The Influence of Advanced Hyperbaric Medical Training on Arterial Gas Embolism Treatment.

3d Reconnaissance Battalion, a forward-deployed Marine Corps unit in Okinawa, Japan, frequently performs diving operations. Often throughout the year, several reconnaissance teams are diving simultaneously in different locations for training. We present a case of an otherwise healthy 30-year-old-male Reconnaissance Marine who surfaced from a dive with abnormal symptoms and received prompt care from exercise participants who were nonmedical personnel. Studies have demonstrated improved morbidity outcomes in decompression illness patients with shorter times to hyperbaric treatment following the onset of symptoms. High-risk military exercises with diving components have a mandatory safety structure that includes recompression chamber support. All United States Marine Corps Reconnaissance, Marine Corps Special Operations Command, and U.S. Navy dive operations are required to have at least one diving supervisor. To expand the diving capabilities of the unit, Marines are encouraged to attend training and qualify as diving supervisors. This case study demonstrates the efficacy and importance of training Recon Marines to recognize decompression illness as diving supervisors.

Decompression sickness with incidental pulmonary cyst.

Decompression sickness (DCS) is a known complication of scuba diving. DCS occurs when bubbles are formed as pressure is reduced during and after ascent from a dive, following inert gas uptake during the dive. The bubbles cause inflammation and hypoxia. The definitive treatment for decompression sickness is hyperbaric oxygen therapy. We present a case of a healthy 16-year-old male who presented with decompression sickness and an incidental pulmonary cyst discovered by chest CT, likely congenital. The patient was successfully treated with U.S. Navy Treatment Table 6 (TT6) for his decompression sickness, but he continued to have chest pain, requiring hospitalization and consultation with pediatric pulmonology and cardiothoracic surgery from the cyst. Three years later he complained of chest pain with changes in altitude. Chest CT showed persistence of this cyst, and additional cysts. Case conference with pulmonologists and chest radiologist could not offer a definite etiology without lung biopsy, felt to not be indicated. We believe that the changes in pressure/volumes during the dives and TT6 exacerbated his pulmonary cyst.

Effects of hyperbaric oxygen pretreatment on brain antioxidant capacity in rats with decompression sickness.

OBJECTIVE: Decompression sickness (DCS) causes serious brain hypoxic-ischemic injury. This experiment was designed to observe whether hyperbaric oxygen (HBO2) pretreatment played a neuroprotective effect in decompression sickness rat models and to explore the mechanism of protective effects. METHODS: Sprague-Dawley (SD) male rats were pretreated with HBO2 and then underwent decompression to establish the DCS rat model. Antioxidant capacities were evaluated by detecting peroxides (GPx), superoxide dismutase (SOD), catalase (CAT) activity and malondialdehyde (MDA) content in brains. The levels of metal elements manganese (Mn), zinc (Zn), iron (Fe) and magnesium (Mg) in brain tissues were assessed by flame atomic absorption spectrometry. Necrosis and apoptosis of neurons were assessed by H-E staining and immunohistochemical staining. RESULTS: HBO2 pretreatment reduced the degree of necrosis and apoptosis in brain tissues of decompression sickness rat models. In addition, HBO2 pretreatment increased GPx, SOD and CAT activities and reduced MDA accumulation. It also increased the content of Mn, Zn, Fe and Mg in brain tissue, which are all related to free radical metabolism. CONCLUSION: These results suggested that HBO2 pretreatment has protective effects on brain injury of rats with decompression sickness. The mechanism of the protective effects may be related to reducing oxidative damage by affecting metal elements in vivo.

Decrease in dysbaric osteonecrosis severity as a result of 45-minute oxygen pre-breathe.

Sudden decompression can result in bubble formation as the result of nitrogen gas (N2) dissolved in tissue during disabled submarine escape (DISSUB). This may cause dysbaric osteonecrosis (DON), a condition in long bones where bubbles in fatty marrow result in ischemia and necrosis. Previous research has shown that oxygen (O2) pre-breathe of two hours resulted in a reduction of DON; however, effects of shorter O2 pre-breathe remain uncertain. This study's aim was to understand the effect of shorter lengths of O2 pre-breathe. Eight adult Suffolk ewes (89.5± 11.5 kg) were exposed to 33 feet of seawater (fsw) for 24 hours. They were placed randomly into four groups and exposed to either 45, 30 or 15 minutes of O2 (91-88%) pre-breathe; the controls received none. They were then rapidly decompressed. Alizarin complexone was later injected intravenously to visualize the extent of DON in the right and left long bones (radii, tibiae, femur and humeri). The 30- and 15-minute pre-breathe groups saw the greatest deposition. There was significant decrease of variance in the 45-minute group when compared with all other treatments, suggesting that 45 minutes of O2 pre-breathe is required to effectively increase confidence in the reduction of DON. Similar confidence was not reflected in the 30-minute and 15-minute groups: 45 minutes of pre-breathe was the minimum amount needed to effectively prevent against DON in DISSUB escape at 33 fsw. However, future research is needed to determine how to calculate effective dosages of O2 pre-breathe to prevent DON in any given scenario.

