Macular edema (EM) represents a final common pathway as retinal response to a variety of possible insults. It is a common clinical problem that, for the most part, is self-limiting and has been reported in association with vascular problems (such as diabetes and obstruction of retinal veins), inflammatory conditions (such as the pars planiti), hereditary diseases (such as retinitis pigmentosa or EM dominant cystoid), tractional problems (as from vitreous traction syndrome - macular), use of medicaments such as epinephrine (adrenaline) and following interventions of cataract removal. The EM cystoid post cataract was first described by Irvine in 1953. The therapeutic problem begins in cases of persistent or chronic EM, for which a gradual therapeutic approach is the optimal solution. The specialists should always be alert to the possible side effects of many effective drugs, but potentially toxic, used to treat this disease; in addition to medicines, for the persistent cases, you should intervene with surgical treatment. Macular edema is a common condition associated with intraocular inflammation, retinal vitreous traction, vascular permeability. The EM CME after cataract surgery is known as syndrome of Irvine - Gass. The extracapsular cataract extraction is associated with EM cystoid, angiographically evident in 20% of uncomplicated cases. The clinically significant cystoid macular edema with decreased visual acuity after modern cataract surgery can be observed in only 1% of the eyes. The complicated interventions torn posterior capsule and / or persistent vitreous traction on the anterior segment structures are at the highest risk. Interestingly capsulotomy obtained with neodymium: yttrium-aluminum: garnet (Nd: YAG), if carried out at least three months after surgery for cataract, does not seem to increase the incidence of EM cystoid. Diabetics with any degree of retinopathy have an increased incidence of EM cystoid after the cataract. The EM cystoid can develop even after other types of intraocular surgery: is common after penetrating keratoplasty, after detachment of interventions of the retina, as well as after filtering interventions for glaucoma. It has been suggested that the EM can develop through various mechanisms including macular vitreous traction, vascular compromise, the secretion of prostaglandins (PG) and inflammation, although the exact cause is still unknown. Despite the initial insult, the accumulation of fluid to Amd is a direct result of retinal vascular endothelial damage. When the extracellular fluid accumulates in the central macula, in the outer plexiform layer, can develop the cystic spaces due to the easing horizontal intracellular adhesion. Many mechanisms may be active in the EM genesis and the most important is the intraocular inflammation. As well as in patients after cataract surgery, the EM occurs more commonly in the context of diabetic retinopathy, in which are obvious associations with microaneurysms and hard exudates. In many diabetics, the EM is present with diffuse macular edema and is rarely an isolated problem. While the "Early Treatment Diabetic Retinopathy Study" showed visual improvement after focal photocoagulation for clinically significant macular edema, cystoid EM does not respond so well to laser treatment. The pan-retinal photocoagulation in diabetics can cause a normally self limiting EM. Retinal venous obstructions are another common cause of EM. Both venous occlusions of the branch is the central ones, they can give rise to a severe macular edema. In these conditions the trigger is a secondary hypoxic damage the endothelium of the capillaries in an increased intravascular hydrostatic pressure. Occlusions of branch are associated, in the acute phase, in blood vessels dilated and tortuous, pinpoint hemorrhages and cotton wool spots and flame, with a provision in the sector. In the chronic phase are present EM persistent perivascular muffs, microaneurysms, collateral vessels, shunts, hard exudates. The "Branch Vein Occlusion Study" showed a visual benefit after applying a grid laser treatment on the area of EM. In the acute phase of the obstruction of the