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Recent advances in the techniques of vitrectomy with membrane peeling [See chapter V.A.2. Vitreo-maculopathy surgery], at times with chromodissection [See chapter V.A.3. Chromodissection in vitreo-retinal surgery], have greatly improved patient outcomes. There are, however, risks associated with these procedures, and on rare occasions there can be much worse vision following surgery than preoperatively. This chapter will review the current concepts of pathogenesis and surgical management of macular holes and macular pucker. Special emphasis will be placed on failed cases and reoperations.

Vitreo-papillary adhesion (VPA) is characterized by persistent adhesion of the posterior vitreous cortex to the optic disc as a direct consequence of anomalous posterior vitreous detachment (PVD) [see chapter III.B. Anomalous PVD and vitreoschisis]. The significance of this pathology has gained increasing attention in the medical literature as traction at the adhesion site can lead to various pathologies depending on the directions of the force vector. As a result, VPA has been implicated in a wide range of retinal disorders such as macular holes and macular puckers, intraretinal cysts, and vascular disorders including peripapillary/subretinal/intrapapillary hemorrhages, proliferative diabetic vitreo-retinopathy, and central retinal vein occlusion. Due to direct traction on the optic disc, it may also play a role in a number of optic neuropathies such as non-arteritic anterior ischemic optic neuropathy, gaze-evoked amaurosis, and optic nerve pit. Optical coherence tomography (OCT) provides direct visualization of the vitreo-papillary interface, allowing us to better understand the underlying pathophysiology of vitreo-papillary adhesion and traction.

The fetal hyaloid vasculature plays a critical role in many aspects of proper ocular development. The hyaloid artery (HA) is a large vessel that extends from the optic disc through the vitreous where it branches and extends to the posterior surface of the lens to anastamose with the tunica vasculosa lentis (TVL) which supplies nutrients to the developing lens in the fetus (Figure I.D-1). In humans, the entire embryonic vascular system regresses by birth, which is necessary for media clarity and normal vision. Regression of the hyaloid vasculature is a very complex process likely requiring the participation of many proteins. The mechanisms of hyaloid vessel regression are not known, but insight could be obtained by understanding how this fetal vasculature forms. One study of human embryonic vitreous revealed the presence of blood islands composed of aggregates of primitive erythroblasts and hemangioblasts, as early as the seventh week of gestation (WG) [1]. These cell aggregates express hematopoietic stem cell markers, and the ligands for these markers are expressed in high concentrations in the lens and retina, probably functioning to guide the cells into the vitreous body assembling the fetal vitreous vasculature by hemo-vasculogenesis [2].

The symptoms and signs of nutritional and toxic optic neuropathies are similar in that they usually present simultaneously and bilaterally. Symptoms are progressive with bilateral symmetric visual loss without pain. Some patients may initially only observe dyschromatopsia, such that certain colors, such as red, are not as bright. Usually only one eye may be involved in the early stages before the other becomes symptomatic. If one eye is severely affected while the other eye has completely normal findings, however, then the diagnosis of nutritional or toxic optic neuropathy is questionable. A gradual progressive blurriness, then cloudiness, often forms at the point of fixation.1

Floaters most commonly occur in the middle age due to age-related changes in vitreous structure and light scattering by the posterior vitreous cortex after collapse of the vitreous body during posterior vitreous detachment (PVD). In youth, floaters are most often due to myopic vitreopathy. Vitreous floaters can have a negative impact on visual function and in turn the quality of life. Techniques to characterize floaters clinically include ultrasound imaging, optical coherence tomography, and dynamic light scattering for structural characterization. Functional impact can be assessed by straylight measurements, as well as contrast sensitivity testing. When the severity of floater symptomatology is significant, commonly used therapies include neodymium:yttrium-aluminum-garnet (YAG) laser and limited 25-gauge vitrectomy. While the former is of unproven efficacy, the latter has been shown to be a safe, effective, and definitive cure that improves patients’ quality of life and eradicates symptomatology produced by light scattering and diffraction. It is thus reasonable to offer limited vitrectomy to individuals who have attempted to cope unsuccessfully and in whom functional deficit can be objectively demonstrated by testing contrast sensitivity, an important aspect of vision.

Experimental animal and human studies have shown the existence of several retinal ganglion cell types, each with different central projections. These separate channels probably subserve different psychophysical functions. It is likely that several parallel visual systems exist in man and that each pathway subserves a different visual task.