Transient keratectasia caused by intraocular pressure elevation after laser in situ keratomileusis.

Transient keratectasia caused by intraocular pressure elevation after laser in situ keratomileusis.
复制标题

DOI:
10.1016/j.jcrs.2004.08.046
复制
发表时间:
2005
影响因子:
2.8
通讯作者:
A. Toshino;T. Uno;Y. Ohashi;N. Maeda;T. Oshika
A. Toshino;T. Uno;Y. Ohashi;N. Maeda;T. Oshika
中科院分区:
医学2区
文献类型:
--
作者:
A. Toshino;T. Uno;Y. Ohashi;N. Maeda;T. Oshika

文献摘要

被引文献

相似文献

讨论据报道,角膜较薄、高IOP和高度近视需要更大激光消融的眼睛在LASIK后容易发生角膜前移。4在这个病例中,角膜扩张似乎可归因于IOP升高,因为IOP降低导致扩张迅速改善,并且在IOP恢复正常后并发症未复发。因为眼压是用Goldmann压平眼压计测量的,据报道该眼压计低估了角膜屈光手术后的眼压,6,7真实的眼压可能高于读数。内部压力的增加可能使角膜扩张和膨胀,角膜在结构上已经被先前的角膜屈光手术改变,导致向前移动和拉伸。对侧眼的近视矫正量相似,但术后过程顺利,未观察到医源性角膜扩张迹象,可能是因为未发生IOP升高。可能会担心IOP升高对扫描狭缝角膜地形图测量的影响。为了解决这一问题,在静脉注射甘露醇治疗IOP升高的眼睛中进行了地形测量,如所述病例中所示。患者为一名38岁女性,患有Posner-Schlossman综合征,无其他疾病或眼部手术史。甘露醇治疗使IOP从46 mm Hg降至16 mm Hg。如图2所示,甘露醇治疗前后的后角膜高度图显示差异很小,渗透剂给药前后的中央角膜厚度分别为575 mm和557 mm。在我们的病例中,LASIK术后IOP的显著升高对结构受损的角膜产生不利影响,导致一过性角膜扩张。角膜扩张是可逆的,通过治疗可以防止复发。眼内压升高可能是角膜屈光手术后医源性角膜扩张的危险因素,可能由类固醇应用引起。
DiscussionEyes with thin corneas, high IOP, and high myopia requiring greater laser ablation are reportedly predisposed to an anterior shift of the cornea after LASIK. 4 In this case, the keratectasia seemed to be attributable to the IOP elevation since reduction of the IOP resulted in prompt improvement of the ectasia and the complication did not recur after the IOP was normalized. Because the IOP was measured with the Goldmann applanation tonometer, which reportedly underestimates IOP after keratorefractive surgery, 6, 7 the true IOP was probably higher than the readings. Increases in the internal pressure may have expanded and distended the cornea, which had been structurally modified by the previous keratorefractive surgery, leading to forward movement and stretching. The contralateral eye had a similar amount of myopic correction, but the postoperative course was uneventful and no sign of iatrogenic keratectasia was seen, possibly because no IOP elevation occurred. There may be concern about the effect of IOP elevation on scanning-slit corneal topography measurements. To address this question, topographical measurements were performed in an eye that was treated with intravenous mannitol for elevated IOP, as in the case presented. The patient was a 38-year-old woman with Posner-Schlossman syndrome with no other disease or history of ocular surgery. The mannitol treatment decreased the IOP from 46 mm Hg to 16 mm Hg. As shown in Figure 2, the posterior corneal elevation maps before and after mannitol treatment showed little difference, and the central corneal thickness was 575 mm and 557 mm before and after administration of the osmotic agent, respectively. After LASIK in our case, marked elevation of the IOP adversely affected the structurally compromised cornea, leading to transient keratectasia. The keratectasia was reversible, and its recurrence was prevented by treatment. Intraocular pressure elevation, which may be caused by steroid application, can be a risk factor for iatrogenic keratectasia after keratorefractive surgery.