Acute Medicine & Surgery最新文献

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.

Not Applicable.

Not Applicable.

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.

Successful embolization controlled active bleeding in a 76-year-old woman with diffuse idiopathic skeletal hyperostosis (DISH) [1] after a lumbar fracture. She originally presented with back pain following a fall. Initial computed tomography (CT) revealed fractures of the first and second lumbar vertebrae (L1, L2) with DISH extending from T8 to L2 (Figure 1A). Two days later, she was pale in complexion with hypotension (92/60 mmHg) and tachycardia (130 bpm). Contrast-enhanced CT revealed extravasation within the L2 vertebral body, indicative of left L2 and L3 arteries' involvement (Figure 1B). Emergency transcatheter arterial embolization was performed. To prevent reflux of embolic material into the aorta and spinal arteries including Adamkiewicz, the microcatheter was advanced beyond the vertebral limbus under fluoroscopic guidance. Selective angiography confirmed extravasation from the left L2 and L3 arteries (Figure 1C), which were embolized using a 1:2 mixture of N-butyl cyanoacrylate that achieved hemostasis after confirming absence of spinal arteries (Figure 1D).

Patients with DISH have an elevated risk of vertebral fracture compared to the general population due to rigidity and ossification [2]. The condition may cause various complications including injuries to intercostal and lumbar arteries, leading to active bleeding within relatively loose tissue spaces [3, 4]. This case demonstrates the importance of prompt intervention in DISH-related fractures with vascular complications, and it highlights the efficacy of embolization for controlling vertebral body bleeding.

The authors have nothing to report.

Written informed consent was obtained from the patient's family for the publication.

The authors declare no conflicts of interest.

The data that supports the findings of this study is available from the corresponding author upon reasonable request.

We read with interest the recent article, “Remifentanil use in intensive care units: Current evidence and future perspectives” by Okano et al. The article suggests that remifentanil should be preferred for analgesia in patients with hepatic failure because plasma esterases metabolise it [1]. We wish to share a related pediatric case. A 4-month-old boy with acute hepatic failure was admitted to the pediatric intensive care unit and intubated. We chose remifentanil infusion (0.25 μg/kg/min) for sedation and analgesia. After ~5 h on remifentanil, the patient acutely desaturated (SpO₂ ≈ 80%), and tidal volume fell to 2 mL/kg. Endotracheal tube position was confirmed using end-tidal carbon dioxide monitoring. However, bag ventilation produced no chest movement. We suspected opioid-induced chest wall rigidity. Remifentanil was immediately stopped, and naloxone (0.1 mg/kg IV) was administered. Chest wall excursion promptly returned, and SpO₂ normalised; tidal volume improved to ~6 mL/kg on mechanical ventilation. Remifentanil was then restarted at a reduced rate (0.15 μg/kg/min) without recurrence of rigidity. As shown by Sivak and Davis, remifentanil's clearance is unaffected by end-stage hepatic or renal failure, making it suitable for use in patients with hepatic failure [2]. However, clinicians must be aware of the rare but serious risk of opioid-induced chest wall rigidity, which can also occur in intubated patients under mechanical ventilation. In such cases, warning signs include a sudden rise in peak airway pressures, reduced tidal volumes despite adequate ventilator settings, poor chest wall expansion, and unexplained oxygen desaturation [3]. Chest wall rigidity may occur with small doses, especially in neonates and infants. A recent systematic review similarly noted that chest wall rigidity is a common side effect of remifentanil in neonates and infants, emphasising prevention by slow infusion and minimal dosing [4]. Our experience is consistent with previous reports: even small opioid doses may induce rigidity in neonates and infants [3].

When rigidity occurs, it must be recognized and treated immediately. As in our patient, chest rigidity is rapidly reversible with naloxone. In our case, naloxone promptly restored adequate ventilation without needing paralysis. This pediatric case supports the use of remifentanil in hepatic failure (extrahepatic metabolism ensures predictable clearance) while highlighting “wooden chest syndrome” as a rare but critical complication. Clinicians should be alert for chest wall rigidity during opioid infusions in intubated patients and be prepared to intervene (naloxone or paralysis) to prevent hypoxemia.

The authors declare no conflicts of interest.

This article is linked to Okano et al. paper. To view this article, visit https://doi.org/10.1002/ams2.70087.

We sincerely thank Dr. Raihan Mohammed Mohiuddin and Dr. Mohammed Misbah Ul Haq for their insightful and thoughtful comments on our study. We greatly appreciate their careful appraisal, which highlights important clinical considerations regarding diagnostic interpretation and treatment selection for secondary postpartum hemorrhage (PPH) associated with subinvolution of the placental site (SIPS).

We fully share their concern that an increased rate of diagnostic imaging, particularly computed tomography (CT), may contribute to potentially excessive angiographic procedures and hemostatic interventions. While uterine artery embolization (UAE) remains a highly reliable and life-saving therapy for hemodynamically unstable cases, its use in stable patients with SIPS requires more nuanced evaluation. Current evidence, though still limited, suggests that uterotonics and curettage constitute the standard initial management for stable SIPS [1].

As noted in our paper, the concept of SIPS has not yet been widely recognized in Japan. Consequently, curettage has seldom been selected as a first-line treatment. Furthermore, the ready availability of CT in Japan has facilitated early imaging; once contrast extravasation is visualized, clinicians often proceed to angiography because of its high procedural success rate and low short-term complication risk. Nevertheless, considering the potential for increased hemorrhagic complications in subsequent pregnancies, UAE should not be chosen indiscriminately.

We agree that broader awareness of SIPS and the establishment of evidence-based management algorithms are essential. In particular, for hemodynamically stable patients, a diagnostic and therapeutic pathway that begins with ultrasonography and proceeds to uterotonics and curettage—rather than immediate embolization—should be further studied and systematically implemented in Japan.

We again thank the authors for their valuable perspectives, which contribute to advancing a balanced and patient-centered approach to managing secondary PPH due to SIPS.

Sincerely.

This study conformed to the provisions of the Declaration of Helsinki (revised in Fortaleza, Brazil in October 2013).

The author has nothing to report.

The author declares no conflicts of interest.