritis include headache and eye pain with eye movement. Many individuals with optic neuritis have multiple sclerosis or will eventually progress to multiple sclerosis. Treatment of Optic Neuritis: Steroids such as prednisone may help quicken recovery from optic neuritis. Optimal treatment of multiple sclerosis is necessary to prevent recurrent episodes of optic neuritis that may result in permanent blindness.

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Atherosclerotic Ischemic Optic Neuropathy: (AION) Ischemic optic neuropathy is caused by an infarction (obstruction of blood supply) of the optic nerve head in the eye. It usually affects patients over 60 years of age. These individuals are likely to have other evidence of vascular disease such as angina (chest pain with exertion) or intermittent claudication (leg pain with exertion). Anterior ischemic optic neuropathy begins with rapid, painless loss of vision in the affected eye. In some individuals the vision loss is only in the upper or lower fields of vision. Unfortunately, there is no treatment for this condition. Visual recovery does not occur.

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Arteritic Ischemic Optic Neuropathy: (AION) This is most commonly due to giant cell arteritis. Temporal arteritis is similar to atherosclerotic optic neuropathy in that it presents with rapid, painless loss of vision in the affected eye that may be in only the upper or lower fields of vision. It s a systemic disorder and patients may also have general malaise, headaches, thickened, tender temporal arteries, pulsating temporal artery, scalp tenderness, muscle tenderness and jaw claudication (pain or weakness when chewing). More than 50% of patients with temporal arteritis have polymylagia rheumatica. Individuals with giant cell arteritis usually have evidence of inflammation such as an elevated ESR or CRP level. It is treatable. High doses of steroids such as prednisone are used to preserve the vision in the other eye which has a 65% chance of being affected within 10 days. Steroid treatment may be required for many years.

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Vitreous Hemorrhage: Symptoms of vitreous hemorrhage may initially include floaters, which can quickly progress to vision loss. These visual symptoms are due to bleeding into the vitreous humor. Common causes of vitreous hemorrhage are diabetic retinopathy and retinal tears following trauma to the eye or head. Subarachnoid hemorrhage may also cause vitreous hemorrhage. Treatment of Vitreous Hemorrhage: The treatment of vitreous hemorrhage may include photocoagulation laser treatment or vitrectomy.

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A 30-year-old woman with acute pancreatitis was referred to eye clinic because of sudden blindness. Visual acuity was reduced to counting fingers in both eyes. Fundoscopy showed cotton-wool spots and intraretinal haemorrhages surrounding a normal optic disc bilaterally .. At 3-month follow-up, the patient's retinal findings had much improved spontaneously. However, her visual acuity did not recover completely (right, 20/40, left, 20/25), although the underlying pancreatitis had been treated successfully

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Purtscher retinopathy Purtscher retinopathy is a form of retinopathy. It is due to the activation of complement and agglutination of red blood cells within retinal vessels. It can threaten vision, leading to temporary or permanent blindness. Purtscher's retinopathy is a hemorrhagic and vascular occlusive abnormality induced by several mechanisms ( Purtscher Syndrome)

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Valsalva manoeuvre has also been reported as a cause of Purtscher'sretinopathy (Kocak et al. 2003) and retinal vein occlusion Purtscher Retinopathy and Necrotizing Vasculitis With Gemcitabine Patients with Purtscher's retinopathy may notice severe visual loss, either immediately or within the first few hrs 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.

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Purtscher retinopathy is a hemorrhagic and vasoocclusive vasculopathy, which, in 1912, was first described as a syndrome of sudden blindness associated with severe head trauma. These patients had findings of multiple white retinal patches and retinal hemorrhages that were associated with severe vision loss

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The original findings of white lesions in the retina associated with intraretinal and preretinal hemorrhages and papillitis were believed to be caused by lymphatic extravasation from trauma. These lesions are known as Purtscher flecken (larger infarcts of the retinal capillary bed) and cotton-wool spots (small retinal microinfarcts at the level of the nerve fiber layer) The most accepted mechanism is leukoembolization that causes arterial occlusion and infarction of the microvascular bed. Leukocyte aggregation, which is induced by complement C5a, is believed to be the most likely mechanism of embolization because of its known association with trauma, acute pancreatitis, and vasculitic diseases.

