Impact of intravesical administration of tranexamic acid on gross hematuria in the emergency department: A before-and-after study.

INTRODUCTION: Local applications of tranexamic acid (TXA) have been effective in treating various hemorrhagic conditions. In patients with gross hematuria, the main treatment in the emergency department (ED) is continuous bladder irrigation (CBI). However, CBI has no pharmacological effects except blood clot removal from dilution. The aim of this study was to evaluate the impact of the intravesical TXA injection before CBI. METHODS: This study was a before-and-after, retrospective, and single-center study. The target population was hematuria patients who received CBI via a 3-way Foley catheter. As the intervention procedure, 1000 mg of TXA was injected through the Foley catheter and after 15 min, the Foley catheter was declamped and CBI started. Since the intervention started in March 2022, the patients from March 2022 to August 2022 were assigned to the after group and the patients from March 2021 to August 2021 were assigned to the before group. The primary outcomes were the length of stay in the ED and duration of Foley catheter placement. The secondary outcomes were the admissions and the revisits for CBI within 48 h after discharge. RESULTS: The numbers of patients in the before group and after group were 73 and 86, respectively. The median length of stay in the ED was shorter in the intervention group than in the group not treated with TXA (274 min vs. 411 mins, P < 0.001). The median duration of Foley catheter placement was also shorter in the intervention group than not treated with TXA (145 min vs. 308 mins, P < 0.001). The revisits after ED discharge were lower in the after group than in the before group (2.3% vs. 12.3%, P = 0.031). There was a trend for lower admissions in the TXA treatment group than before group (29.1% vs. 45.2%, P = 0.052). CONCLUSION: After the TXA intervention, reduction in the length of stay in the ED, the duration of Foley catheter placement, and the revisits after ED discharge was observed.

Clinical effects of adjunctive atropine during ketamine sedation in pediatric emergency patients.

INTRODUCTION: The prophylactic coadministration of anticholinergics during dissociative sedation has been considered necessary to mitigate ketamine-associated hypersalivation. Given recent conflicting conclusions regarding adjunctive atropine, we compared the incidence of hypersalivation, degree of secretion, and related side effects with atropine or placebo as an adjunct to intravenous (IV) ketamine sedation for children. METHODS: This controlled trial randomized children, 1 to 10 years old, requiring ketamine sedation in a tertiary emergency department to receive 0.01 mg/kg of atropine or placebo, along with IV ketamine (2 mg/kg). A nurse rated preprocedure and postprocedure salivation on a 100-mm visual analog scale and recorded the frequency and nature of airway complications and interventions for hypersalivation. RESULTS: During 27 months, 140 patients were enrolled. Baseline characteristics did not differ between the 2 groups (P > .05). Secretion was significantly less in the atropine vs placebo group (mean visual analog scale score ± SD, 21.2 ± 13.1 [preprocedure] to 16.5 ± 9.9 [postprocedure] vs 22.4 ± 13.5 [preprocedure] to 27.0 ± 15.9 [postprocedure], respectively; P < .05). Visual analog scale scores greater than 50 were assigned to 7 (9.7%) of 72 and 1 (1.5%) of 68 patients in the placebo and atropine groups, respectively; these patients needed only medical procedures such as suction or airway repositioning. Heart rate was significantly higher in the atropine group compared with the placebo group (P < .05). There were no significant differences between the groups in terms of other adverse events. CONCLUSION: Atropine as an adjunct to IV ketamine sedation in children significantly reduced hypersalivation, without providing a clinical benefit.

The therapeutic effect and mechanism of niacin on acute lung injury in a rat model of hemorrhagic shock: Down-regulation of the reactive oxygen species-dependent nuclear factor κB pathway.

BACKGROUND: The purpose of the current study was to investigate the protective effect of niacin on acute lung injury by the down-regulation of the nuclear factor κB (NF-κB) pathway in hemorrhagic shock (HS) rats. METHODS: HS was induced in male Sprague-Dawley rats by withdrawing blood to maintain a mean arterial pressure of 20 mm Hg to 25 mm Hg for 40 minutes. The rats were resuscitated by the reinfusion of the drawn blood, and a vehicle (HS), a low-dose of niacin (360 mg/kg, HS + LD-NA), or a high dose of niacin (1,080 mg/kg, HS + HD-NA) were administered orally. The survival of the subjects was observed for 72 hours, and a separate set of animals was killed at 6 hours after HS induction. We measured cytoplasmic phosphorylated inhibitor κB-α and inhibitor κB-α expressions, nuclear NF-κB p65 expression, NF-κB p65 DNA-binding activity, MEK partner 1 activity, tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), IL-8, nicotinamide adenine dinucleotide (NAD+), reduced nicotinamide adenine dinucleotide phosphate, reduced glutathione, glutathione disulfide, malondialdehyde levels, and histologic damage in the lung tissue. We also measured TNF-α, IL-6, and IL-8 levels in the serum. RESULTS: The survival rates of the sham, HS, HS + LD-NA, and HS + HD-NA groups were 6 of 6 (100%), 0 of 9 (0%), 1 of 9 (11.1%), and 3 of 9 (33.3%), respectively. A high dose of niacin increased lung NAD+, nicotinamide adenine dinucleotide phosphate levels, and glutathione-glutathione disulfide ratios; decreased lung malondialdehyde levels; down-regulated the NF-κB pathway; suppressed TNF-α, IL-6, and IL-8 levels in the lung tissue and serum; and attenuated histologic lung damage. CONCLUSION: A high dose of niacin attenuated lung inflammation, suppressed proinflammatory cytokine release, reduced histologic lung damage, and improved survival after HS in rats. Its therapeutic benefits were associated with the down-regulation of the reactive oxygen species-dependent NF-κB pathway.