central retinal vein are apparent retinal hemorrhages and dilated retinal veins. In the chronic phase may develop perivascular muffs, absorption of retinal hemorrhage and side opto ciliary vessels. The macula may submit an EM, an epiretinal membrane and the formation of a lamellar hole. The "Central Retinal Vein Occlusion Study" showed that there is no benefit in the use of grid photocoagulation for the treatment of edema associated; However, a possible improvement can be observed in younger patients treated. It is not unusual for the EM overlap to a choroidal neovascular membrane or in a serous retinal detachment. Often it goes unnoticed compared to the severe abnormalities subretinal and / or intraretinal. Other rarer forms of retinal diseases produce the EM. Retinal telangiectasia (also called Leber miliary aneurysms or Coats disease) is a unilateral condition that occurs more commonly in boys. The retinal vasculature is abnormal and produces an increased permeability with a diffuse cystoid macular edema. Cryotherapy or laser treatment is recommended if these injuries are threatening macular function. Patients who receive radiation therapy involving the head and neck may develop signs of retinopathy radiation from 6 months to 3 years after treatment. Macroaneurismi retinal arterial acquired, choroidal tumors as nevi, malignant melanomas, cavernous hemangiomas, a multitude of ocular inflammation and infection can cause EM. The major symptom is the decrease of EM central visual acuity. The accompanying symptoms may include metamorphopsia, micropsia, scotoma, eye irritation, photophobia, and conjunctival injection. Clinically, the EM is best seen using the slit lamp with a contact lens; edema, in fact, gives rise to a dispersion of light caused by the numerous interfaces created by the separate retinal cells. Light leakage decreases the translucency of the neurosensory retina, so that the normal retinal pigment epithelium and the background choroidal prove confused. They are seen delimited accumulations of fluid in the outer plexiform layer, with the widest part centrally and peripherally progressively smaller. The backlight can help delineate the spaces of pseudo cysts. A yellow spot, which is believed to be due to the spread of the luteal pigment, may be evident in the central macula. The underlying causes instead of EM does not alter its appearance, but the signs associated vary widely depending on the etiology. As a result of EM, a rupture of the cyst of the inner retina may cause a lamellar macular hole. Prolonged EM can induce atrophy of macular photoreceptors, resulting in a low visual acuity. Retinal fluorescein angiography showed better than clinical examination, the EM. It was shown that there is a close correlation between the average thickness and retinal visual acuity. However, the retinal fluorescein angiography only provides qualitative information. Quantitative data on retinal thickness can be studied only through the OCT examination. The literature shows, unfortunately, the lack of EM response to laser therapy, which is why the last decade has opened the border to the use of anti-angiogenic and steroid levels in intraocular substances, based on their nature at times to altered permeability vascular, sometimes distinctly inflammatory, EM. Prior Bevacizumab (Avastin®), then the pegaptanib sodium (Macugen®), then the ranibizumab (Lucentis®), triamcinolone (Triesence®), then the dexamethasone (Ozurdex®), have given new hope and good results in the battle against this nosographic entities very disabling and that inevitably affects the quality of life of the same. The need to offer a more effective treatment approach has led to the search for a new molecule that can offer better results both qualitatively and quantitatively. The following study aims to determine primarily the efficacy of intravitreal Aflibercept the best corrected visual acuity and its safety profile, monitoring secondarily for both local and systemic adverse effects to Amd secondary to neovascular AMD, and secondary to OVCR secondary to diabetic retinopathy also in association with the use of yellow laser micropulsato subthreshold.
