Dear Readers, Welcome to this year's third issue of the International Maritime Health Magazine. Every medical specialty has a history, but not every history is preserved. Hyperbaric medicine in Latin America did not emerge from a single institution or a single pioneering individual. Rather, it evolved through diverse national experiences that were shaped by geography, maritime traditions, military and civilian medicine, engineering, scientific curiosity, and the dedication of countless, often silent, professionals. The articles in this issue offer more than historical accounts of individual countries; together, they reveal the collective story of a specialty that developed along many different paths while pursuing a common goal: the care and well-being of patients exposed to exceptional conditions of pressure and oxygen. This month's issue of our Journal brings a strong contemporary focus on diving and hyperbaric medicine. Complementing these historical perspectives, our scientific section presents recent contributions addressing decompression strategies in technical diving, risk factors for decompression sickness among commercial divers, and the physiological and behavioral challenges of extreme cold-water diving.

Cognitive impairment is a common and disabling consequence of various neurological disorders. Due to its high prevalence, high conversion rate, and significant burden, it has increasingly become a major challenge for aging societies worldwide. Existing treatment strategies have limited efficacy in halting disease progression, making effective intervention strategies urgently needed. As a non-invasive physical therapy, hyperbaric oxygen therapy (HBOT) exerts its effects by increasing arterial oxygen partial pressure and improving tissue oxygenation. Historically widely used for treating carbon monoxide poisoning and decompression sickness, HBOT has recently demonstrated potential in alleviating symptoms of neurological disorders. Mechanistically, HBOT modulates the hypoxic microenvironment, promotes angiogenesis, restores neurovascular integrity, enhances neurogenesis and synaptic plasticity, and reduces neuroinflammation and oxidative stress. This paper systematically reviews the mechanisms of action, application progress, and existing limitations of HBOT in neurological disorders causing cognitive impairment. As a promising therapeutic modality, HBOT holds the potential to overcome current treatment limitations and become a key component of comprehensive neurological rehabilitation strategies.

This hypothesis-driven narrative review synthesizes physiological, clinical, and neuroimaging evidence to advance an integrated pulmonary-cerebral framework for decompression illness (DCI) in repetitive breath-hold diving. Three unresolved features are addressed: the predominance of cerebral involvement, the characteristic localization of lesions to external watershed and distal arterial territories, and the gradual evolution of neurological deficits. Drawing on converging evidence from pulmonary vascular physiology and cerebral gas kinetics, we propose that venous nitrogen bubbles generated during repetitive dives intermittently bypass pulmonary filtration through transient recruitment of intrapulmonary arteriovenous anastomoses (IPAVA), providing a plausible route for episodic arterialization. Once lodged in distal cerebral arteries, these bubbles may enlarge through diffusion of nitrogen from supersaturated brain tissue, potentially contributing to progressive vascular obstruction, endothelial activation, blood-brain barrier disruption, and vasogenic edema. This review articulates a hypothesis-generating integrative framework in which IPAVA-mediated arterialization and diffusion-driven bubble enlargement may together provide a plausible physiological interpretation for the progressive, watershed-predominant cerebral injury unique to repetitive breath-hold diving. Although direct evidence remains limited-particularly regarding dynamic IPAVA behavior and quantitative nitrogen kinetics- the available data appear broadly compatible with a proposed mechanism centered on episodic arterialization followed by diffusion-driven bubble growth. By framing breath-hold diving-related DCI as a coupled pulmonary-cerebral process, this review proposes a testable conceptual foundation for future integrative research aimed at clarifying IPAVA dynamics, cerebral microvascular vulnerability, and nitrogen transport within supersaturated tissues.

Decompression sickness (DCS) is a severe condition caused by rapid reductions in ambient pressure during diving, altitude exposure, or aerospace operations, with circulating gas bubbles serving as a central initiating event. Stable nanobubbles on active hydrophobic spots along the vascular lumen can grow under decompression-induced supersaturation, detach, and enter the circulation. Their subsequent behavior is shaped by blood flow, vessel geometry, and coagulation and may lead to thrombosis and microvascular stasis. DCS pathogenesis involves three linked interfaces: the blood-bubble interface activates coagulation and complement; the bubble-endothelium interface causes mechanical injury, endothelial dysfunction, oxidative stress, and cell death; and the endothelium-immune interface, which promotes neutrophil recruitment and NETosis, driving sterile inflammation and microthrombosis. Experimental approaches reproduce different stages of this pathogenic sequence and can be broadly distinguished according to the origin of the bubbles. Whole-animal decompression models and whole-blood decompression systems incorporate pressure reduction or gas supersaturation and can therefore generate bubbles within the experimental system. Many endothelial-cell, vessel-based, and microfluidic platforms use pre-existing or externally generated gas bubbles that are introduced directly into the experimental system. These directly introduced-bubble models do not reproduce decompression-induced bubble genesis; however, they provide precise control over bubble size, flow, vascular geometry, and cellular interactions. They are therefore valuable for dissecting post-formation processes shared by decompression-generated and directly introduced intravascular bubbles, including bubble transport, vascular retention, endothelial injury, thrombosis, and inflammation. Recognizing this distinction in bubble origin is essential for defining the translational relevance and limitations of individual experimental models.

