Hemodynamic instability following intravenous dexmedetomidine infusion for sedation under brachial plexus block: Two case reports.

BACKGROUND: Dexmedetomidine (DMED) is frequently used as a sedative in several medical fields. The benefits of DMED include enhanced quality of regional anesthesia, prolonged analgesia, and postoperative opioid-sparing when administered intravenously or perineurally in combination with regional anesthesia. Severe hemodynamic complications, such as profound bradycardia and hypotension, can occur after DMED administration in critically ill patients or overdosage; however, there are few reports of complications with DMED administration following brachial plexus block (BPB). CASE SUMMARY: We present two cases of hemodynamic instability that occurred following the initial loading of DMED under supraclavicular BPB. A healthy 29-year-old man without any medical history showed profound bradycardia after receiving a loading dose of DMED 0.9 µg/kg for 9 min. DMED administration was promptly stopped, and after receiving a second dose of atropine, the heart rate recovered. A 62-year-old woman with a history of cardiomyopathy became hypotensive abruptly, requiring the administration of inotrope and vasopressors after receiving a reduced loading dose of 0.5 µg/kg for 10 min. Half of the recommended loading dose of DMED was administered due to the underlying heart dysfunction. Decreased blood pressure was maintained despite the intravenous administration of ephedrine. With continuous infusion of dopamine and norepinephrine, the vital signs were maintained within normal ranges. Inotropic and vasopressor support was required for over 6 h after the initial loading dose of DMED. CONCLUSION: DMED administration following BPB could trigger hemodynamic instability in patients with decreased cardiac function as well as in healthy individuals.

Casein Kinase 2 Alpha Inhibition Protects against Sepsis-Induced Acute Kidney Injury.

Sepsis-induced acute kidney injury (AKI) is a common complication in critically ill patients, often resulting in high rates of morbidity and mortality. Previous studies have demonstrated the effectiveness of casein kinase 2 alpha (CK2α) inhibition in ameliorating ischemia-reperfusion-induced AKI. In this study, our aim was to investigate the potential of the selective CK2α inhibitor, 4,5,6,7-tetrabromobenzotriazole (TBBt), in the context of sepsis-induced AKI. To assess this, we initially confirmed an upregulation of CK2α expression following a cecum ligation and puncture (CLP) procedure in mice. Subsequently, TBBt was administered to a group of mice prior to CLP, and their outcomes were compared to those of sham mice. The results revealed that, following CLP, the mice exhibited typical sepsis-associated patterns of AKI, characterized by reduced renal function (evidenced by elevated blood urea nitrogen and creatinine levels), renal damage, and inflammation (indicated by increased tubular injury score, pro-inflammatory cytokine levels, and apoptosis index). However, mice treated with TBBt demonstrated fewer of these changes, and their renal function and architecture remained comparable to that of the sham mice. The anti-inflammatory and anti-apoptotic properties of TBBt are believed to be associated with the inactivation of the mitogen-activated protein kinase (MAPK) and nuclear factor κB (NF-κB) signaling pathways. In conclusion, these findings suggest that inhibiting CK2α could be a promising therapeutic strategy for treating sepsis-induced AKI.

Rapid correction of severe hyponatremia and control of subsequent overcorrection in operative hysteroscopy intravascular absorption syndrome: A case report.

RATIONALE: Operative hysteroscopy intravascular absorption syndrome (OHIAS) results from systemic absorption of hypotonic solution during hysteroscopy, which may induce severe hyponatremia within hours. Depending on the serum sodium (Na+) level, this can be life-threatening and requires prompt and careful remedial treatment. PATIENT CONCERNS AND DIAGNOSES: A 53-year-old woman underwent hysteroscopic myomectomy for submucosal leiomyoma. Approximately 3 hours postoperatively, the serum Na+ level decreased to 82 mM/L, accompanied by pulmonary edema and lactic acidosis. The patient was strongly suspicious of OHIAS. INTERVENTIONS AND OUTCOMES: A rapid correction was made using 3% NaCl to prevent brain edema as an initial response. After the serum Na+ level reached 120 mM/L, gradual correction was performed considering osmotic demyelination syndrome, and desmopressin was administered to prevent overcorrection caused by excessive water diuresis. Serum Na+ level normalized in 4 days and the patient recovered without any specific sequelae. LESSONS: The detection of OHIAS may be delayed under general anesthesia, and prior vigilance is important if the operation time is prolonged. In severe hyponatremia with an apparently rapid onset, such as OHIAS, a two-step correction process may be safe and useful: rapid correction followed by more gradual correction.