L’edema maculare (EM) rappresenta una via comune finale come risposta della retina a una varietà di possibili insulti. Rappresenta un comune problema clinico che, per la maggior parte, è auto-limitante ed è stato riportato in associazione con problemi vascolari (come diabete e ostruzioni delle vene retiniche), condizioni infiammatorie (come pars planiti), malattie ereditarie (come retinite pigmentosa o EM cistoide dominante), problemi trazionali (come sindrome da trazione vitreo - maculare), uso di medicamenti come l’epinefrina (adrenalina) e in seguito a interventi di rimozione di cataratta. L’EM cistoide post cataratta fu inizialmente descritto da Irvine nel 1953. Il problema terapeutico inizia nei casi di EM persistente o cronico, per cui un approccio terapeutico graduale è la soluzione ottimale. Gli specialisti devono sempre essere attenti ai possibili effetti collaterali di molti farmaci efficaci, ma potenzialmente tossici, usati per trattare questa patologia; in aggiunta ai farmaci, per i casi persistenti, si dovrebbe intervenire con il trattamento chirurgico. L’edema maculare è una comune condizione associata a infiammazioni intraoculari, trazioni vitreo retiniche, permeabilità vascolare. L’EM cistoide dopo intervento di cataratta è conosciuto come sindrome di Irvine – Gass. L’estrazione extracapsulare di cataratta è associata con EM cistoide, angiograficamente evidente nel 20% dei casi non complicati. L’edema maculare cistoide clinicamente significativo con diminuzione dell’acutezza visiva dopo il moderno intervento di cataratta è osservabile solo nell’1% degli occhi. Gli interventi complicati da rottura della capsula posteriore e/o persistente trazione vitreale sulle strutture del segmento anteriore sono al più alto rischio. È interessante osservare che la capsulotomia ottenuta con neodimio:ittrio-alluminio:granato (Nd:YAG), se eseguita ad almeno 3 mesi di distanza dall’intervento di cataratta, non sembra aumentare l’incidenza dell’EM cistoide. I diabetici con qualsiasi grado di retinopatia hanno un’aumentata incidenza di EM cistoide dopo la cataratta. L’EM cistoide può svilupparsi anche dopo altri tipi di chirurgia intraoculare: è comune dopo cheratoplastica perforante, dopo interventi di distacco di retina, così come dopo interventi filtranti per il glaucoma. È stato ipotizzato che l’EM può svilupparsi attraverso vari meccanismi che includono la trazione vitreo maculare, la compromissione vascolare, la secrezione di prostaglandine (PG) e l’infiammazione, sebbene l’esatta causa sia ancora sconosciuta. Malgrado l’iniziale insulto, l’accumulo di liquido nell’EM è la diretta conseguenza di danni dell’endotelio vascolare retinico. Quando il liquido extracellulare si accumula nella macula centrale, nello strato plessiforme esterno, possono svilupparsi gli spazi cistici dovuti all’allentamento orizzontale dell’adesione intracellulare. Molti meccanismi possono essere attivi nella genesi dell’EM e il più importante è l’infiammazione intraoculare. Oltre che nei pazienti dopo l’intervento di cataratta, l’EM si manifesta più comunemente nel quadro della retinopatia diabetica, in cui sono evidenti associazioni con i microaneurismi ed essudati duri. In molti diabetici, l’EM è presente con l’edema maculare diffuso e raramente è un problema isolato. Mentre il “Early Treatment Diabetic Retinopathy Study” dimostrò il miglioramento visivo dopo fotocoagulazione focale per l’edema maculare clinicamente significativo, l’EM cistoide non risponde così bene al trattamento laser. La fotocoagulazione panretinica nei diabetici può provocare un EM normalmente auto limitante. Le ostruzioni venose retiniche rappresentano un’altra comune causa di EM. Sia le occlusioni venose di branca sia quelle centrali, possono dare origine a un severo edema maculare. In queste condizioni la causa scatenante è un danno ipossico dell’endotelio dei capillari secondario a una aumentata pressione idrostatica intravascolare. Le occlusioni di branca sono associate, nella fase acuta, a vasi sanguigni dilatati e tortuosi, emorragie puntiformi e a fiamma ed essudati cotonosi, con una disposizione a settore. Nella fase cronica sono presenti EM persistente, manicotti perivasali, microaneurismi, vasi collaterali, shunts, essudati duri. Il “Branch Vein Occlusion Study” dimostrò un beneficio visivo dopo l’applicazione di un trattamento laser a griglia sull’area dell’EM. Nella fase acuta dell’ostruzione della vena centrale della retina sono evidenti emorragie retiniche e vene retiniche