The International Space Station maintains normoxic atmospheric conditions of 14.7 psia (101 kPa) and 21% oxygen. Astronauts don spacesuits to conduct extravehicular activities (EVAs), which operate at a reduced pressure of 4.3 psia (29.6 kPa), and a hyperoxic atmosphere of 100% oxygen. The reduction in pressure presents a risk of decompression sickness and is mitigated by a several hour denitrogenation (aka, prebreathe) protocol. To reduce the time required for prebreathe, future lunar and planetary exploration habitats and vehicles are expected to maintain a hypobaric, mildly hypoxic habitable environment in order to facilitate faster transitions to hypobaric hyperoxic EVAs. Among other things, hypoxic environments can influence oxidative stress and alter glucose metabolism, or other adaptive remodeling.

An error was identified in Figure 3 of the published article. The images in the figure were incorrectly placed, resulting in the same image being shown for each part of the figure. The online version of the article has been corrected, and the corrected figure will also be included in the version deposited in PubMed Central. However, three versions of the article had already been distributed before the error was identified and cannot be corrected retrospectively. The error is limited to Figure 3 and does not affect the text, data, results or conclusions of the article. The journal apologises for the error.

This report presents the case of a diver who suffered from ciguatera intoxication (CTX). After three days of consecutive diving, he arrived at hospital with symptoms of chest pain, shortness of breath, nausea, and had sensory abnormalities across his body, arms and legs. Although his clinical signs and symptoms may have suggested cardiac involvement or decompression sickness (DCS), ultimately his condition was caused by CTX after eating fish. This case illustrates the similarities between DCS and food intoxication. The common pathology of CTX is described and its differential diagnosis with DCS is discussed.

An experienced recreational diver developed a severe multisystem life-threatening decompression sickness following a series of eight dives over four days, the profiles of which were all within acceptable limits. The diver had marked haemoconcentration and required large volume intravenous fluid replacement during initial treatment. Similar presentations have previously only been described following deep dives, fast ascents or where mandatory decompression had been missed. The management of this case, including the involvement of a hyperbaric unit co-located to an intensive care department, and the underlying pathophysiology are discussed.

Breath-hold diving exposes humans to repeated episodes of profound hypoxia and hypercapnia, eliciting physiological adaptations that enable prolonged underwater performance. This article summarises current knowledge on chronic adaptations in elite breath-hold athletes and traditional diving populations, including the Bajau sea nomads of Southeast Asia and the Korean Haenyeo divers. Evidence indicates that repeated apnoea induces adaptations across multiple physiological systems. Haematological changes include increased spleen size and enhanced splenic contraction, augmenting circulating haemoglobin and oxygen stores during apnoea. In elite divers, structured training can increase resting spleen volume, whereas the Bajau exhibit genetically associated splenic enlargement linked to variants near the PDE10A gene. Cardiopulmonary adaptations include modified pulmonary vascular responses to hypoxia, improved oxygen conservation, and metabolic shifts favoring efficient mitochondrial energy production. Molecular adaptations involve enhanced antioxidant defenses and activation of hypoxia-responsive pathways that may mitigate oxidative stress associated with repeated hypoxia-reoxygenation cycles. Emerging evidence also suggests neural plasticity and possible structural brain adaptations, although the long-term neurological consequences of chronic intermittent hypoxia exposure remain uncertain. Studies of traditional diving populations indicate that both phenotypic plasticity and genetic selection contribute to diving capacity, highlighting interactions between training and evolution. Despite these benefits, breath-hold diving also carries risks, including hypoxic blackout, decompression sickness, and potential neurological injury. Understanding the mechanisms underlying human tolerance to extreme hypoxia may have implications beyond diving physiology, including applications in cardiovascular medicine, hypoxic diseases, and rehabilitation. Further longitudinal, genomic, and mechanistic studies are needed to clarify the limits, benefits, and clinical relevance of these adaptations.