Why does vitreoretinal traction create macular oedema?

Abstract

A 65-year-old taxi driver was referred due to blurry vision in the right eye of two-day duration and described his symptoms as if he was ‘looking through ice’. There were no other symptoms. Visual acuity (VA) was 0.7 in the right eye and 0.8 in the left eye. Slit lamp examination revealed macular oedema in the right eye (Fig. 1). Optical coherent tomography (OCT, Topcon 3D OCT-2000 FA plus) revealed vitreomacular traction (VMT) and macular oedema involving the inner layers of the retina in the right eye. In the left eye, a partial posterior vitreous detachment (PVD) was seen, without VMT (Fig. 1). A diagnosis of VMT syndrome, due to incomplete PVD, was entertained. The patient was advised of the situation and did not receive any treatment. A follow-up appointment was scheduled few weeks later. Before that appointment, he came to the clinic complaining of floaters in the right eye. On examination, the vision was 1.0 in both eyes, a Weiss ring was visible on biomicroscopy in the vitreous cavity of the right eye and there were no signs of maculopathy. Optical coherent tomography (OCT) imaging was normal, except for minimal shadows on the image due to vitreous floaters. He was diagnosed with complete PVD. Vitreomacular traction is caused by an incomplete PVD where the vitreous remains attached to the posterior retina, exerting traction on the macula. The traction causes retinal distortion and can cause various macular disorders, including cystoid macular oedema, macular hole and epiretinal membrane (Duker et al. 2013). In our case, the initial OCT image showed clear vitreous traction on the central macular area resulting in distortion and macular oedema. No epiretinal membrane was noted. The distortion is easy to understand, but what is the mechanism that translates mechanical traction into tissue oedema? Newton's third law states: ‘To every action there is always opposed an equal reaction’ (Newton 1726), which in current terminology means that for every force, there is a counter-force acting in the opposite direction. The force exerted by the vitreous gel pulls anteriorly on the retina, and this is met by an equal force in the retina pulling posteriorly towards the back of the eye. The opposite pulling forces lower the hydrostatic pressure in the tissue between the forces (Fig. 2). Starling's law describes the formation of oedema in tissues. It states that fluid transport between tissue and blood vessels is controlled by hydrostatic and osmotic forces. The hydrostatic pressure difference (created by the heart) between blood vessels and tissue drives water down a pressure gradient into the interstitial space. The osmotic pressure difference pulls water from tissue into blood vessels due to high osmotic activity of the macromolecules in blood. In normal conditions, the hydrostatic and osmotic pressure differences between tissue and blood vessels are equal and opposite and no net transport of water takes place; oedema is neither formed nor reduced (Hall & Guyton 2011). This steady state is upset by the VMT. The traction reduces the hydrostatic pressure in the retina, thus increasing the pressure difference between blood vessel and retinal tissue. Water flows down this pressure gradient and accumulates in the tissue as oedema. Water accumulation lowers the osmotic pressure in the interstitial space and increases the osmotic pressure difference, until a new equilibrium is established between the hydrostatic and osmotic pressure differences. At this time, the net transport of water again is zero and the tissue reaches a steady state – with macular oedema (Stefánsson 2009). Vitreomacular traction (VMT) with macular oedema can be managed conservatively as spontaneous resolution occurs in some cases. When the VMT is persistent, it is usually treated surgically with pars plana vitrectomy, but pharmacological vitreolysis with ocriplasmin and pneumatic release with intravitreal gas have also shown to be effective (Jackson et al. 2013). Surgical, spontaneous, pneumatic or enzymatic release of the VMT reverses the situation described above. Hydrostatic pressure in the retina increases back to normal, water flows back into the blood vessels, and the macular oedema disappears.