Use Of Protocol And Evaluation Of Postoperative Residual Curarization Incidence In The Absence Of Intraoperative Acceleromyography - Randomized Clinical Trial

Objective: Evaluate the incidence of PORC in the post-anesthesia care unit (PACU) after the use of protocol and absence of intraoperative acceleromyography (AMG). Methods: Randomized clinical trial with 122 patients divided into two groups (protocol and control). Protocol group received initial and additional doses of rocuronium (0.6. mg/kg and 10. mg, respectively); the use of rocuronium was avoided in the final 45. minutes; blockade reversal with neostigmine (50. μg/kg); time ≥ 15. minutes between reversion and extubation. Control: initial and additional doses of rocuronium, blockade reversal, neostigmine dose, and extubation time, all at the discretion of the anesthetist. AMG was used in the PACU and PORC considered at T4/T1 ratio. <. 1.0. Results: The incidence of PORC was lower in protocol group than in control group (25% vs. 45.2%, p = 0.02). In control group, total dose of rocuronium was higher in patients with PORC than without PORC (0.43 vs. 0.35. mg/kg/h, p = 0.03) and the time interval between the last administration of rocuronium and neostigmine was lower (75.0 vs. 101.0. min, p <. 0.01). In protocol group, there was no difference regarding the analyzed parameters (with PORC vs. without PORC). Considering the entire study population and the presence or absence of PORC, total dose of rocuronium was higher in patients with PORC (0.42 vs. 0.31. mg/kg/h, p = 0.01), while the time interval between the last administration of rocuronium and neostigmine was lower (72.5 vs. 99.0. min, p ≤ 0.01). Conclusion: The proposed systematization reduced PORC incidence in PACU in the absence of intraoperative AMG. © 2017

Lipoid Proteinosis And Otolaryngology [lipoproteinoses E Otorrinolaringologia]

