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PURPOSE To demonstrate the technique and report the results of endoscopic-assisted lateral orbitotomy for 6 patients with huge intraorbital dermoid cyst causing orbital roof bone erosion and dural invasion. METHODS Patients had unilateral cystic tumor with proptosis and hypoglobus for more than 6 months. There was no compressive optic neuropathy. Lateral orbitotomy procedure was performed from 2004 to 2016 by 1 surgeon. Cysts were dissected, and fluid content was aspirated to reduce the size. Selleckchem Onametostat Solid contents were then suctioned, its cavity was repeatedly irrigated, and orbital part of epithelial lining was removed. The remained epithelial lining and keratinized content at the orbital roof (abutting the dura) were removed using the rigid endoscope lenses (4 mm, 0° and 30°) and curettage. Orbital tissue was pulled away from the roof (inferior) by an assistant surgeon to make a space for introducing the lens and curette. The surgical field was frequently irrigated. No orbital drain was used, and all the patients were discharged on the same day after 8-10 hours of observation. Skin sutures were removed 1 week later. RESULTS They were 4 men and 2 women with age range of 19-48 years. A large superolateral orbital tumor with roof erosion and dural invasion was observed on imaging. Procedures were performed uneventfully. Dermoid was the pathological diagnosis. While one patient lost to follow up after 1 week, others had 6-18 months follow-up time with no recurrence. CONCLUSIONS Endoscopic-assisted lateral orbitotomy approach provided a good field of view, illumination, and magnification to totally remove all the content and epithelial lining of very large orbital roof dermoid cysts with dural invasion.INTRODUCTION Correction of lower eyelid retraction commonly involves one or more techniques, including recession of the eyelid retractors, spacer grafts, horizontal lid tightening, and midface lifting. However, patients presenting with cicatricial lower lid retraction following prior eyelid surgery often have scarring and concomitant ectropion or entropion that cause unpredictable wound healing, recicatrization, and suboptimal outcomes. The modified Hughes tarsoconjunctival flap is typically used to repair full-thickness eyelid defects. Prior reports describe treating refractory lower lid retraction with a modified Hughes flap placed beneath the tarsus after full-thickness blepharotomy. We present our experience with a novel surgical technique for treating refractory cicatricial lower lid retraction using a modified Hughes flap above the tarsus after excision of the scarred lid margin. METHODS Three patients were treated using this technique. The upper edge of the lower eyelid and associated scar tissue are excised. A modified Hughes flap is mobilized and secured above the posterior lamellar remnant. A full-thickness skin graft is placed over the flap. The flap is divided 4-5 weeks later. RESULTS This surgical technique was employed in all 3 cases. All cases were revisional, with 2 having extensive multioperative histories with multiple unsuccessful reconstructions and lid retraction repairs. All patients had improvement in cicatricial eyelid retraction, lagophthalmos, exposure keratopathy, and resolution of concomitant cicatricial ectropion. CONCLUSIONS The technique of using a modified Hughes flap to reconstruct above the tarsus with excision of the scarred lid margin was effective in correcting refractory cicatricial lower lid retraction. This procedure can be considered in multioperative cases in which traditional techniques for lower lid retraction repair have failed. Reconstructing a new lid margin reduces the risk of recicatrization and suboptimal results.Coronavirus disease 2019 has spread around the world. In the 3 months since its emergence, we have learned a great deal about its clinical management and its relevance to the pediatric critical care provider. In this article, we review the available literature and provide valuable insight into the clinical management of this disease, as well as information on preparedness activities that every PICU should perform.Anakinra is a recombinant human interleukin 1 receptor antagonist that competes and blocks the biologic effects of interleukin 1, reducing systemic inflammatory responses. In the 2015 guidelines for the diagnosis and management of pericardial diseases of the European Society of Cardiology, anakinra was established as a third-line therapy option for refractory recurrent pericarditis. Recently, important studies that investigates the effect and safety of anakinra in recurrent pericarditis were published, such as the AIRTRIP trial and the International Registry of Anakinra for Pericarditis. This article presents the current evidence about the effectiveness and safety of anakinra in recurrent pericarditis and discusses its clinical application and mechanisms.Previous studies have demonstrated that nicotine can induce relaxation of the middle cerebral artery (MCA). However, whether this relaxation is associated with the activity of sensory calcitonin gene-related peptide (CGRP) nerves, and whether this is modulated by H facilitating the release of CGRP from sensory CGRPergic nerve terminals in the MCA remains unclear. In this study, we examined the role of H in the modulation of neurogenic vasomotor responses in rat-isolated endothelium-denuded MCA. Wire-myography was used to measure vasoreactivity, and indicated that nicotine-induced relaxation was sensitive to tetrodotoxin and lidocaine, and drastically reduced levels of guanethidine (an adrenergic neuronal blocker), N-nitro-L-arginine (L-NNA), CGRP8-37, vasoactive intestinal polypeptide (VIP)6-28, capsaicin, capsazepine (a transient receptor potential vanilloid-1 inhibitor) and tetraethylammonium. However, this nicotine-induced relaxation was not sensitive to propranolol. Lowering the pH of buffer solution with HCl caused pH-dependent vasorelaxation and deceased intracellular pH in the MCA rings, which was sensitive to L-NNA, CGRP8-37, VIP6-28, capsazepine, 4-aminopyridine (a voltage-gated potassium channel antagonist), and paxilline (a large conductance Ca-activated K channels antagonist). However, HCl-induced relaxation was not inhibited by glibenclamide (an ATP-sensitive K channel blocker). These results suggested that electrical and chemical activation of cerebral perivascular adrenergic nerves led to the release H which then facilitated the release of NO, VIP and CGRP, resulting in vasorelaxation. Lowering the pH of buffer solution caused potassium channels of vascular smooth muscle cells and perivascular nerves to open. In conclusion, our results demonstrated that H may act as a modulator on MCA perivascular nerves and/or smooth muscles.
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