[A case of pulmonary barotrauma complicated with cerebral arterial air embolism in a diver].

Pulmonary barotrauma is a kind of disease caused by the injury of lung tissue or blood vessel when the gas pressure of lung is too high or too lower than the external pressure of the body, which causes the air to enter the blood vessel and adjacent tissue. It could be happened in the escape of the divers with the light diving equipment or the sailors from submarine. Generally, the decompression chamber was used to treating the disease, and the minimum air pressure of 0.5 MPa recompression therapeutic schedule was used to selecting. In November 2019, a patient with pulmonary barotrauma combined with cerebral arterial gas embolism caused by improper underwater escape with light diving equipment was admitted to the General Hospital of Eastern War Zone. He was treated with 0.12 MPa oxygen inhalation recompression scheme in the oxygen chamber pressurized with air. 7 days later, the patient recovered and discharged.

Retroperitoneal extensive free air bubbles due to decompression illness.

Decompression illness (DCI) is a rare condition caused by air bubbles that arise because of a rapid decrease in ambient pressure. These air bubbles exert both physical and chemical effects associated with a range of findings from asymptomatic clinical presentation to death. In the literature, changes in consciousness, severe musculoskeletal and abdominal pain, respiratory distress, and skin changes have been described. The diagnosis of DCI is difficult, but anamnesis and physical examination are helpful. Radiologic evaluation is useful for determining possible complications in patients with severe disease and excluding other acute pathologies. In computed tomography (CT) images of patients diagnosed with DCI, air bubbles in the portal venous system, iliac and mesenteric veins, the vena cava inferior (VCI), and the cerebral and spinal arteries have been described before. Herein, we present the clinical and CT findings of two cases of DCI with extensive intra-abdominal free bubbles evident on abdominal CT.

Massive gas embolisms in diving fatalities visualized by radiology and neuropathology.

Massive vascular gas embolism is a feared and often lethal symptom of decompression illness, resulting from diving accidents. The aim of this case report was to correlate post-mortem computed tomography scan (PMCT) findings with autopsy in cases of massive vascular gas embolism. Two cases of fatal diving accidents were retrospectively selected from a forensic radiological pathological database. The PMCT results were initially shared with the forensic pathologist prior to autopsy, enabling a more accurate overall assessment. Both cases were in retrospect thoroughly studied to compare the PMCT findings with the autopsy results. In general, intra- and extra-vascular gas collections are easily detected on PMCT in all body regions. We focused on abundant intravascular gas collections, mainly in the large brain vessels. General autopsy findings are described in both cases, and in one case we elaborate on specific intracerebral changes found at autopsy. Both cases were diagnosed as pulmonary barotrauma with subsequent vascular gas embolisms. We conclude that PMCT excels in the detection of macroscopic gas collections in the body, whereas microscopic gas collections identified at autopsy aid in the differentiation between decompression sickness and pulmonary barotrauma followed by vascular gas embolism. The presented cases highlight the advantages of using both PMCT and autopsy in the post-mortem evaluation of fatal diving accidents.

Gas in coronary artery: A case of fatal decompression sickness evaluated by computed tomography.

A 54-year-old man suffered a leg cramp while diving in the ocean at a depth of 20 meters. He began to surface, with his ascent based on a decompression table. He lost consciousness at the surface and was rescued by a nearby boat. The boat staff judged him to be in cardiac arrest, so they performed chest compressions. When the boat reached port where an ambulance was waiting, emergency medical technicians confirmed that the patient was in cardiac arrest; his initial rhythm was asystole. Treated with basic life support, the patient was then transported to a rendezvous point, where a physician-staffed helicopter waited. The patient remained in cardiac arrest, so the staff of the helicopter performed tracheal intubation with mechanical ventilation, securing a venous route, infusion of adrenaline, and mechanical chest compression. On arrival at our hospital 100 minutes after collapse, he remained in cardiac arrest. Continued advanced cardiac life support failed to obtain spontaneous circulation. Whole-body computed tomography (CT) at 120 minutes after the collapse showed multiple gas bubbles in the heart, aorta, inferior vena cava, cerebral artery, coronary artery and portal vein with lung edema. This is the first case to show gas in the bilateral coronary arteries on CT. The present case clearly demonstrates that decompression sickness can also induce acute coronary syndrome.

Hyperbaric treatment of air or gas embolism: current recommendations.