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Other possible sources of emboli include fat emboli in cases of long bone fractures and perhaps pancreatitis from enzymatic digestion of omental fat, amniotic fluid embolization during childbirth and postpartum, air emboli from traumatic chest compression, and granulocyte aggregation resulting from complement activation . Other proposed mechanisms of vascular occlusion include angiospasm

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Patients may present with unilateral or bilateral vision loss (possibly severe) generally within 2 days. Purtscher-like retinopathy has been reported in diverse vasculitic and related diseases, including thrombocytopenia purpura, cryoglobulinemia, hemolytic uremic syndrome, juvenile dermatomyositis, and multiple myeloma Unexplained vision loss in patients with these conditions (eg, systemic lupus erythematosus, dermatomyositis, scleroderma) should raise the possibility of Purtscher-like retinopathy. SLE with microvascular encephalopathy and retinopathy S O D H A R C O U R T E S Y

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Physical The most common retinal findings in Purtscher retinopathy are cotton-wool spots, Purtscher flecken around the optic nerve, and intraretinal hemorrhages. Less common reported findings include serous detachment of the macula, preretinal hemorrhages, dilated vessels, and optic disc edema. Confluence of cotton-wool spots in the central macula may simulate the cherry-red spot that is seen in central retinal artery occlusion. Retinal microinfarcts that are observed in patients with fat embolization are usually smaller in size and located in the peripheral, not central, retina. Pigment migration and optic atrophy have been reported as late findings in the disease.

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Causes Traumatic chest compression and blunt head trauma are common causes. Chest trauma that is associated with Purtscher retinopathy ranges from mild to severe; the degree is not necessarily indicative of the risk of developing retinopathy. Compressive chest injuries often are seen with unrestrained drivers in motor vehicle accidents (MVAs). Patients with known vasculitic disease (eg, systemic lupus erythematosus, scleroderma, dermatomyositis) are at risk for developing a Purtscher-like retinopathy with microvascular occlusion. Childbirth and the uncommon complication of amniotic fluid embolism are known risk factors. There have been several case reports of Purtscher retinopathy in the setting of preeclampsia without other known risk factors. Acute pancreatitis is a known risk factor. The risk from acute pancreatitis may be due to fat embolization or complement activation with secondary leukocyte aggregation and occlusive vasculopathy.

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Differential Diagnoses Central Retinal Artery Occlusion Giant Cell Arteritis Hypertension Ocular Manifestations of HIV Ocular Manifestations of Syphilis Sjogren Syndrome Terson Syndrome S O D H A R C O U R T E S Y

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Laboratory Studies Amylase level: Purtscher-like retinopathy is associated with acute pancreatitis; thus, an elevated amylase level may be diagnostic of this condition. Complement C5a level Activated complement C5a is associated with the development of Purtscher-like retinopathy in numerous conditions. This test may be diagnostic in presentations without an antecedent history of trauma. A positive antinuclear antibody (ANA) test is helpful in establishing the diagnosis of certain collagen vascular diseases, such as lupus (>95% positive) and scleroderma (about 40% positive). Dermatomyositis rarely shows a positive ANA. Similarly, anti–double-stranded DNA antibody is frequently positive in lupus (>75% positive) and scleroderma (about 15-50% positive).

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Evidence of muscle disease and breakdown may be present in patients with dermatomyositis, to include the following: Elevated serum transaminase Elevated serum creatine phosphokinase Elevated serum aldolase Elevated serum myoglobin Elevated urine myoglobin In patients with lupus, antiphospholipid antibodies may be associated with an increased risk of retinal vascular thrombosis.

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Procedures Fluorescein angiography studies (early in the disease) demonstrate capillary leakage and staining of the retinal arteries. In severe disease, the following are often noted together:Nonperfusion of the small arterioles that surround the central macula Perivenous staining Venous dilation and leakage Fluorescein angiogram of a patient who sustained blunt chest compression as an unrestrained driver in a motor vehicle accident shows focal microvascular occlusion in the area of the cotton-wool spot. Mild venous leakage and staining is seen in the perifoveal capillary bed just beneath the central fovea. A small amount of fluorescein leakage is also seen beneath the fovea

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Histologic Findings Histopathologic examination of an eye with prior Purtscher retinopathy shows evidence of inner retinal atrophy, which is consistent with inner retinal arterial occlusion. Late findings include nerve fiber layer dropout and evidence of optic atrophy.

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Medical Care 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

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Jasakum Allah khairan For your patience listening Dr. Sajid Mumtaz Sodhar S O D H A R C O U R T E S Y “The major sins are associating other objects of worship with God, disobedience to parents, murder, and deliberate perjury.”

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