Postoperative Clinical Outcomes Using Standard Variables Following Levator-Mullerectomy Advancement Blepharoptosis Surgery.

ABSTRACT: The Muller muscle-conjunctival resection is a common technique used to treat blepharoptosis, but there is variability with the target surgical resection and expected postoperative outcomes measured by marginal reflex distance-1 (MRD1). A Levator-Mullerectomy is a novel surgical approach described by Morris et al to incorporate the levator palpebrae superioris in the same incision as the classic Muller muscle-conjunctival resection in the treatment of blepharoptosis. This a retrospective study of patients who underwent Levator-Mullerectomy for ptosis repair showing the clinical outcomes based on MRD1. Statistical analysis was performed using analysis of variance and a nonparametric Kruskal-Wallis test. One hundred-twelve eyes of 83 patients (29 bilateral cases) with a mean age 64.6 years (7-92 years) were included. The types and prevalence of blepharoptosis were involutional (83%), neurogenic (8.0%), traumatic (3.6%), apraxia (2.7%), and congenital (2.7%). There was no significant difference in clinical outcome based on type of blepharoptosis (P = 0.7). Target resection lengths of 8 mm, 10 mm, and 12 mm were compared with postoperative MRD1 change. The mean change in MRD 1 between 8 mm and 10 mm was found to be statistically significant (P = 0.001 for both) but was not statistically significant for the 12 mm resection (P = 0.8). In patients with blepharoptosis and a positive response to 2.5% phenylephrine can benefit from Levator-Mullerectomy with either an 8 mm or 10 mm resection. This novel surgical approach allows surgeons to produce a more predictable and consistent clinical outcome.

Dematiaceous fungal endophthalmitis: report of a case and review of the literature.

BACKGROUND: Pleurostomophora richardsiae (formerly Phialophora richardsiae) is a dematiaceous fungus that is an uncommon cause of ocular infection. Herein, we present a case of endogenous endophthalmitis associated with disseminated P. richardsiae infection. FINDINGS: This is a descriptive case report with a brief review of literature. A 43-year-old male admitted to the hospital following an acute cerebellar hemorrhage was found to have a swollen and tender wrist. The patient was afebrile with leukocytosis. Visual acuity was hand motion in the right eye and 20/20 in the left. Right eye examination noted anterior chamber cells and flare, vitreous haze and multiple large, and fluffy retinal infiltrates. Diagnostic vitrectomy revealed a mixed inflammatory cell infiltrate with numerous fungal elements. Blood cultures were negative, multiple transesophageal echocardiography studies revealed no vegetations, and synovial fluid aspiration of the wrist and biopsy of the radius were unremarkable. The patient was treated with intravitreal cefazolin, vancomycin, and amphotericin B, topical ciprofloxacin and natamycin, and intravenous amphotericin B and voriconazole. Visual acuity in the right eye declined to light perception, and examination revealed increasing anterior and posterior chamber inflammation. The patient died several weeks after presentation due to a massive intracranial hemorrhage. Fungal culture results from the vitrectomy were received post mortem and were positive for P. richardsiae. CONCLUSIONS: P. richardsiae endophthalmitis is rare, and outcomes are typically poor. Infections typically occur following traumatic skin inoculation; however, a long refractory period may occur before symptoms develop. Early diagnosis and combination antimicrobial therapy are essential to optimize visual outcomes.

Signaling via P2Y12 may be critical for early stabilization of platelet aggregates.

P2Y(12) receptor antagonism inhibits platelet aggregation by preventing adenosine diphosphate (ADP)-mediated amplification of activation pathways downstream of primary agonists, such as thrombin and collagen. However, the role of ADP signaling in maintaining aggregate stability and the effects of P2Y(12) antagonists on preestablished aggregates in vitro and arterial thrombus in vivo are not well understood. This study evaluated the impact of P2Y(12) signaling on platelet aggregate stability and early thrombotic occlusion using a reversible P2Y(12) antagonist, ticagrelor. There were 2 study objectives: (1) to determine if there was a time-dependent factor on the capacity of a P2Y(12) antagonist to affect human platelet aggregate stability in vitro using light transmission aggregometry and (2) to evaluate the extent of arterial thrombus reversal in a preclinical model upon administration of ticagrelor in vivo. Platelet aggregates were exposed to ticagrelor after ADP or collagen activation, monitored for stability by aggregometry, and visualized by microscopy. Freshly formed ADP- and collagen-induced platelet aggregates were more rapidly dispersed by a P2Y(12) antagonist than drug carrier control at clinically relevant concentrations (P < 0.05). However, stable aggregates were not noticeably affected. A murine arterial thrombosis model was used to evaluate thrombus stability in an in vivo mouse model. Thrombotic occlusion was induced by FeCl(3), followed by a bolus intravenous administration of ticagrelor or vehicle control. Doppler blood flow was monitored before injury and 30 minutes after bolus administration. Arteries were retrieved for inspection for residual thrombus. Early arterial thrombotic occlusion in vivo was partially reversed by ticagrelor administration. Blood flow through the injured artery increased, and thrombus size within the artery decreased (P < 0.05, n = 3). In conclusion, P2Y(12) antagonism disrupts the stability of newly formed platelet aggregates, promoting disaggregation, and reverses thrombotic vascular occlusion. Thus, in addition to activating platelets, signaling via P2Y(12) seems to be required for stabilizing platelet thrombi.