dilatate. Nella fase cronica si possono sviluppare manicotti perivasali, assorbimento delle emorragie retiniche e vasi collaterali opto ciliari. La macula può presentare un EM, una membrana epiretinica e la formazione di un foro lamellare. Il “Central Retinal Vein Occlusion Study” dimostrò che non c’è alcun beneficio nell’uso della fotocoagulazione a griglia per il trattamento dell’edema associato; tuttavia, un possibile miglioramento può essere osservato in pazienti più giovani trattati. Non è inusuale per l’EM sovrapporsi ad una membrana neovascolare coroideale o a un distacco sieroso retinico. Spesso passa inosservato rispetto alle severe anomalie sottoretiniche e/o intraretiniche. Altre più rare forme di patologie retiniche producono l’EM. Le telangectasie retiniche (anche chiamate aneurismi miliari di Leber o malattia di Coats) sono una condizione unilaterale che avviene più comunemente nei ragazzi. La vascolarizzazione retinica è anomala e produce un’aumentata permeabilità con un diffuso edema maculare cistoide. La crioterapia o il trattamento laser è consigliato se queste lesioni minacciano la funzione maculare. I pazienti che ricevono il trattamento radiante coinvolgente la testa e il collo possono sviluppare segni di retinopatia da radiazione da 6 mesi a 3 anni dopo il trattamento. Macroaneurismi retinici arteriosi acquisiti, tumori coroideali come i nevi, i melanomi maligni, gli emangiomi cavernosi, una moltitudine di infiammazioni oculari e di infezioni posso provocare EM. Il maggiore sintomo dell’EM è la diminuzione dell’acuità visiva centrale. I sintomi di accompagnamento possono includere metamorfopsie, micropsia, scotoma, irritazione oculare, fotofobia e iniezione congiuntivale. Clinicamente, l’EM è meglio visibile usando la lampada a fessura con una lente a contatto; l’edema, infatti, dà origine a una dispersione della luce causata dalle numerose interfacce create dalle cellule retiniche separate. La dispersione della luce diminuisce la traslucenza della retina neurosensoriale, così che il normale epitelio pigmentato retinico e lo sfondo coroideale risultino confusi. Sono visti accumuli delimitati di fluido nello strato plessiforme esterno, con la parte più larga centralmente e progressivamente più piccola perifericamente. La retroilluminazione può aiutare a delineare gli spazi delle pseudo cisti. Una macchia gialla, che si crede sia dovuta alla diffusione del pigmento luteale, può essere evidente nella macula centrale. Le cause alla base dell’EM invece non alterano il suo aspetto, ma i segni associati variano ampiamente a seconda dell’eziologia. Come risultato dell’EM, una rottura delle cisti della retina interna può provocare un foro maculare lamellare. Un prolungato EM può indurre atrofia dei fotorecettori maculari, con bassa acuità visiva conseguente. La fluorangiografia retinica evidenzia meglio, rispetto all’esame clinico, l’EM. È stato dimostrato che vi è una stretta correlazione tra lo spessore medio retinico e l’acuità visiva. Tuttavia, la fluorangiografia retinica fornisce solo informazioni qualitative. I dati quantitativi sullo spessore retinico possono essere studiati solo attraverso l’esame OCT. Dalla letteratura emerge, purtroppo, la scarsa risposta dell’EM alla terapia laser, motivo per cui nell’ultimo decennio si è aperta la frontiera all’utilizzo di sostanze anti angiogeniche e steroidee a livello intraoculare, basandosi proprio sulla natura alle volte per alterata permeabilità vasale, alle volte spiccatamente flogistica, dell’EM. Prima il Bevacizumab (Avastin®), poi il Pegaptanib sodico (Macugen®), poi il Ranibizumab (Lucentis®), Triamcinolone (Triesence®), poi il Desametasone (Ozurdex®), hanno dato nuove speranze e discreti risultati nella battaglia contro questa entità nosografica estremamente invalidante e che inevitabilmente si ripercuote sulla qualità della vita dello stesso. La necessità di offrire un approccio terapeutico maggiormente efficace ha spinto alla ricerca di una nuova molecola che possa offrire migliori risultati sia in termini qualitativi che in termini quantitativi. Il seguente studio si propone di determinare primariamente l’efficacia dell’utilizzo di Aflibercept intravitreale sulla miglior acuità visiva corretta e sul suo profilo di tollerabilità, monitorandone secondariamente gli effetti avversi sia locali che sistemici nell’EM secondario ad AMD neovascolare, secondario ad OVCR e secondario a retinopatia diabetica anche in associazione all’utilizzo del laser giallo micropulsato sottosoglia.
