Vitreous Lecture Notes PDF

5LMS0069 Abnormal Ocular Conditions and Pharmacology Vitreous Aneela Raja Lecture overview Aims: A brief overview of the structure and function of the vitreous To determine the signs / symptoms a patient may present with Differential diagnoses of related eye conditions Management in...

5LMS0069 Abnormal Ocular Conditions and Pharmacology Vitreous Aneela Raja Lecture overview Aims: A brief overview of the structure and function of the vitreous To determine the signs / symptoms a patient may present with Differential diagnoses of related eye conditions Management in both primary and secondary care Prognosis: is the condition sight or life threatening What to do during the lecture: Take notes as we review the slides Prior / expected knowledge: The anatomy and physiology of the ocular adnexa (module 4LMS0241) Revision - function Transparent gel consisting mostly of water, in addition to collagen, hyaluronic acid and other substances Regulate eye growth and shape during development Provides structural support to the globe / maintains the shape of the eye Transmit light Act as a shock absorber against trauma (due to the shape, strength, flexibility, and resistance of the fibrillar proteins) Protect the lens and retina by lowering oxygen tensions Role in metabolism and immunological response It liquefies with age (syneresis), and there is no repair mechanism Revision - structure Consequences of damage / abnormal growth What can go wrong? Age-related degeneration, inflammation, trauma This may cause direct / indirect damage to the surrounding structures Management 1. Does your patient require treatment +/- referral? 2. What is the cause of the problem, and the risk to their sight/eye/life? What symptoms / signs might this cause? The most common symptoms are: Muscae volitantes (floaters) Photopsia (flashing lights) – only if there are adhesions to the retina Vision – depends on the severity and nature of the vitreo-retinal disease: Metamorphopsia Blurring or loss of vision Visual field defect Optical coherence tomography scans – in brief OCT is one of the most commonly used imaging modalities both in practice and in the HES Non-invasive, high resolution, cross-sectional imaging You will be given detailed lectures into how it works, but for the purposes of today the important information is as follows: Highly reflective structures: drusen, microaneurysm, hard exudates, cotton wool spots, naevus Low reflective structures: vitreous, oedema, intra-/sub-retinal fluid, cysts  Vitreo- retinal interface Area affected by retinal circulatory changes Area affected by chorioretinal circulatory changes A link to this diagram (pdf) is provided in the lecture references section, and also on the unit information page Vitreous pathology Posterior vitreous detachment (PVD) Vitreous opacities Muscae volitantes (floaters) Asteroid hyalosis Synchisis scintillans Vitreous haemorrhage (persistent foetal vasculature) Vitreomacular interface disorders Vitreomacular traction (VMT) Epiretinal membrane (ERM) Macular Hole Posterior vitreous detachment (PVD) Pockets of liquid appear within the central vitreous that gradually coalesce (A), whilst the posterior vitreoretinal adhesions weaken. Eventually, the gel liquefies (synchysis) to form fluid filled cavities which coalesce and condense (syneresis) leading to separation of the cortical vitreous from the neurosensory retina (B), posterior to the vitreous base It usually occurs spontaneously, and takes a few months to detach fully Whom? Prevalence increases with age, but can be precipitated by trauma, surgery, uveitis, PRP laser Posterior vitreous detachment (PVD) Symptoms Flashing lights (photopsia) – arc like, more noticeable in dim illumination, usually in temporal field of vision Floaters – spots, cobwebs, flies, more noticeable against a bright pale background Less frequently – blurred vision (if associated with a VH) Signs Detached hyaloid membrane You may see a Weiss ring near the optic disc margin Pigment granules in the anterior vitreous (Shafer sign “tobacco dust”) – bigger and less reflective than red blood cells. Usually seen when there has been a retinal break Vitreous haemorrhage (look very carefully for retinal breaks) Posterior vitreous detachment (PVD) Management in practice You must dilate this patient Review patient within 24-48hrs for a dilated fundus examination (urgency depends on severity of symptoms and any associated risk factors) If no suspicious findings and no other risk factors then advise them of the signs/symptoms of a RD and to report these ASAP (give oral and written info) Management in HES Routinely refer to HES if high risk (trauma, shower of floaters, hazy vision, high myope with sig retinal thinning) or any suspicious signs (VH) Vitreous opacities Muscae volitantes (floaters) Asteroid hyalosis Synchisis scintillans Vitreous haemorrhage Less common: persistent foetal vasculature (Bergmeister papilla) Vitreous opacities - muscae volitantes “Floaters” – an entoptic phenomenon (a visual effect whose source is in the eye) Vitreous opacities – asteroid hyalosis Common degenerative process Small round yellow/white opacities (lipid & calcium particles) collect within the vitreous gel. These move relatively little with eye movement Usually unilateral Rarely causes any symptoms Vitreous opacities – synchisis scintillans Degenerative process Cholesterol crystals in liquified vitreous, usually as a result of vitreous haemorrhage Moves more with eye movement than asteroid hyalosis, sinking inferiorly when the eye is immobile Can occ involve the anterior chamber Vitreous opacities - vitreous haemorrhage Causes Acute PVD associated with retinal tear or avulsion of a peripheral vessel Proliferative retinopathy (DR, RVO, vasculitis, sickle cell) Miscellaneous retinal disorders (microaneurysm, telangiectasia, capillary hemangioma) Trauma Systemic (bleeding disorders) Vitreous opacities - vitreous haemorrhage Symptoms Mild VH - sudden onset floaters and sl.blurred vision Severe VH - severe LOV Management Ultrasound B-scan (to look beyond VH to determine the cause) Treatment depends on the cause (either leave to self-resolve or perform a vitrectomy) Vitreous opacities – persistent foetal vasculature Remnants of the hyaloid vessels can form a Bergmeisters papilla Mittendorf dot (a form of posterior polar cataract) on the posterior lens surface (persistent hyperplastic primary vitreous) Vitreomacular interface disorders Epiretinal membrane (ERM) Macular Hole Vitreomacular traction (VMT) Epiretinal membrane (ERM) This is a fibrocellular structure that develops on the retinal surface. As it proliferates and contracts, it can distort the underlying retina, which can cause visual symptoms and the development of other macular abnormalities including CMO and holes Why? Idiopathic: mostly occur after a PVD, where remnants of vitreous tissue on the retinal surface proliferate Secondary: to surgery (RD, PRP, cryotherapy), trauma, inflammation Epiretinal membrane (ERM) Symptoms Metamorphopsia, and (depending on the extent of the ERM) blurred vision (i.e. VA variable) Signs Irregular translucent sheen - cellophane maculopathy (esp with red-free light) Later thickens into a macular pucker Use an OCT (often seen before symptoms develop) or Amsler grid Epiretinal membrane (ERM) Management in practice Advise the patient of the diagnosis and optimise their refraction Only refer for surgery if they have distortion affecting their binocular vision. Why? The retinal architecture will never be the same as it was prior to developing this condition (often the underlying layer of retina is peeled off along with the membrane) i.e. counsel your patient that vision (VA) will not likely recover significantly, due to damage from the membrane to the retina Management in HES Vitrectomy and ERM peel Success rate: 70-80% within the first few months Depends on how badly the vision is affected, surgical complications, original cause Macular hole – full thickness As the vitreous separates following a strong VMT or PVD, it can remove a section of retina leading to the development of a hole This can be a partial or full thickness hole, and the effect on vision depends on the severity of the hole Incidence? F:M 2:1, myopia, >60yrs (1/500 Px) Fellow eye involved in 10%  Macular hole – full thickness Symptoms Metamorphopsia, and (depending on the extent of the hole) blurred vision. Note that even if the VA is sig reduced, the Px may not have symptoms if they retain good binocular vision Signs Stage 0: VMA Stage 1a: Impending hole – flattening of foveal pit, underlying yellow spot Stage 1b: Occult hole – photoreceptor layer displaced Stage 2: small or medium FTMH with VMT (400microns), yellowish dots at the base, and operculum Stage 4: FTMH with complete PVD (or any size FTMH without VMT) Spontaneous resolution: near normal architecture Macular hole – full thickness How to test for it? OCT, Amsler, Watzke-Allen test Management in practice Advise your patients to monitor their vision in either eye monocularly on a daily basis, and to report any sudden change/distortion/LOV ASAP 50% of early / stage 1 holes resolve spontaneously (only 10% of FTMH do) Refer new onset FTMH (we can only operate successfully on these ones), and early treatment can reduce the risk of significant visual loss Macular hole – full thickness Management in HES Surgery to improve symptoms of distortion and stabilise VA (will not necessarily improve VA) FTMH are closed with vitrectomy, ILM peel and gas Success rate: if caught early, 75% get 2-3 lines visual improvement (better for smaller lesions present for