Characteristics of surgically induced astigmatism after standardized microincisional cataract surgery with a superior limbal incision.

PURPOSE: To determine (1) if measurements of surgically induced astigmatism (SIA) as measured by keratometry (K) and total keratometry (TK) differ (2) if SIA affects the magnitude and/or meridian of keratometric astigmatism (3) if SIA evolves over time. SETTING: Tertiary care center. DESIGN: Retrospective data analysis. METHODS: A swept-source optical coherence tomography biometry dataset (IOLMaster700) consisting of 498 eyes (327 patients) from a tertiary care center was analyzed. For all eyes preoperative and postoperative biometric measurements at 1-month, 3-month, and 6-months postoperative visits were considered for vector analysis of SIA K and SIA TK . RESULTS: Centroids in right and left eyes were 0.26 diopters (D) @5 degrees/0.31 D @1 degree for SIA K and 0.27 D @4 degrees/0.34 D @1 degree for SIA TK . Centroids for difference vectors K-TK in right and left eyes were 0.02 D @ 176 degrees/0.03 D @6 degrees. The mean SIA magnitudes in right and left eyes were 0.48 ± 0.41 D and 0.50 ± 0.37 D for SIA K and 0.53 ± 0.42 D and 0.54 ± 0.40 D for SIA TK . In eyes with ATR astigmatism, an increase in postoperative astigmatism magnitude was more common than a decrease. More than 30% of eyes showed changes in the meridian of more than 15 degrees. CONCLUSIONS: Overall, we observed differences in K- and TK-derived SIA, and changes in SIA magnitude over time. For postsurgical interventions, postoperative astigmatism meridian values should be measured to base treatments. Astigmatism magnitude showed a tendency to decrease for steep-meridian incisions and to increase in flat-meridian incisions.

Late onset of a persistent, deep stromal and endothelial scarring after corneal collagen crosslinking for keratoconus: A case report.

INTRODUCTION: To report a late onset, deep stromal and endothelial corneal scar in a keratoconus patient after corneal collagen cross-linking (CXL). CASE DESCRIPTION: Observational case report. A 29-year-old man with bilateral keratoconus received an accelerated (A-CXL 10*9) epithelium-off CXL procedure in the left eye.6-months postoperatively, a 2.2 × 1.2 mm inferocentral corneal scar was detected, which was located in the posterior stroma ranging from approximately 350 µm until the endothelium, therefore was situated below the demarcation line. A topical corticosteroid treatment did not influence the magnitude or configuration of the scar. Visual acuity was never affected, which includes the examination 12 months postoperatively. CONCLUSIONS: We report a case of a late onset deep stromal and endothelial corneal scar 6 months after accelerated CXL as postoperative complication without affecting visual acuity.

Biomechanical Response After Corneal Cross-linking With Riboflavin Dissolved in Dextran Solution Versus Hydroxypropyl Methylcellulose.

PURPOSE: To evaluate corneal stiffening in porcine eyes induced by corneal cross-linking (CXL) using riboflavin dissolved in either aqueous dextran or hydroxypropyl methylcellulose (HPMC) solution. METHODS: Fifty-one porcine corneas were divided into three groups of 17 each. After deepithelialization, the first (Dresden) group was treated for 30 minutes with 0.1% riboflavin (riboflavin-5-monophosphate in 0.9% NaCl) dissolved in hypertonic 20% dextran and the second (HPMC) group for 30 minutes with isotonic solution containing 0.1% riboflavin and 1.1% HPMC. Thereafter, corneas of both groups were irradiated using 5.4 J/cm2 (irradiance of 9 mW/cm2 for 10 minutes; 10*9). After CXL, all corneas were kept in an isotonic 16% dextran bath for 2 hours to obtain an equal hydration state. The third group served as the control group. Stress-strain measurements were performed on 5-mm-wide strips. Corneal thickness was monitored throughout the entire course of the experiments. RESULTS: The required stress for a 10% strain was increased by 83% in the Dresden group and 35% in the HPMC group compared to the control group. Resultant Young's modulus (at 10% strain) was 2.53 ± 0.73, 1.87 ± 0.50, and 1.47 ± 0.44 Pa for the Dresden, HPMC, and control groups, respectively. The differences between the Dresden and HPMC groups (P = .006), the Dresden and control groups (P < .001), and the HPMC and control groups (P = .014) were statistically significant. Pachymetry measurements showed a significantly increased corneal thickness after application of HPMC compared with the Dresden group (P = .002) and control group (P = .041). CONCLUSIONS: The biomechanical stiffening of the cornea by CXL can be achieved using dextran- and HPMC-based riboflavin solutions in porcine corneas with an application time of 30 minutes. Dextran-based riboflavin solutions seem to induce a slightly stronger biomechanical response in this setting. HPMC solutions induce less thinning than dextran solutions. [J Refract Surg. 2021;37(9):631-635.].