Lipoproteinosis is an autossomal recessive disease characterized by the deposition of diffuse hyaline material in skin, mucous membranes, blood vessels and other organs. It is caused by mutations in a gene encoding a glycoprotein of the extracellular matrix (ECM1), and different mutations may lead to the distinct epithelial changes. The disease has a chronic and benign course, and the main changes observed are: skin lesions of early presentation and varied aspects, blepharosis, intracranial calcifications with neuropsychiatric manifestations, symptoms of heartburn and fullness associated with nodules around gastrointestinal tract. The main otorhinolaryngological manifestation is dysphonia, which usually begins early in life, may present irregularities on the surface of the vocal cords and thickening of the interarytenoid region. The diagnosis is made by clinic associated with the classic findings of biopsy or by mapping the gene ECM1. Treatment is directed to the signs and symptoms of the affected organs, and the main impact of the disease is in the quality of life for its esthetic and functional damage. This article proposes a review of the literature, based on detailed description of four clinical cases, focusing on otorhinolaryngological manifestations.708/SetDi, G.S., Masi, R., Cassandrini, D., Lipoid proteinosis: Case report and review of the literature (2006) Acta Otorhinolaryngol Ital, 26 (3), pp. 162-167Acar, A., Eryilmaz, A., Gocer, C., Akmansu, H., Lipoid proteinosis of larynx: Review of four cases (2004) Int J Pediatr Otorhinolaryngol, 68 (12), pp. 1557-1561Toosi, S., Ehsani, A.H., Treatment of lipoid proteinosis with acitretin: A case report (2009) Journal of European Academy of Dermatology and Venereology, 23, pp. 482-483Duke-Elder, S., MacFaul, P.A., Lipoid proteinosis (1974) The Ocular Adnexa. System of Ophthalmology, 13, pp. 310-314. , Duke-Elder S (ed), Henry Kimpton, LondonFonseca, E.C., Fendi, L.I., Andretta, P.S., Síndrome de urbach-wiethe: Relato de caso (2007) Arq Bras Oftalmol, 70 (4), pp. 689-692Blodi, F.C., Whinery, R.D., Hendricks, C.A., Lipoid-proteinosis (urbach-wiethe) involving the lids (1960) Trans Am Ophthalmol Soc, 58, pp. 155-166Baykal, C., Topkarci, Z., Yazganoglu, D., Lipoid proteinosis: A case series from istanbul (2007) International Journal of Dermatology, 46, pp. 1011-1016Bozdag, K.E., Gul, Y., Karaman, A., Lipoid proteinosis (2000) International Journal of Dermatology, 39, pp. 203-204Kumar, J., Ramesh, V., Beena, K.R., Clinicopathological cases: Case 1 (2002) Clinical and Experimental Dermatology, 27, pp. 531-532Chaudhary, S.J., Dayal, P.K., Hyalinosis cutis et mucosae. Review with a case report (1995) Oral Surg Oral Med Oral Pathol Oral Radiol Endod, 80, pp. 168-171Hamada, T., McKean, W.H.I., Ramsay, M., Lipoid proteinosis maps to 1q21 and is caused by mutations in the extracelular matrix protein 1 gene (ECM1) (2002) Human Molecular Genetics, 11 (7), pp. 833-840Hamada, T., Wessagowit, V., South, A.P., Extracellular matrix protein 1 gene (ECM1) mutations in lipoid proteinosis and genotype-phenotype correlation (2003) The Journal of Investigative Dermatology, 120 (3), pp. 345-350Smits, P., Ni, J., Feng, P., Wauters, J., The human extracellular matrix gene 1 (ECM1): Genomic structure, cDNA cloning, expression pattern and chromosomal localization (1997) Genomics, 45, pp. 487-495Mongiat, M., Fu, J., Oldershaw, R., Perlecan protein core interacts with extracellular matrix protein 1 (ECM1), a glycoprotein involved in bone formation and angiogenesis (2003) J Biol Chem, 278, pp. 17491-17499Horev, L., Potikha, T., Ayalon, S., A novel splice-site mutation in ECM-1 gene in a consanguineous family with lipoid proteinosis (2005) Exp Dermatol, 14, pp. 891-897Chan, I., The role of extracelular matrix protein 1 in human skin (2004) Clinical and Experimental Dermatology, 29, pp. 52-56Sercu, S., Poumay, Y., Herphelin, F., Functional redundancy of extracelular matrix protein 1 in epidermal differentiation (2007) British Journal of Dermatology, 157, pp. 771-775Dyer, J.A., Yu, Q.C., Paller, A.S., Free-floating desmosomes in lipoid proteinosis: An inherent defect in keratinocyte adhesion (2006) Pediatric Dermatology, 23 (1), pp. 1-6Fujimoto, N., Terlizzi, J., Aho, S., Extracellular matrix protein 1 inhibits the activity of matrix metalloproteinase 9 through high-affinity protein/protein interactions (2006) Exp Dermatol, 15, pp. 300-307Claeys, K.G., Claes, L.R.F., Goethem, J.W.M.V., Epilepsy and migraine in a patient with urbach-wiethe disease (2007) Seizure, 16, pp. 465-468Mirancea, N., Hausser, I., Matze, D., Junctional basement membrane anomalies of skin and mucosa in lipoid proteinosis (hyalinosis cútis et mocosae) (2007) Journal of Dermatological Science, 45, pp. 175-185Mirancea, N., Hausser, I., Beck, R., Vascular anomalies in lipoid proteinosis (hyalinosis cutis et mucosae): Basement membrane componentes and ultrastructure (2006) Journal of Dermatologinal Science, 42, pp. 231-239Hu, S., Kuo, T., Hong, H., Lipoid proteinosis: Report of a possible localized formo n both hands and wrists (2005) International Journal of Dermatology, 44, pp. 408-410Uchida, T., Hayashi, H., Inaoki, M., A failure of mucocutaneous lymphangiogenesis may underlie the clinical features of lipoid proteinosis (2007) British Journal of Dermatology, 156, pp. 152-157Kowalewski, C., Kozlowska, A., Chan, I., Three-dimensional imaging reveals major changes in skin microvasculature in lipoid proteinosis and lichen sclerosus (2005) Journal of Dermatological Science, 38, pp. 215-224Holme, S.A., Lenane, P., Krafchik, B.R., What syndrome is this? (2005) Pediatric Dermatology, 22 (3), pp. 266-267Ehsani, A.H., Ghiasi, M., Robati, R.M., Lipoid proteinosis: Report of three familial cases (2005) Dermatology Online Journal, 12 (1), p. 16Kini, S., Jain, A., Shet, T.M., Lipoid proteinosis in a 12-yea-old: A report from west India (2006) Dermatology Online Journal, 12 (1), p. 10Rao, R., Prabbu, S., Sprpathi, H., (2006) Dermatology Online Journal, 14 (7), p. 16Cole, J.A., Novosel, T.A., Willians, J.V., Pocklike scarring and sublingual papules in a child (2008) Arch Dermatol, 144 (10), pp. 1383-1388Desmet, S., Devos, S.A., Hamada, T., At, Al., Clinical and Molecular Abnormal