Acute Medicine & Surgery最新文献

Aim: To reassess the efficacy of hyperbaric oxygen (HBO) therapy for acute carbon monoxide (CO) poisoning through a systematic review and meta-analysis, including a subgroup analysis of treatment pressures exceeding 2.5 atm absolute (ATA).

Methods: We conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) evaluating HBO therapy for acute CO poisoning. A literature search was performed in MEDLINE, CENTRAL, and Ichushi-Web databases, focusing on RCTs published up to June 2024. Only adult patients (≥ 18 years) were included, and studies were screened following PRISMA guidelines. Data extraction and quality assessment were conducted by two independent reviewers using the Cochrane risk of bias tool and the GRADE approach. Statistical analysis used a random effects model, with outcomes expressed as odds ratios (OR) and 95% confidence intervals (CI).

Results: Six studies were included, and no significant benefit of HBO therapy was observed in terms of reducing mortality or improving neurological outcomes. The subgroup analysis of HBO at ≥ 2.5 ATA also showed no significant advantage over control treatments. Moderate to significant heterogeneity was found across included studies, and the quality of evidence was rated as low to very low.

Conclusions: The efficacy of HBO therapy, even at ≥ 2.5 ATA, for improving outcomes in acute CO poisoning remains unproven. Despite these findings, HBO therapy may still hold potential benefits that require further exploration. High-quality, multicenter RCTs are necessary to better define its role in the treatment of CO poisoning.

Trial registration: UMIN Clinical Trials Registry: UMIN000054641.

Six months after a CT scan showed a linear hyperdense focus within the liver, an 81-year-old man was diagnosed with a hepatic abscess. Emergency laparotomy with abscess drainage was performed. A foreign body was extracted from the hepatic penetration site and identified as a fish bone.

An illustrative image of periorbital necrotizing soft tissue infection. In any patient presenting with severe facial pain and systemic signs of infection, this rare but life-threatening condition must be considered.

We read with great interest the study by Tanaka et al. [1]. Investigated hydrogen inhalation therapy in a swine model of non-occlusive mesenteric ischemia (NOMI). The authors should be commended for establishing a reproducible model combining hemorrhagic shock and vasopressor administration and for being the first to evaluate hydrogen therapy in this setting. Given the poor prognosis of NOMI and the absence of widely effective therapies, this study is timely and valuable.

The reported findings that hydrogen inhalation did not significantly mitigate histological ischemic injury in the absence of transmural necrosis are important, as they suggest that hydrogen therapy alone may not be sufficient for NOMI treatment. However, we wish to highlight two issues that influence clinical interpretation.

First, the model design may not have allowed for the assessment of the potential benefits of hydrogen. The study was terminated at 4 h without the development of transmural necrosis; however, clinical NOMI typically evolves over days with progressive microcirculatory compromise. In this relatively early phase, mucosal changes may be subtle and below the threshold at which antioxidant effects translate into measurable histological benefits. Therefore, the absence of an effect within this time frame may reflect the study design rather than true therapeutic inefficacy. From a clinical standpoint, this distinction matters [2]; clinicians may wrongly conclude that hydrogen therapy has no role at any stage of NOMI when, in fact, its impact may emerge under longer observation or more severe ischemic injury.

Second, the sample size was insufficient to detect modest differences. The power calculation indicated that 64 animals per group were needed, yet only four were studied. While practical constraints are understandable in large-animal research, a small cohort increases the risk of type II error. A nonsignificant result should not be interpreted as the absence of an effect, but rather as inconclusive. Translating this into clinical terms, the current findings should temper enthusiasm for hydrogen inhalation as a standalone therapy but should not dismiss its potential contribution as part of a multimodal approach, for example, combined with early vasodilator infusion or optimized hemodynamic support [3].

Despite these limitations, this study makes a valuable contribution by demonstrating the safety and feasibility of hydrogen inhalation in a critical illness model. This is an essential prerequisite for further translational studies. Importantly, this opens the door for future investigations into whether hydrogen might synergize with other therapies in NOMI, particularly at later disease stages, where oxidative stress is more pronounced.

No funding was received.

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The authors declare that they have no conflicts of interest.

We sincerely thank Dr. Mishba Ur Haq et al. for their thoughtful comments, which provided valuable insight and critical appraisal of our publication “Hydrogen inhalation therapy alone may not alleviate intestinal mucosal damage in NOMI without total-layer necrosis: An experimental swine model study”. We would like to address two key comments raised.

First, we agree that both the 4-h observation period and treatment intensity are areas for future consideration. Previous studies [1-3] implemented hydrogen inhalation therapy for only a few hours. Therefore, extending the duration of hydrogen inhalation could potentially yield.

Unlike conditions characterized by complete ischemia–reperfusion injury, such as cardiac arrest, large-vessel occlusive stroke, or coronary artery occlusion, our NOMI model did not involve superior mesenteric artery occlusion and did not induce full-thickness necrosis. Under these conditions, a lower quantity of reactive oxygen species (ROS) potentially attenuated the measurable effects of hydrogen as an antioxidant adjunct. This interpretation aligns with our findings showing no intergroup differences in 8-OHdG levels and similar progression of histological injury grades over time. We also note that achieving uniform intensity was technically challenging due to variations in individual responses to vasopressors. While macroscopic serosal images occasionally suggested transmural necrosis, histological confirmation consistently revealed only partial layer injury. Given the limited number of animals, comprehensive histological sampling at multiple time points was not feasible.

Second, we acknowledge that the limited sample size, imposed by ethical constraints of large-animal research, restricted statistical power. This study was designed as a pilot feasibility experiment, intended to generate preliminary data for subsequent investigations with adequate power and longer observation periods.

In conclusion, we appreciate the reviewers' constructive criticism and share the goal of improving outcomes in NOMI. We believe that further studies exploring hydrogen therapy, as part of a multifaceted strategy, under optimized timing and dosage conditions, represent the most promising path. We hope that our preliminary findings, together with such academic dialogue, will contribute to future translational research in this challenging field.

The Committee for Animal Ethics at Jichi Medical University approved the present experimental study (Approval number: 21054-01).

The authors have nothing to report.

The authors declare no conflicts of interest.