Interleukin-33 Promotes Recruitment of Microglia/Macrophages in Response to Traumatic Brain Injury.

Traumatic brain injury (TBI) is a devastating condition, often leading to life-long consequences for patients. Even though modern neurointensive care has improved functional and cognitive outcomes, efficient pharmacological therapies are still lacking. Targeting peripherally derived, or resident inflammatory, cells that are rapid responders to brain injury is promising, but complex, given that the contribution of inflammation to exacerbation versus improved recovery varies with time post-injury. The injury-induced inflammatory response is triggered by release of alarmins, and in the present study we asked whether interleukin-33 (IL-33), an injury-associated nuclear alarmin, is involved in TBI. Here, we used samples from human TBI microdialysate, tissue sections from human TBI, and mouse models of central nervous system injury and found that expression of IL-33 in the brain was elevated from nondetectable levels, reaching a maximum after 72 h in both human samples and mouse models. Astrocytes and oligodendrocytes were the main producers of IL-33. Post-TBI, brains of mice deficient in the IL-33 receptor, ST2, contained fewer microglia/macrophages in the injured region than wild-type mice and had an altered cytokine/chemokine profile in response to injury. These observations indicate that IL-33 plays a role in neuroinflammation with microglia/macrophages being cellular targets for this interleukin post-TBI.

Mast cell mediators cause early allergic bronchoconstriction in guinea-pigs in vivo: a model of relevance to asthma.

One feature of allergic asthma, the EAR (early allergic reaction), is not present in the commonly used mouse models. We therefore investigated the mediators involved in EAR in a guinea-pig in vivo model of allergic airway inflammation. Animals were sensitized using a single OVA (ovalbumin)/alum injection and challenged with aerosolized OVA on day 14. On day 15, airway resistance was assessed after challenge with OVA or MCh (methacholine) using the forced oscillation technique, and lung tissue was prepared for histology. The contribution of mast cell mediators was investigated using inhibitors of the main mast cell mediators [histamine (pyrilamine) and CysLTs (cysteinyl-leukotrienes) (montelukast) and prostanoids (indomethacin)]. OVA-sensitized and challenged animals demonstrated AHR (airway hyper-responsiveness) to MCh, and lung tissue eosinophilic inflammation. Antigen challenge induced a strong EAR in the sensitized animals. Treatment with a single compound, or indomethacin together with pyrilamine or montelukast, did not reduce the antigen-induced airway resistance. In contrast, dual treatment with pyrilamine together with montelukast, or triple inhibitor treatment, attenuated approximately 70% of the EAR. We conclude that, as in humans, the guinea-pig allergic inflammation model exhibits both EAR and AHR, supporting its suitability for in vivo identification of mast cell mediators that contribute to the development of asthma. Moreover, the known mast cell mediators histamine and leukotrienes were major contributors of the EAR. The data also lend further support to the concept that combination therapy with selective inhibitors of key mediators could improve asthma management.