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圆锥角膜(一)

西医的认识:

? ? ? ? 圆锥角膜是一种双侧非炎症性角膜扩张为特征,致角膜中央部向前凸出呈圆锥形及产生高度不规则近视散光和不同视力损害的原发性角膜变性疾病。其可以是一种独立的疾病,也可以是多种综合征的组成部分。其多发生于青春期前后,也有部分发生于中老年更年期前后,不伴有炎症。晚期会出现急性角膜水肿,形成瘢痕,视力严重受损。早期无典型临床表现易漏诊,很多患者起初都是在误认为是近视导致的视物模糊去配镜验光时发现的,或因原来的镜片佩戴不合适到医院进行验光配镜时因为散光无法纠正时查出圆锥角膜的,圆锥角膜首先表现为因近视和近视散光而导致的裸眼视力下降,而且散光度数较高,并常带有不规则散光。其发病机制是角膜中央区进行性变薄、膨隆,呈圆锥状突出,到晚期会突然发生急性角膜水肿、混浊,使得视力在短期内更进一步下降。这时,就无法用RGP矫正。

中医的认识:

? ? ? ?古代中医医学书籍上记载圆锥角膜(旋胪泛起)比较少见,近年来发病却逐年增多,众多医学书籍都有记载,却无有效诊治方案。《证治准绳?杂病》指出该病是风轮高耸而起的疾病。本病与旋螺突起之翳色青白、累及瞳神不同。旋胪泛起证气轮自平。水轮自明。惟风轮泛起也。或半边泛起者。亦因半边火盛。火郁风轮。故随火胀起。非旋螺突起。已成证而顶尖俱凸。不可医治之比也。《审视瑶涵》记载:火郁风轮,则旋胪泛起;血瘀火炽,则旋胪尖生。精亏血少虚损,则起坐生花;竭视酒色思虑,则昏蒙干涩。暴盲似祟,痰火思虑并头风。赤痛如邪,肝肾亏损荣卫弱。枣花障起痰火色酒怒劳瞻。萤星满目,辛燥火痰劳酒色。眼若虫行因酒欲,悲思惊恐怒所伤,云翳移睛见旗旆,蝇蛇异形虚所致。淫欲多而邪气侵,则膜入乎水轮。

简要临床分类:

按Duke-Elder(1946)和Eapbenb(1960)的分类为: (1)前部形圆锥角膜。 (2)后部型圆锥角膜:又分为完全型和局限型(3)也可以分为早期、中期、晚期、水肿期

起病要点:

1.遗传学说 较多学者认为本病为常染色体隐性遗传。如Ammon(1830)报告6个家系均有不规律的病例。高桥报告一家同胞3人均患此病。还发现这些病例的亲代往往有近亲通婚史。但有些病例可连续2或3代出现,有时发生中断现象,提示为外显不全,这些应考虑为规律或不规律的显性遗传。常染色体显性遗传的圆锥角膜致病基因位于染色体16q22和3q23。在某些遗传性疾病如视网膜色素变性,Downs综合征、蓝色巩膜病和Marfan综合征等都可能合并圆锥角膜。 2.发育障碍学说 Collins等(1925)认为本病是角膜中央部胶原纤维坚韧性降低所致。Mihalyhegy(1954)指出,本病不仅角膜中央变薄,弯曲度增加,巩膜亦有相似改变。认为其病因与间质发育不全有关。有些病例除圆锥角膜外,尚发生晶状体脱位或视网膜脱离,亦提示与胶原组织脆弱相关。 3.内分泌紊乱学说 Siegrist(1912)、Knapp(1929)和Stitcherska(1932)均认为甲状腺功能减退与本病发生有重要关系。Hippel(1913)强调胸腺在本病发生中的重要作用。 4.代谢障碍学说 Myuhnk(1959)发现本病患者的基础代谢率明显降低。Tntapeho(1978)报告本病患者血液中锌、镍含量明显降低,钛、铅和铝的含量升高,而锰的含量正常,因此认为这些微量元素的变化对发生本病有一定的影响。Yukobckaa等(1979)报告,在本病患者的血液和房水中,6-磷酸葡萄糖脱氢酶的活性明显下降致谷胱甘肽氧化作用不全,使过氧化物过多堆积,这些过氧化物就可能是促使角膜发病的重要因子。此外患者的胶原酶活性有所提高,致胶原组织的丧失大于蛋白合成,使基质层变薄。 5.变态反应学说 圆锥角膜常与春季卡他性角结膜炎等变态反应性疾病同时发病,其特点是IgA反应降低,IgE反应增高,细胞免疫也有缺陷。Boland(1963)统计,本病患者中有32.6%患过花粉症,有33.3%患过哮喘病。Ruedeman报告本病86%的患者有过敏反应病史。 6.戴角膜接触镜可以诱发圆锥角膜 Hartstein(1968)报告4例戴角膜接触镜后发生圆锥角膜者,认为戴接触镜可能诱发此病。眼球及角膜硬度降低可能是戴接触镜后发生本病的危险因素。 7.PRK、LASIK等准分子激光角膜切除术后继发圆锥角膜。 8.慢性眼部干燥性病变及泪液缺少时会使下方角膜变陡,并产生高度角膜散光,形成继发性圆锥角膜。

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