Compartment Syndrome Secondary to Calcium Gluconate Extravasation.

This case report highlights a rare yet severe complication of calcium gluconate extravasation, namely, compartment syndrome. We present the case of an 86-year-old female who developed compartment syndrome following an extravasation of intravenously administered calcium gluconate for the management of hyperkalemia. Initially, mild erythema and edema were observed at the site of extravasation, which eventually progressed to severe pain, a reduction in the joint range of motion due to increased compartment pressure. Despite undergoing a series of fasciotomies, the patient's condition did not improve, and extensive tissue necrosis and gangrene necessitated amputation. This case emphasizes that calcium gluconate extravasation can lead to life-threatening complications, such as compartment syndrome, underscoring the critical importance of employing proper infusion techniques.

Gestational intermittent hyperoxia rescues murine genetic congenital heart disease in part.

Cardiac development is a dynamic process, temporally and spatially. When disturbed, it leads to congenital cardiac anomalies that affect approximately 1% of live births. Genetic variants in several loci lead to anomalies, with the transcription factor NKX2-5 being one of the largest. However, there are also non-genetic factors that influence cardiac malformations. We examined the hypothesis that hyperoxia may be beneficial and can rescue genetic cardiac anomalies induced by an Nkx2-5 mutation. Intermittent mild hyperoxia (40% PO2) was applied for 10 h per day to normal wild-type female mice mated with heterozygous Nkx2-5 mutant males from gestational day 8.5 to birth. Hyperoxia therapy reduced excessive trabeculation in Nkx2-5 mutant mice compared to normoxic conditions (ratio of trabecular layer relative to compact layer area, normoxia 1.84 ± 0.07 vs. hyperoxia 1.51 ± 0.04) and frequency of muscular ventricular septal defects per heart (1.53 ± 0.32 vs. 0.68 ± 0.15); however, the incidence of membranous ventricular septal defects in Nkx2-5 mutant hearts was not changed. Nkx2-5 mutant embryonic hearts showed defective coronary vessel organization, which was improved by intermittent mild hyperoxia. The results of our study showed that mild gestational hyperoxia therapy rescued genetic cardiac malformation induced by Nkx2-5 mutation in part.