Ophthalmic surgery may have the potential to temporarily induce or worsen dry eye conditions such as photorefractive keratectomy and laser-assisted in situ keratomileusis (LASIK), in especial during the short postoperative stage. 20,21 Furthermore, cataract surgery has been shown the same effects on dry eye symptoms, with dry eye being one of the most frequent complaints in the postoperative period.5 The multifactorial aetiology of dry eye is still not fully understood.22 Patients with DED experienced the stimulation of cataract surgery can increased the severity of the disease. In the past, academe’s study of postoperative dry eye focuses on changes of ocular symptoms and signs, such as OSDI questionnaire, TBUT, TMH, corneal fluorescein staining, Schirmer test and so on. Combined, these series are commonly used for the assessment the degrees of severity. When the inconsistent symptoms and signs, these methods provide poor direct information on ocular surface status. It is widely known that whether DED or cataract surgery would damage corneal nerve by ICVM examination. Moreover, both can increase corneal aberration by Pentacam. To assess the ocular surface status more comprehensively, our study presents a continuous and comprehensive evaluation system for dry eye of perioperative cataract period by combing the locatable IVCM, Pentacam and Oculus.
Choi et al.23 showed the TBUT were not notably altered during the perioperative periods after cataract operation. Consistent with this report, we also found these results. While some studied shown a reduced TBUT only during the early postoperative phase.24,25 Others reported TBUT decreased at 1 month or 3 months postoperatively.2,26 These divergences could be partly attributed to the differences of measurements. Keratograph was used, which permits an automated, hypersensitivity, and examiner independent technique for measuring TBUT. TBUT as measured using the Keratograph was consistently lesser than the subjective observer recordings since it can record the first incident of break-up anywhere in the tear film.27 Or the different target population in each study, we only enrolled DED patients, others enrolled patients with or without DE syndromes. Meibography scores had deteriorated dramatically in one month after the operation. One study said that Meibomian gland function may be altered without accompanying structural changes after cataract surgery.26 Our results suggested possible transient structural changes related to cataract surgery or medication which aggravated symptoms of ocular surface discomfort. We assessed the lower tear meniscus using Oculus which has shown high repeatability.28 And yet TMH shown significantly increased at 1 month. We compared each dry eye symptom of OSDI questionnaire, because it was hard to distinguish the reasons for changes of blurred vision. Apart from the painful eyes that aggravated at 1 month compared to pre-op, the sensitivity to light, foreign body sensation and blurred vision were not significantly changed. The results mean painful eyes may the primary manifestation of postoperative dry eye aggravation. That could be explanation for why TMH increased at 1 month, owing to irritant tear secretion.
Previous studies showed that the injured nerves degenerate after cataract surgery resulting in reduced sub-basal nerve density and reflectivity and increased beading.3,6 They usually measure the central cornea by IVCM, but due to less observed range and on positioning function. These result in each measurement was conducted in different position, increased variability, poor reproducibility, and decreased comparability. Corneal vortex is a recently recognized peculiar structure which is universally present in population.8 Moreover, it is easy to recognize and has relatively fixed site that located in approximately 1 to 2 mm inferior or nasal to the corneal apex.29 Dipika et al. suggested that the mean sub-basal nerve density was greatest centrally.30 For assessment in corneal nerve at different locations, we measured separately corneal vortex and periphery before and after cataract. It turned out that corneal vortical nerve average density and maximum length significantly reduced until 3 months or longer. However, the damage around the corneal periphery only until 1 month. The corneal density and length have not yet returned to preoperative status at the last phase. Consistent with early studies, corneal central and temporal incised sub-basal nerve density is reduced one month after cataract surgery in patients.3,6 These changes are due to temporal clear cornea incision to a small extent, as it also happened in corneal center. Our research also certainly confirmed this conjecture. However, we tested the corneal vortex which is more fixed and corneal periphery that apart from the temporal surgical incision. We ruled out the effect of corneal incision and found there had other factors affecting corneal nerve. Some people consider it is due to ultrasonic energy damage, ocular medicated toxicity or others that relating to surgery. Interestingly, the damage of peripheral corneal nerve lasted only 1 mouth, but central corneal damage until 3 months or more. It seems to have other factors that continue to harm corneal vortex. Yet there had no relevant research which concerning corneal vortical nerve after cataract surgery or of dry eye. Then, referring the studies about corneal center, we would hazard a guess that the persistent injury of corneal vortical nerve is due to lasting dry eye condition-in others word the inflammation.31 We will explain it in combination with the changes of corneal aberration.
