Purpose: To assess the effect of etomidate injection on succinylcholine-induced fasciculations through a randomized controlled trial.
Methods: Intravenous succinylcholine (2 mg/kg) was administered to 100 adult patients undergoing elective vocal cord surgery, with allocation to two groups: immediate group, where succinylcholine was administered immediately, and delayed group, where succinylcholine was administered 15 sec after injection of etomidate 0.2 mg/kg. The two groups were compared in terms of the severity and duration of muscle fasciculation caused by succinylcholine and the incidence of postoperative myalgia.
Findings: The severity of fasciculations graded on a 4-point scale was considered the primary outcome. Compared with the delayed group, the immediate group exhibited substantially reduced fasciculation severity scores (P = 0.005). A lower incidence of postoperative myalgia was observed in the immediate group than in the delayed group (P = 0.031). Furthermore, in the delayed group, the heart rate after intervention decreased more significantly (P = 0.014). No differences in other adverse effects were observed.
Implications: The severity of succinylcholine-induced fasciculations and the incidence of postoperative myalgia were significantly reduced without adversely affecting intubation conditions or hemodynamics by injecting a 0.2 mg/kg dose of etomidate immediately before administering 2 mg/kg succinylcholine.
Purpose: Hereditary anemias are a cause of nonimmune hydrops fetalis (NIHF). Our objective was to review the spectrum of hereditary anemia genes in NIHF diagnosed by exome sequencing (ES).
Methods: We performed a systematic review of ES studies in NIHF from January 1, 2000 to August 1, 2024 with emphasis on genes causing fetal anemia as a primary phenotype.
Findings: Forty-one ES studies with 207 genetically diagnosed NIHF cases met our inclusion criteria; 6 cases within 6 studies involved NIHF and hereditary anemia. Among the six cases, five had definitive diagnosis or likely diagnosis supported by pathogenic or likely pathogenic variants, while one case harbored only variants of uncertain significance and was classified as a possible diagnosis. The six different hereditary anemia genes included SEC23B, SPTA1, KLF1, RPL11, UNC13D, and RFWD3.
Implications: Overall, ES confirmed the etiology of hereditary anemia in 2.4% (5/207) of genetically diagnosed NIHF cases. Hereditary anemias, therefore, represent a distinct and clinically relevant subset of ES-diagnosed NIHF cases. ES should be considered first line in fetuses with NIHF, as common non-genetic causes such as fetomaternal hemorrhage, infectious etiologies, and alloimmunization are excluded. It is also indicated when fetal anemia is suspected, particularly in the setting of elevated MCA Dopplers with a negative evaluation for common hemoglobinopathies and nongenetic etiologies.