Laser Giallo Micropulsato come coadiuvante nella terapia intravitreale nel trattamento degli edemi maculari / Defranco, Edoardo. - (2017 Mar 01).
Laser Giallo Micropulsato come coadiuvante nella terapia intravitreale nel trattamento degli edemi maculari
DEFRANCO, EDOARDO
2017-03-01
Abstract
Macular edema (EM) represents a final common pathway as retinal response to a variety of possible insults. It is a common clinical problem that, for the most part, is self-limiting and has been reported in association with vascular problems (such as diabetes and obstruction of retinal veins), inflammatory conditions (such as the pars planiti), hereditary diseases (such as retinitis pigmentosa or EM dominant cystoid), tractional problems (as from vitreous traction syndrome - macular), use of medicaments such as epinephrine (adrenaline) and following interventions of cataract removal. The EM cystoid post cataract was first described by Irvine in 1953. The therapeutic problem begins in cases of persistent or chronic EM, for which a gradual therapeutic approach is the optimal solution. The specialists should always be alert to the possible side effects of many effective drugs, but potentially toxic, used to treat this disease; in addition to medicines, for the persistent cases, you should intervene with surgical treatment. Macular edema is a common condition associated with intraocular inflammation, retinal vitreous traction, vascular permeability. The EM CME after cataract surgery is known as syndrome of Irvine - Gass. The extracapsular cataract extraction is associated with EM cystoid, angiographically evident in 20% of uncomplicated cases. The clinically significant cystoid macular edema with decreased visual acuity after modern cataract surgery can be observed in only 1% of the eyes. The complicated interventions torn posterior capsule and / or persistent vitreous traction on the anterior segment structures are at the highest risk. Interestingly capsulotomy obtained with neodymium: yttrium-aluminum: garnet (Nd: YAG), if carried out at least three months after surgery for cataract, does not seem to increase the incidence of EM cystoid. Diabetics with any degree of retinopathy have an increased incidence of EM cystoid after the cataract. The EM cystoid can develop even after other types of intraocular surgery: is common after penetrating keratoplasty, after detachment of interventions of the retina, as well as after filtering interventions for glaucoma. It has been suggested that the EM can develop through various mechanisms including macular vitreous traction, vascular compromise, the secretion of prostaglandins (PG) and inflammation, although the exact cause is still unknown. Despite the initial insult, the accumulation of fluid to Amd is a direct result of retinal vascular endothelial damage. When the extracellular fluid accumulates in the central macula, in the outer plexiform layer, can develop the cystic spaces due to the easing horizontal intracellular adhesion. Many mechanisms may be active in the EM genesis and the most important is the intraocular inflammation. As well as in patients after cataract surgery, the EM occurs more commonly in the context of diabetic retinopathy, in which are obvious associations with microaneurysms and hard exudates. In many diabetics, the EM is present with diffuse macular edema and is rarely an isolated problem. While the "Early Treatment Diabetic Retinopathy Study" showed visual improvement after focal photocoagulation for clinically significant macular edema, cystoid EM does not respond so well to laser treatment. The pan-retinal photocoagulation in diabetics can cause a normally self limiting EM. Retinal venous obstructions are another common cause of EM. Both venous occlusions of the branch is the central ones, they can give rise to a severe macular edema. In these conditions the trigger is a secondary hypoxic damage the endothelium of the capillaries in an increased intravascular hydrostatic pressure. Occlusions of branch are associated, in the acute phase, in blood vessels dilated and tortuous, pinpoint hemorrhages and cotton wool spots and flame, with a provision in the sector. In the chronic phase are present EM persistent perivascular muffs, microaneurysms, collateral vessels, shunts, hard exudates. The "Branch Vein Occlusion Study" showed a visual benefit