Patients with dry eye have greater corneal aberration that usually due to instability of tear film.32 Based on our previous studies,33 DED patients had increased corneal intrinsic aberrations except for the aberration caused by tear film. Pentacam was used to measure corneal intrinsic aberrations. Our research found that the anterior, posterior and total corneal surface higher-order aberrations increased one month after operation. There was no difference in corneal intrinsic aberrations after operation and before operation except from the posterior HOAs that postoperative increased between three months. They believed that corneal aberrations may be related to postoperative ocular surface condition such as dry-eye symptoms. Significant changes in the anterior, posterior and total HOAs over the 4.0 mm zone at 1-month. He et al. reported changes can only be found in the 6mm area. In part that’s because we recruited DED patients who themselves with larger corneal aberration and imbalance of ocular surface homeostasis. Current strategy on dry eye treatment is also mainly based on eliminating exacerbating factors, inhibiting inflammation and restoring homeostasis.34 It is indisputable that cataract surgery is a harsh blow to ocular surface homeostasis, especially to patients with dry eyes before operation who were already imbalance. Thus, the aberrations of dry eye patients after cataract surgery are greater and we detected significant aberration changes over the 4.0 mm zone at 1-month. One study said that persistent DE symptoms after cataract surgery were associated with a high OSDI score at baseline, low TBUT, low digital pressure score, and extended MG dropout at 1 month postoperative.23 Undeniably, the surgical incision, intraoperative flushing, and application of eyedrops may have short-term implications for corneal HOAs.35 Our study also found the long-term changes of the posterior surface corneal HOAs after cataract surgery and agrees with findings in previous studies and attributed to corneal inflammation ,corneal edema, keratic precipitates, the incision, endothelial damage, or localized Descemet membrane detachment can affect the posterior surface more than anterior surface.35,36 There were no significant differences in anterior and total aberration between three months after operation and before operation. Some of these changes can be attributed to postoperative corneal remodeling. Incision remodeling continues slowly for months to years after surgery, a process that is thought to be associated with collagen deposits on the posterior endothelial surface of the incision.37 Late posterior wound retraction can last up to 15 years, what maybe implied long-term incision remodeling. The clinical effect of posterior wound retraction may induce changes in anterior and posterior corneal curvatures and thereby alter corneal power and astigmatism.38 Cataract surgery can damage corneal epithelium and epithelial thickness is associated with local irregularities of corneal topography that contribute to the optical power of the cornea.39Furthermore, significant changes in epithelial thickness have been correlated with corneal instability.40 It was found that epithelial thickness increased 1 day postoperatively and decreased after 1 week. Then it returned to the pre-operative levels at 1-month and remained stable until at 3-months by using spectral-domain OCT measurement. These findings might clinically affect visual function.41 When the cornea is damaged, wound healing primarily progresses toward reestablishing the continuity of the corneal epithelium, followed by remodeling of the stromal tissue via activated keratocytes.42 Although the operation led to exacerbating of dry eye, changing of corneal regularity and then increasing of corneal intrinsic aberration, epithelial or stromal remodeling might restore corneal regularity to preoperative level. While there is no remission of dry eye. Inflammation might be the possible internal reason for epithelial changes. A previous study showed significant Langerhans cell infiltration was seen at 3 days and 5 days after cataract surgery. Langerhans cell infiltration contributed to deranged epithelial renewal and the thinning of the corneal epithelium.43 Inevitably, the infiltration of inflammatory cells will aggravate dry eye. Thus, surgical incision leads to direct injury and indirect injury of inflammation.
In our study, we found the corneal vortical nerve average density and maximum length were negatively correlated anterior corneal aberrations including total aberrations, LOAs and HOAs. As we all known the density of the corneal sub-basal nerve tends to reduce in DED.44,45 We wonder if the changes of corneal nerve will lead to increasing corneal aberrations in DED. Our previous studies have verified this hypothesis and considered it has a certain impact. Only the corneal vortical nerve maximum length had negative correlation with correlated anterior corneal aberrations one month after the operation. However, these correlations disappeared 3 months after operation. The corneal vortical nerve average density and maximum length were positive correlatively with posterior corneal surface aberration 3 months after operation. One cause may be the loss of corneal endothelium. Other corneal anterior aberrations changes disappeared due to corneal remodeling. Moreover, preoperative and postoperative changes and correlation mostly found in corneal vortex which proved to be unique site relating to dry eye.
Our study has some limitations. The total corneal aberrations, corneal nerve length, corneal vortical and peripheral nerve density and length were analysed. However, each aberration, corneal nerve width, branch number, nerve tortuosity required further analysis. The basis of corneal remodeling is also needed, such as anterior-segment optical coherence tomography.