Pharmacology and Vitreoretinal Surgery (Developments in Ophthalmology)
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More than 35 years have passed since the advent of pars plana vitrectomy, and vitreoretinal surgery has developed to highly sophisticated techniques to treat retinal diseases. Removal of the vitreous gel and hemorrhage not only clears the optical axis of the eye, but enables the surgeon to approach the retina and the vitreoretinal interface directly, thereby relieving traction and removing pathological tissue, such as epiretinal membranes. Peeling off the internal limiting membrane has proven to be a safe and effective technique in macular surgery, resulting in macular hole closure. Twenty years ago, nobody would have imagined this. Today, final success rates beyond 90% can be achieved in macular and reattachment surgery.
However, there are limitations of current vitreoretinal surgery techniques, which are mechanically based. Removal of the vitreous is incomplete, especially at the vitreo retinal interface and at the vitreous base. This may lead to persistent or recurrent traction on the retina, resulting in retinal tear formation or reproliferation. More aggressive removal of the vitreous by mechanical means, however, carries the risk of damaging the retina. When epiretinal membranes are removed in PVR cases and in diabetic eyes with traction retinal detachment, gliotic scar tissue is removed but neural retina is not treated. Thus, despite anatomical reattachment, visual results are often disappointing.
Pharmacology-assisted vitreoretinal surgery can help to overcome these limitations. There areenzymes which cleave the vitreoretinal junction without damaging the retina, and those for liquefaction. Thereby, vitreolysis and induction of posterior vitreous detachment has become possible without the need for vitrectomy. Recent results from clinical trials show that up to 40% of eyes achieve release of traction without surgery.
Pharmacologic vitreolysis will change our current indications and concepts in treating retinal and macular diseases, and earlier intervention might save visual function before advanced stages have destroyed the retinal cytoarchitecture. In diabetic eyes, for example, enzymatic PVD induction at an early stage of the disease might inhibit fibrovascular and fibrocellular proliferations at the vitreoretinal interface, thereby preventing progression to proliferative disease.
Neuroprotective and antiproliferative agents may hold the promise of preserving neuronal function when the retina is detached or when PVR has developed. This again may change the time point of intervention from currently advanced stages to an earlier disease stage with less pathology. Fibrinolytic and antiproliferative agents help to treat disasters in ophthalmology such as massive submacular hemorrhage or retinal detachment in retinopathy of prematurity. It is now time to combine pharmacological concepts and vitreoretinal surgery. World renowned experts and opinion leaders in their field have contributed their knowledge and skills to make this book the first summary on pharmacology-assisted vitreoretinal surgery. I am greatly indebted to the authors, and my hopes are that this book was a basis and motivation for clinicians and researchers who want to bring retinal surgery further by introducing pharmacology-assisted vitreoretinal surgery.
However, there are limitations of current vitreoretinal surgery techniques, which are mechanically based. Removal of the vitreous is incomplete, especially at the vitreo retinal interface and at the vitreous base. This may lead to persistent or recurrent traction on the retina, resulting in retinal tear formation or reproliferation. More aggressive removal of the vitreous by mechanical means, however, carries the risk of damaging the retina. When epiretinal membranes are removed in PVR cases and in diabetic eyes with traction retinal detachment, gliotic scar tissue is removed but neural retina is not treated. Thus, despite anatomical reattachment, visual results are often disappointing.
Pharmacology-assisted vitreoretinal surgery can help to overcome these limitations. There areenzymes which cleave the vitreoretinal junction without damaging the retina, and those for liquefaction. Thereby, vitreolysis and induction of posterior vitreous detachment has become possible without the need for vitrectomy. Recent results from clinical trials show that up to 40% of eyes achieve release of traction without surgery.
Pharmacologic vitreolysis will change our current indications and concepts in treating retinal and macular diseases, and earlier intervention might save visual function before advanced stages have destroyed the retinal cytoarchitecture. In diabetic eyes, for example, enzymatic PVD induction at an early stage of the disease might inhibit fibrovascular and fibrocellular proliferations at the vitreoretinal interface, thereby preventing progression to proliferative disease.
Neuroprotective and antiproliferative agents may hold the promise of preserving neuronal function when the retina is detached or when PVR has developed. This again may change the time point of intervention from currently advanced stages to an earlier disease stage with less pathology. Fibrinolytic and antiproliferative agents help to treat disasters in ophthalmology such as massive submacular hemorrhage or retinal detachment in retinopathy of prematurity. It is now time to combine pharmacological concepts and vitreoretinal surgery. World renowned experts and opinion leaders in their field have contributed their knowledge and skills to make this book the first summary on pharmacology-assisted vitreoretinal surgery. I am greatly indebted to the authors, and my hopes are that this book was a basis and motivation for clinicians and researchers who want to bring retinal surgery further by introducing pharmacology-assisted vitreoretinal surgery.
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