after applying a grid laser treatment on the area of EM. In the acute phase of the obstruction of the central retinal vein are apparent retinal hemorrhages and dilated retinal veins. In the chronic phase may develop perivascular muffs, absorption of retinal hemorrhage and side opto ciliary vessels. The macula may submit an EM, an epiretinal membrane and the formation of a lamellar hole. The "Central Retinal Vein Occlusion Study" showed that there is no benefit in the use of grid photocoagulation for the treatment of edema associated; However, a possible improvement can be observed in younger patients treated. It is not unusual for the EM overlap to a choroidal neovascular membrane or in a serous retinal detachment. Often it goes unnoticed compared to the severe abnormalities subretinal and / or intraretinal. Other rarer forms of retinal diseases produce the EM. Retinal telangiectasia (also called Leber miliary aneurysms or Coats disease) is a unilateral condition that occurs more commonly in boys. The retinal vasculature is abnormal and produces an increased permeability with a diffuse cystoid macular edema. Cryotherapy or laser treatment is recommended if these injuries are threatening macular function. Patients who receive radiation therapy involving the head and neck may develop signs of retinopathy radiation from 6 months to 3 years after treatment. Macroaneurismi retinal arterial acquired, choroidal tumors as nevi, malignant melanomas, cavernous hemangiomas, a multitude of ocular inflammation and infection can cause EM. The major symptom is the decrease of EM central visual acuity. The accompanying symptoms may include metamorphopsia, micropsia, scotoma, eye irritation, photophobia, and conjunctival injection. Clinically, the EM is best seen using the slit lamp with a contact lens; edema, in fact, gives rise to a dispersion of light caused by the numerous interfaces created by the separate retinal cells. Light leakage decreases the translucency of the neurosensory retina, so that the normal retinal pigment epithelium and the background choroidal prove confused. They are seen delimited accumulations of fluid in the outer plexiform layer, with the widest part centrally and peripherally progressively smaller. The backlight can help delineate the spaces of pseudo cysts. A yellow spot, which is believed to be due to the spread of the luteal pigment, may be evident in the central macula. The underlying causes instead of EM does not alter its appearance, but the signs associated vary widely depending on the etiology. As a result of EM, a rupture of the cyst of the inner retina may cause a lamellar macular hole. Prolonged EM can induce atrophy of macular photoreceptors, resulting in a low visual acuity. Retinal fluorescein angiography showed better than clinical examination, the EM. It was shown that there is a close correlation between the average thickness and retinal visual acuity. However, the retinal fluorescein angiography only provides qualitative information. Quantitative data on retinal thickness can be studied only through the OCT examination. The literature shows, unfortunately, the lack of EM response to laser therapy, which is why the last decade has opened the border to the use of anti-angiogenic and steroid levels in intraocular substances, based on their nature at times to altered permeability vascular, sometimes distinctly inflammatory, EM. Prior Bevacizumab (Avastin®), then the pegaptanib sodium (Macugen®), then the ranibizumab (Lucentis®), triamcinolone (Triesence®), then the dexamethasone (Ozurdex®), have given new hope and good results in the battle against this nosographic entities very disabling and that inevitably affects the quality of life of the same. The need to offer a more effective treatment approach has led to the search for a new molecule that can offer better results both qualitatively and quantitatively. The following study aims to determine primarily the efficacy of intravitreal Aflibercept the best corrected visual acuity and its safety profile, monitoring secondarily for both local and systemic adverse effects to Amd secondary to neovascular AMD, and secondary to OVCR secondary to diabetic retinopathy also in association with the use of yellow laser micropulsato subthreshold.File | Dimensione | Formato | |
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