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Catarina Oliveira Catarina Marques Vânia Simões Leina Spencer Rita Poeira Margarida Casteleira 《Brazilian Journal of Anesthesiology》2019,69(2):218-221
Background and objectives
Sugamadex is a modified gamma‐cyclodextrin, the first selective agent for reversal of neuromuscular blockade induced by steroidal non‐depolarizing muscle relaxants, with greater affinity for rocuronium. In this article we present a case of severe bradycardia and asystole following sugammadex administration.Case report
A 54‐year‐old male patient, ASA II, with a history of hypertension, dyslipidemia and obesity, who underwent an emergency umbilical herniorrhaphy under balanced general anesthesia. Intraoperative muscle relaxation was maintained with rocuronium. At the end of the surgery, the patient maintained a neuromuscular block with two TOF responses, and sugammadex (200 mg) was administered. About thirty seconds after its administration, the patient developed marked bradycardia (HR 30 bpm) followed by asystole.Conclusions
Documented bradycardia and asystole were attributed to the administration of sugammadex. This case shows that, although rare, cardiac arrest is a possible adverse effect of this drug, and that the knowledge of this situation can be determinant for the patient's evolution. 相似文献943.
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Emmanuelle Ranza Anne Guimier Alain Verloes Yline Capri Charles Marques Martine Auclair Michèle Mathieu-Dramard Gilles Morin Julien Thevenon Laurence Faivre Christel Thauvin-Robinet A. Micheil Innes David A. Dyment Corinne Vigouroux Jeanne Amiel 《Clinical genetics》2020,98(1):10-18
Overlapping syndromes such as Noonan, Cardio-Facio-Cutaneous, Noonan syndrome (NS) with multiple lentigines and Costello syndromes are genetically heterogeneous conditions sharing a dysregulation of the RAS/mitogen-activated protein kinase (MAPK) pathway and are known collectively as the RASopathies. PTPN11 was the first disease-causing gene identified in NS and remains the more prevalent. We report seven patients from three families presenting heterozygous missense variants in PTPN11 probably responsible for a disease phenotype distinct from the classical Noonan syndrome. The clinical presentation and common features of these seven cases overlap with the SHORT syndrome. The latter is the consequence of PI3K/AKT signaling deregulation with the predominant disease-causing gene being PIK3R1. Our data suggest that the phenotypic spectrum associated with pathogenic variants of PTPN11 could be wider than previously described, and this could be due to the dual activity of SHP2 (ie, PTPN11 gene product) on the RAS/MAPK and PI3K/AKT signaling. 相似文献
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Familial thrombotic risk based on the genetic background of Protein C Deficiency in a Portuguese Study
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