Stefánsson Einar
University of Iceland, National University Hospital, 101 Reykjavı´k, Iceland.
Saudi J Ophthalmol. 2009 Jul;23(2):143-8. doi: 10.1016/j.sjopt.2009.06.002. Epub 2009 Aug 5.
A variety of treatment options are available for the treatment of diabetic macular edema. They include laser photocoagulation, anti-VEGF drugs, intravitreal steroids, and vitrectomy with or without release of vitreoretinal traction. A full understanding of the physiological mechanisms of these treatment modalities allows sensible combination of treatment options. Retinal photocoagulation has repeatedly been shown to improve retinal oxygenation, as does vitrectomy. Oxygen naturally reduces VEGF production and thereby decreases leakage of plasma proteins from capillaries into the tissue. In addition, vitrectomy allows faster clearance of cytokines, such as VEGF, from the retina into the vitreous cavity. The VEGF-lowering effect of photocoagulation and vitrectomy can be augmented with anti-VEGF drugs and corticosteroids reduce the effect of VEGF on capillary permeability. Starling's law explains vasogenic edema, which is controlled by osmotic and hydrostatic gradients between vessel and tissue. It explains how VEGF-induced vascular permeability causes plasma protein to leak into the tissue interstitial space, thus decreasing the osmotic pressure gradient between vessel and tissue, resulting in water accumulation, i.e. edema. This is reversed by reducing VEGF production, which is achieved with laser treatment; or by removing VEGF with antibodies or vitrectomy; or by reducing the permeability effect with steroids. At the same time, Starling's law takes into account hemodynamic changes that affect the hydrostatic gradient. High arterial blood pressure and hypoxic vasodilatation increase the hydrostatic pressure in the microcirculation, which increases water flux from vessel to tissue and induce edema. Treatment of arterial hypertension or reversal of retinal hypoxia with laser reverses this pathophysiology and reduces edema. Newton's third law explains, that vitreoretinal traction decreases hydrostatic tissue pressure in the retina, increases the pressure gradient between vessel and tissue, and stimulates water fluxes from vessel into tissue, leading to edema. Release of vitreoretinal traction reverses this mechanism and reduces edema.
糖尿病性黄斑水肿有多种治疗选择。这些选择包括激光光凝、抗血管内皮生长因子（VEGF）药物、玻璃体内注射类固醇，以及有或无玻璃体视网膜牵拉松解的玻璃体切除术。充分了解这些治疗方式的生理机制有助于合理组合治疗方案。视网膜光凝已反复证明可改善视网膜氧合，玻璃体切除术也有同样效果。氧气可自然减少VEGF生成，从而减少血浆蛋白从毛细血管渗漏到组织中。此外，玻璃体切除术能使细胞因子（如VEGF）更快地从视网膜清除到玻璃体腔。光凝和玻璃体切除术降低VEGF的作用可通过抗VEGF药物增强，而皮质类固醇可降低VEGF对毛细血管通透性的影响。斯塔林定律解释了血管源性水肿，它由血管与组织之间的渗透和流体静力梯度控制。该定律解释了VEGF诱导的血管通透性如何导致血浆蛋白渗漏到组织间隙，从而降低血管与组织之间的渗透压梯度，导致水积聚，即水肿。通过激光治疗减少VEGF生成可逆转这种情况；或者用抗体或玻璃体切除术清除VEGF；或者用类固醇降低通透性作用。同时，斯塔林定律考虑了影响流体静力梯度的血流动力学变化。高动脉血压和缺氧性血管舒张会增加微循环中的流体静力压力，这会增加从血管到组织的水流量并诱发水肿。治疗动脉高血压或用激光逆转视网膜缺氧可逆转这种病理生理过程并减轻水肿。牛顿第三定律解释了玻璃体视网膜牵拉会降低视网膜中的流体静力组织压力，增加血管与组织之间的压力梯度，并刺激水从血管流入组织，导致水肿。解除玻璃体视网膜牵拉可逆转这一机制并减轻水肿。
