Rocuronium anaphylaxis in a 7-year-old boy during the induction of anesthesia.

We report a case of rocuronium-induced anaphylaxis in a previously healthy 7-year-old boy. The first presenting sign of anaphylaxis was bronchospasm, appearing 11 min after he received intravenous doses of rocuronium (1 mg/kg) (Eslax®, MSD Co. Ltd., Tokyo, Japan), propofol (2 mg/kg), and cefazolin sodium (25 mg/kg). After the administration of adrenalin and ephedrine hydrochloride, bronchospasm resolved, and the vital signs became stable. Percutaneous pinning of his left humeral supracondylar fracture was performed without problems. The next day, he was successfully liberated from the ventilator support and discharged on the fifth hospital day. On the 76th postoperative day, we performed intradermal tests of rocuronium, propofol, and cefazolin. It showed that diluted rocuronium alone induced 14 mm of flare and 8 mm of wheal within 5 min, both of which disappeared within 15 min after the intradermal injection. The reaction was too quick to mention the possible contribution of rocuronium-specific IgE. His rapid reaction at the rocuronium skin test and anaphylactic reaction upon the first exposure to this drug may highlight the association of rocuronium anaphylaxis with IgE independent mast cell stimulation through mas-related G-protein coupled receptor X2 (MRGPRX2 receptor).

A randomized prospective study on the use of 2 g-IVIG or 1 g-IVIG as therapy for Kawasaki disease.

A single, 2 g/kg dose of immune globulin (IG), denoted 2 g-intravenous (IV)IG, has become a standard regimen for treating Kawasaki disease (KD) because of its highly preventive effect on coronary arterial lesions (CAL). However, IG is obtained from blood specimens, a drawback to many patients, and is also very expensive. This randomized prospective study reported here was carried out with the aim of developing a treatment regimen that would reduce the total dose of IG. The study tested two protocols (A: 2 g-IVIG; B: 1 g-IVIG) that included the strategy of administering additional IVIG to IVIG-resistant patients based on the criteria we described previously. In protocol A, an additional 2 g-IVIG was administered only once; in protocol B, the first additional IVIG was 1 g-IVIG and the second was 2 g-IVIG. One hundred and nine patients who were admitted before the seventh day of illness and had no CAL at the time of admission were enrolled in the study (protocol A: 54 patients; B: 55 patients). In the protocol A group, 7.4% (4/54) of the patients received 4 g/kg IG. In protocol B, 41.8% (23/55) were treated only with 1 g/kg IG, and 10.9% (6/55) received 4 g/kg IG. No significant differences were observed between the patients of the two subgroups receiving 4 g/kg IG in each protocol group. Discriminate analysis also suggested that 52.4% of the patients in the protocol A group could be treated only with 1 g/kg IG. On the other hand, no significant difference was observed in the incidence of aneurysms between patients in the protocol A group (1/54) and those in the protocol B group (4/55). Our protocol based on 1 g-IVIG, including additional IVIG, was assessed to be an effective treatment and to provide a considerably useful means to reduce the total dose of IG.