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全视网膜激光光凝术（panretinal photocoagulation, PRP）通过激光热效应封闭无灌注及血管渗漏点，改善视网膜缺血；玻璃体腔内注射抗血管内皮生长因子（VEGF）药物来抑制VEGF从而抑制新生血管生成及血管渗漏，二者是控制糖尿病性视网膜病变（DR）及糖尿病性黄斑水肿（DME）病情的一线治疗方法。在增殖型糖尿病性视网膜病变（PDR）患者中，进行PRP及玻璃体腔内抗VEGF药物注射需密切观察玻璃体视网膜界面情况。在部分病例中，对PDR患者进行PRP或抗VEGF药物治疗后，纤维血管膜的收缩可能导致牵拉性视网膜脱离，既往报道将PRP及抗VEGF药物治疗后导致的牵拉性视网膜脱离称为Crunch综合征（Crunch syndrome）。Crunch综合征的发生率为1.5%～5.3%，糖尿病病程15年以上、后极部环形增殖的PDR患者出现Crunch综合征的风险较高。其背后的机制可能是在使用抗VEGF药物治疗后，患者玻璃体腔内VEGF浓度下降，而结缔组织生长因子（connective tissue growth factor）浓度不变，血管发生收缩的同时纤维组织继续增殖，易导致患者出现牵拉性视网膜脱离。此外，在PRP治疗后，激光的热效应也可导致增殖的血管纤维膜发生收缩，从而引起Crunch综合征。因此，对PDR患者，尤其是增殖严重的患者行抗VEGF及PRP治疗后，应进行密切观察，如出现Crunch综合征或原有增殖膜牵拉加重，应在7日内行玻璃体切割术（PPV）进行干预。然而，在既往的病例报道及笔者研究团队的观察中，Crunch综合征并非都会引起视网膜脱离，也存在有利的Crunch综合征（favorable Crunch syndrome）。抗VEGF药物及PRP治疗后引起的纤维收缩也可促进玻璃体后皮质及视网膜前增殖膜完全与视网膜分离，解除纤维组织对视网膜的牵拉，从而在不进行PPV手术的情况下，改善牵拉性视网膜脱离及玻璃体视网膜牵拉引起的DME（图2-2-1）。
2022-03-16第1次抗VEGF治疗
2022-04-18第2次抗VEGF治疗
2022-05-18第3次抗VEGF治疗
2022-09-21第4次抗VEGF治疗
A
2022-05-05第1次激光
2022-05-23第2次激光
2022-06-15第3次激光
B
图2-2-1 抗VEGF及PRP治疗后玻璃体后脱离范围显著扩大的PDR案例
A．PDR合并玻璃体视网膜牵拉引发的相关DME，既往已行PRP，行4次抗VEGF药物治疗后，黄斑区玻璃体后界膜与视网膜分离（白色箭头所示），玻璃体视网膜牵拉解除，黄斑水肿较前明显好转。B．PDR合并玻璃体视网膜牵拉性相关DME，在行3次视网膜激光光凝治疗后，黄斑区玻璃体后界膜与视网膜分离（白色箭头所示），玻璃体视网膜牵拉缓解，黄斑水肿较前好转。
Müller细胞的胞体位于视网膜内核层，其突起向上延伸至视网膜表面的内界膜、向下延伸至光感受器细胞及外界膜，以此为视网膜提供张力、维持视网膜神经层的完整性。Müller细胞突起的末端含有整合素细胞表面受体，这些受体介导内界膜与视网膜内层的黏附。在PDR的PPV手术中，血管增殖膜与视网膜粘连紧密，剥膜时用力，特别是反复用力牵拉血管增殖膜时，机械牵拉力必定会过度刺激Müller细胞，引起炎症因子释放、胶原增生，易引起术后增殖膜再形成，导致二次手术风险增加。在玻璃体切割手术过程中，当视网膜破裂甚至缺损的时候，Müller细胞的过度修复在术后增殖瘢痕的形成中起到显著作用。
（陈若瑜 王子诚 张良）
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