Qing Sun

In severe carbon monoxide poisoning complicated by compartment syndrome, prompt fasciotomy combined with hyperbaric oxygen and multidisciplinary supportive care was associated with full neurological recovery and limb salvage. Brain MRI abnormalities did not parallel the favorable clinical course in this patient.

Tracheo-innominate artery fistula is a rare but life-threatening complication of tracheostomy, even in chronic cases. A 22-year-old comatose man with a 2-year tracheostomy presented with sentinel bleeding followed by massive hemorrhage. Immediate measures included airway control, digital compression, and fluid resuscitation. Angiography confirmed a 3-mm fistula, and endovascular stenting achieved hemostasis. The patient was extubated on Day 5, with patent stent at 1-month follow-up but remained vegetative. Early recognition of sentinel bleeding and prompt endovascular intervention are critical for survival.

Objective: Cerebral arterial gas embolism (CAGE) is a life‐threatening acute critical illness in compressed‐air diving, primarily induced by pulmonary barotrauma (PBT). This study aimed to analyze the chest computed tomography (CT) imaging features of CAGE patients, clarify the detection rules of PBT‐related lesions, and evaluate the clinical value of chest CT in the diagnosis and treatment guidance of CAGE. Methods: A retrospective analysis was conducted on the medical records of 8 male compressed‐air divers diagnosed with CAGE who were admitted to the hyperbaric oxygen therapy (HBOT) center of No. 971 Hospital of the Chinese People’s Liberation Army Navy from August 2018 to September 2024. All patients underwent chest CT scans within 72 h of admission. Relevant data, including demographic information, diving details, clinical symptoms, chest CT findings, treatment regimens, and prognosis, were collected and analyzed using descriptive statistical methods. Results: The main etiologies of the 8 patients were gas supply interruption (6 cases, 75%) and breath‐holding during decompression (2 cases, 25%). All patients presented with neurological symptoms, including unconsciousness (5 cases, 62.5%), hemiplegia (3 cases, 37.5%), and dizziness (3 cases, 37.5%), while 7 cases (87.5%) had concurrent respiratory symptoms. Chest CT detected pulmonary injuries in 7 cases (87.5%), including pneumothorax (6 cases, 75.0%), mediastinal emphysema (4 cases, 50.0%), subcutaneous emphysema (2 cases, 25.0%), and pulmonary bulla (1 case, 12.5%). All patients received comprehensive treatments, such as basic supportive care, recompression therapy, and/or HBOT. Follow‐up at 6 months showed that all patients achieved favorable outcomes, with most fully recovered and no severe disabilities. Conclusion: CAGE in compressed‐air divers is highly associated with PBT. Chest CT exhibits high sensitivity in detecting pulmonary lesions, such as pneumothorax and mediastinal emphysema, providing potentially valuable evidence for early diagnosis, individualized treatment planning, and prognosis evaluation. Chest CT examination may be considered as part of the emergency evaluation for CAGE patients, particularly in cases with respiratory symptoms or when pneumothorax is clinically suspected, though further prospective studies are warranted to validate its routine use.

The report focuses on mooring operations-related accidents, especially those involving mooring line partings for bulk carriers. It presents a case of a young seafarer who suffered severe injuries from a snap-back mooring line during disembarking. The causes of the accident, including factors like abnormal fendering compression and meteorological/hydrological conditions, are analyzed. Moreover, it discusses prevention measures for such accidents, treatment strategies for snap-back trauma which is a complex and multidisciplinary process, and key aspects regarding the long-term prognosis and quality of life of the cases. The study emphasizes the importance of establishing comprehensive plans and training programs due to the common occurrence of such accidents and their potentially severe consequences, as there's a lack of systematic reviews on on-site emergency care strategies in general.

In clinical management of carbon monoxide (CO) poisoning, serum cardiac enzyme biomarkers and electrocardiogram (ECG) are both highly recommended emergency check-ups to evaluate myocardial injuries. Medical imaging – including head CT or MRI – are not routine for CO poisoning emergency management. We herein report on a comatose patient who was diagnosed with cerebral infarction secondary to 24 hours previous acute CO poisoning, warned by a typical cerebral-type T waves on ECG in advance, and confirmed by a head MRI. Fortunately, the patient made a full recovery based on a timely treatment with medications and hyperbaric oxygen (HBO2) therapy. We would like to propose that a vital, stable, conscious CO poisoning patient who remains a higher risk for hemorrhagic or ischemic stroke should be closely monitored for potential neurological abnormalities, and a continuous ECG monitoring should be reinforced throughout the treatment. A head MRI or CT is a priority in evaluating the secondary cerebral stroke and should be arranged immediately in the event of an abnormal ECG or if unusual new symptoms are apparent. Keywords: carbon monoxide poisoning; cerebral infarction; cerebral T-wave; magnetic resonance imaging (MRI)

Demyelination of the cerebral white matter is the most common pathological change after carbon monoxide (CO) poisoning. Notch signaling, the mechanism underlying the differentiation of astrocytes and oligodendrocytes, is critical to remyelination of the white matter after brain lesion. The purpose of this work was to determine the effects of hyperbaric oxygen (HBO) on Notch signaling pathway after CO poisoning for the explanation of the protective effects of HBO on CO-poisoning-related cerebral white matter demyelination. The male C57 BL/6 mice with severe CO poisoning were treated by HBO. And HBO therapy shortened the escape latency and improved the body mass after CO poisoning. HBO therapy also significantly suppressed protein and mRNA levels of Notch1 and Hes5 after CO poisoning. Our findings suggested that HBO could suppress the activation of Notch signaling pathway after CO poisoning, which is the mechanism underlying the neuroprotection of HBO on demyelination after severe CO poisoning.