A booster dose can result in a similar reaction to the initial dose. Neuromuscular blocking agents (NMBAs) can produce a comparable reaction in the absence of specific pathophysiologic alterations. Case: An initial dose of rocuronium 40 mg was given to a male patient (50 years old, height 168 cm, weight 54 kg, body mass index 19.13 kg/m2 ) for anesthesia. The onset was usual, but the duration was brief. Two booster doses were administered at 20 min intervals, but recovery came quickly. So, acute tolerance was suspected. Muscle function was restored to greater than train-of-four ratio 0.75 while spontaneous aided breathing was maintained without the need of further NMBAs. Following the operation, sugammadex (1.85 mg/kg) was provided to prevent residual neuromuscular inhibition. Conclusions: Anesthetists must be able to suspect acute tolerance to NMBAs in patients with no unique medical history and have a plan to resolve it.

A booster dose can result in a similar reaction to the initial dose. Neuromuscular blocking agents (NMBAs) can produce a comparable reaction in the absence of specific pathophysiologic alterations. Case: An initial dose of rocuronium 40 mg was given to a male patient (50 years old, height 168 cm, weight 54 kg, body mass index 19.13 kg/m2 ) for anesthesia. The onset was usual, but the duration was brief. Two booster doses were administered at 20 min intervals, but recovery came quickly. So, acute tolerance was suspected. Muscle function was restored to greater than train-of-four ratio 0.75 while spontaneous aided breathing was maintained without the need of further NMBAs. Following the operation, sugammadex (1.85 mg/kg) was provided to prevent residual neuromuscular inhibition. Conclusions: Anesthetists must be able to suspect acute tolerance to NMBAs in patients with no unique medical history and have a plan to resolve it.

A booster dose can result in a similar reaction to the initial dose. Neuromuscular blocking agents (NMBAs) can produce a comparable reaction in the absence of specific pathophysiologic alterations. Case: An initial dose of rocuronium 40 mg was given to a male patient (50 years old, height 168 cm, weight 54 kg, body mass index 19.13 kg/m2 ) for anesthesia. The onset was usual, but the duration was brief. Two booster doses were administered at 20 min intervals, but recovery came quickly. So, acute tolerance was suspected. Muscle function was restored to greater than train-of-four ratio 0.75 while spontaneous aided breathing was maintained without the need of further NMBAs. Following the operation, sugammadex (1.85 mg/kg) was provided to prevent residual neuromuscular inhibition. Conclusions: Anesthetists must be able to suspect acute tolerance to NMBAs in patients with no unique medical history and have a plan to resolve it.

A booster dose can result in a similar reaction to the initial dose. Neuromuscular blocking agents (NMBAs) can produce a comparable reaction in the absence of specific pathophysiologic alterations. Case: An initial dose of rocuronium 40 mg was given to a male patient (50 years old, height 168 cm, weight 54 kg, body mass index 19.13 kg/m2 ) for anesthesia. The onset was usual, but the duration was brief. Two booster doses were administered at 20 min intervals, but recovery came quickly. So, acute tolerance was suspected. Muscle function was restored to greater than train-of-four ratio 0.75 while spontaneous aided breathing was maintained without the need of further NMBAs. Following the operation, sugammadex (1.85 mg/kg) was provided to prevent residual neuromuscular inhibition. Conclusions: Anesthetists must be able to suspect acute tolerance to NMBAs in patients with no unique medical history and have a plan to resolve it.

A booster dose can result in a similar reaction to the initial dose. Neuromuscular blocking agents (NMBAs) can produce a comparable reaction in the absence of specific pathophysiologic alterations. Case: An initial dose of rocuronium 40 mg was given to a male patient (50 years old, height 168 cm, weight 54 kg, body mass index 19.13 kg/m2 ) for anesthesia. The onset was usual, but the duration was brief. Two booster doses were administered at 20 min intervals, but recovery came quickly. So, acute tolerance was suspected. Muscle function was restored to greater than train-of-four ratio 0.75 while spontaneous aided breathing was maintained without the need of further NMBAs. Following the operation, sugammadex (1.85 mg/kg) was provided to prevent residual neuromuscular inhibition. Conclusions: Anesthetists must be able to suspect acute tolerance to NMBAs in patients with no unique medical history and have a plan to resolve it.

