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BackgroundIn-hospital cardiac arrest (IHCA) is a critical medical event with outcomes less researched compared to out-of-hospital cardiac arrest. This retrospective observational study aimed to investigate key aspects of IHCA epidemiology and prognosis in patients with Code Blue activation.MethodsThis retrospective observational study enrolled patients with Code Blue events in our hospital between January 2010 and October 2019. Participant characteristics, including age and sex, and IHCA characteristics, including the time of cardiac arrest, witnessed event, bystander cardiopulmonary resuscitation (CPR), initial shockable rhythm, vital signs at 1 and 6 h before IHCA, survival to hospital discharge (SHD), and the cardiac arrest survival postresuscitation in-hospital (CASPRI) score were included in univariate and multivariate logistic regression analyses with SHD as the primary endpoint.ResultsFrom the 293 Code Blue events that were activated during the study period, 81 participants were enrolled. Overall, the SHD rate was 28.4%, the median CPR duration was 14 (interquartile range, 6–28) min, and the rate of initial shockable rhythm was 19.8%. There were significant intergroup differences between the SHD and non-SHD groups in the CPR duration, shockable rhythm, and CASPRI score on univariate logistic regression analysis. Multivariate logistic regression analysis showed that the CASPRI score was the most accurate predictive factor for SHD (OR = 0.98, p = 0.006).ConclusionsThe CASPRI score is associated with SHD in patients with IHCA during Code Blue events. Therefore, the CASPRI score of IHCA patients potentially constitutes a simple, useful adjunctive tool for the management of post-cardiac arrest syndrome.

BackgroundThyroid storm (TS) is a fatal disease that leads to multiple organ failure and requires prompt diagnosis. Diabetic ketoacidosis (DKA) is a trigger for thyroid crisis. However, TS and DKA rarely occur simultaneously. Moreover, owing to the rarity of the co-occurrence, the clinical course remains unclear. In this study, we present a case of TS that developed during the follow-up for repeated DKA in a young patient.Case PresentationA 25-year-old man with a history of recurrent DKA was brought to the emergency room frequently with similar symptoms. DKA treatment was initiated, but his tachycardia and disturbance of consciousness did not improve. Further examination of the patient revealed a Burch–Wartofsky Point Scale score of 80 points, consistent with the Japan Thyroid Association criteria. Therefore, DKA coexisting with TS was diagnosed. Antithyroid medication, inorganic iodine, and corticosteroids were then started as treatment for TS, and β-blockers were administered to manage tachycardia. With these treatments, the patient’s health improved and he recovered.ConclusionsIn severe cases of recurrent DKA, the presence of TS should be considered, and early treatment should be initiated before the patient’s condition worsens.

Severe muscle weakness concomitant with preferential depletion of myosin has been observed in several pathological conditions. Here, we used the steroid-denervation (S-D) rat model, which shows dramatic decrease in myosin content and force production, to test whether electrical stimulation (ES) treatment can prevent these deleterious changes. S-D was induced by cutting the sciatic nerve and subsequent daily injection of dexamethasone for 7 days. For ES treatment, plantarflexor muscles were electrically stimulated to produce four sets of five isometric contractions each day. Plantarflexor in situ isometric torque, muscle weight, skinned muscle fiber force, and protein and mRNA expression were measured after the intervention period. ES treatment partly prevented the S-D-induced decreases in plantarflexor in situ isometric torque and muscle weight. ES treatment fully prevented S-D-induced decreases in skinned fiber force and ratio of myosin heavy chain (MyHC) to actin, as well as increases in the reactive oxygen/nitrogen species-generating enzymes NADPH oxidase (NOX) 2 and 4, phosphorylation of p38 MAPK, mRNA expression of the muscle-specific ubiquitin ligases muscle ring finger-1 (MuRF-1) and atrogin-1, and autolyzed active calpain-1. Thus, ES treatment is an effective way to prevent muscle impairments associated with loss of myosin.