Dantrolene sodium (DS) was first introduced as an oral antispasmodic drug. However, in 1975, DS was demonstrated to be effective for managing malignant hyperthermia (MH) and was adopted as the primary therapeutic drug after intravenous administration. However, it is difficult to administer DS intravenously to manage MH. MH is life-threatening, pharmacogenomically related, and induced by depolarizing neuromuscular blocking agents or inhalational anesthetics. All anesthesiologists should know the pharmacology of DS. DS suppresses Ca2+ release from ryanodine receptors (RyRs). RyRs are expressed in various tissues, although their distribution differs among subtypes. The anatomical and physiological functions of RyRs have also been demonstrated as effective therapeutic drugs for cardiac arrhythmias, Alzheimer’s disease, and other RyR-related diseases. Recently, a new formulation was introduced that enhanced the hydrophilicity of the lipophilic DS. The authors summarize the pharmacological properties of DS and comment on its indications, contraindications, adverse effects, and interactions with other drugs by reviewing reference articles.

Background: Chronic glucocorticoid exposure is associated with resistance to nondepolarizing neuromuscular blocking agents. Therefore, we hypothesized that sugammadex-induced recovery would occur more rapidly in subjects exposed to chronic dexamethasone compared to those who were not exposed. This study evaluated the sugammadex-induced recovery profile after neuromuscular blockade (NMB) in rats exposed to chronic dexamethasone. Methods: Sprague–Dawley rats were allocated to three groups (dexamethasone, control, and pair-fed group) for the in vivo study. The mice received daily intraperitoneal dexamethasone injections (500 μg/kg) or 0.9% saline for 15 days. To achieve complete NMB, 3.5 mg/kg rocuronium was administered on the sixteenth day. The recovery time to a train-of-four ratio ≥ 0.9 was measured to evaluate the complete recovery following the sugammadex injection. Results: Among the groups, no significant differences were observed in the recovery time to a train-of-four ratio ≥ 0.9 following sugammadex administration (P = 0.531). The time to the second twitch of the train-of-four recovery following rocuronium administration indicated that the duration of NMB was significantly shorter in Group D than that in Groups C and P (P = 0.001). Conclusions Chronic exposure to dexamethasone did not shorten the recovery time of sugammadex-induced NMB reversal. However, the findings of this study indicated that no adjustments to sugammadex dosage or route of administration is required, even in patients undergoing long-term steroid treatment.

Background: The Omicron variant has become the most prevalent SARS-CoV-2 variant. Omicron is known to induce milder lesions compared to the original Wuhan strain. Fatal infection of the Wuhan strain into the brain has been well documented in COVID-19 mouse models and human COVID-19 cases, but apparent infections into the brain by Omicron have not been reported in human adult cases or animal models. In this study, we investigated whether Omicron could spread to the brain using K18-hACE2 mice susceptible to SARS-CoV-2 infection. Results: K18-hACE2 mice were intranasally infected with 1 × 105 PFU of the original Wuhan strain and the Omicron variant of SARS-CoV-2. A follow-up was conducted 7 days post infection. All Wuhan-infected mice showed > 20% body weight loss, defined as the lethal condition, whereas two out of five Omicron-infected mice (40%) lost > 20% body weight. Histopathological analysis based on H&E staining revealed inflammatory responses in the brains of these two Omicron-infected mice. Immunostaining analysis of viral nucleocapsid protein revealed severe infection of neuron cells in the brains of these two Omicron-infected mice. Lymphoid depletion and apoptosis were observed in the spleen of Omicron-infected mice with brain infection. Conclusion Lethal conditions, such as severe body weight loss and encephalopathy, can occur in Omicron-infected K18-hACE2 mice. Our study reports, for the first time, that Omicron can induce brain infection with lymphoid depletion in the mouse COVID-19 model.