Gas can enter arteries (arterial gas embolism, AGE) due to alveolar-capillary disruption (caused by pulmonary over-pressurization, e.g. breath-hold ascent by divers) or veins (venous gas embolism, VGE) as a result of tissue bubble formation due to decompression (diving, altitude exposure) or during certain surgical procedures where capillary hydrostatic pressure at the incision site is subatmospheric. Both AGE and VGE can be caused by iatrogenic gas injection. AGE usually produces stroke-like manifestations, such as impaired consciousness, confusion, seizures and focal neurological deficits. Small amounts of VGE are often tolerated due to filtration by pulmonary capillaries; however VGE can cause pulmonary edema, cardiac "vapor lock" and AGE due to transpulmonary passage or right-to-left shunt through a patient foramen ovale. Intravascular gas can cause arterial obstruction or endothelial damage and secondary vasospasm and capillary leak. Vascular gas is frequently not visible with radiographic imaging, which should not be used to exclude the diagnosis of AGE. Isolated VGE usually requires no treatment; AGE treatment is similar to decompression sickness (DCS), with first aid oxygen then hyperbaric oxygen. Although cerebral AGE (CAGE) often causes intracranial hypertension, animal studies have failed to demonstrate a benefit of induced hypocapnia. An evidence based review of adjunctive therapies is presented.

PDTC ameliorates decompression induced-lung injury caused by unsafe fast buoyancy ascent escape via inhibition of NF-κB pathway.

Nuclear factor kappa B (NF-κB) is the critical transcriptional factor in the pathogenesis of acute lung injury (ALI). NF-κB regulates the expression changes of inflammatory factors such as tumor necrosis factor alpha (TNF-α), interleukin-1ß (IL-1ß) and interleukin 6 (IL-6). In a previous study we showed that decompression sickness (DCS) caused by simulated unsafe fast buoyancy ascent escape (FBAE) could result in ALI, which was characterized by expression changes of inflammatory factors in rat lung tissue. The purpose of the present work was to study the roles of NF-κB and TNF-α in the process of DCS-induced rat lung injury caused by simulated unsafe FBAE. The research methods aimed to detect the rat lung tissue messenger ribonucleic acid (mRNA) and protein level variations of NF-κB, inhibitory ×B (I×B), TNF-α, IL-1ß, IL-6, IL-10 and IL-13 by using pretreatment of the NF-κB inhibitor pyrrolidine dithiocarbamate (PDTC) and TNF-α antibody (Ab). Our experimental results demonstrated that PDTC could improve the survival rate of the rats with DCS caused by unsafe FBAE more effectively than TNF-α Ab. However, the inhibition of TNF-α Ab on the nuclear translocated protein expression of NF-κB was more effective than PDTC. Both PDTC and TNF-α Ab can abrogate the increment of the rat lung tissue mRNA levels of TNF-α, IL-1ß, IL-6 and protein levels of NF-κB, TNF-α, IL-1ß effectively and increase the rat lung tissue content of I×B significantly. In conclusion, TNF-α-mediated NF-κB signaling may be one of the critical signaling pathways in the pathogenesis of DCS-induced rat lung injury caused by simulated unsafe FBAE. PDTC may ameliorate this type of injury partly through inhibiting the NF-κB pathway.

Implementation of Targeted Temperature Management in a Patient with Cerebral Arterial Gas Embolism.

Cerebral arterial gas embolism (CAGE) shows various manifestations according to the quantity of gas and the brain areas affected. The symptoms range from minor motor weakness, headache, and confusion to disorientation, convulsions, hemiparesis, unconsciousness, and coma. A 46-year-old man was transferred to our emergency department due to altered sensorium. Immediately after a controlled ascent from 33 m of seawater, he complained of shortness of breath and rigid extremities, lapsing into unconsciousness. He was intubated at another medical center, where a brain computerized axial tomography scan showed no definitive abnormal findings. Pneumothorax and obstructing lesions were apparent in the left thorax of the computed tomography scan. Following closed thoracostomy, we provided hyperbaric oxygen therapy (HBOT) using U.S. Navy Treatment Table (USN TT) 6A. A brain magnetic resonance imaging diffusion image taken after HBOT showed acute infarction in both middle and posterior cerebral arteries. We implemented targeted temperature management (TTM) to prevent worsening of cerebral function in the intensive care unit. After completing TTM, we repeated HBOT using USN TT5 and started rehabilitation therapy. He fully recovered from the neurological deficits. This is the first case of CAGE treated with TTM and consecutive HBOTs suggesting that TTM might facilitate salvage of the penumbra in severe CAGE.

Representações sociais de pescadores com lesão medular: repercussões e trajetória de vida / Representaciones sociales de pescadores con lesión medular: repercusiones e historia de vida / Social representations of fishermen with spinal cord injury: impacts and life trajectory

RESUMO Objetivo: analisar as representações sociais da trajetória de vida dos pescadores artesanais com lesão medular vítimas de acidente por mergulho nas praias do litoral Norte do Rio Grande do Norte. Método: estudo descritivo, de natureza qualitativa, desenvolvido com 31 pescadores entre outubro de 2013 e agosto de 2014, mediante entrevista semiestruturada. Empregou-se a análise lexicográfica e classificação hierárquica descendente dos textos (software ALCESTE), sob a ótica das Representações Sociais. Resultados: as representações sociais dos pescadores com lesão medular apresentaram as experiências com as limitações físicas e expectativas de aposentadoria, estas últimas configurando-se como uma realidade distante das exigências impostas por nossas leis trabalhistas. Conclusão: exigem-se medidas de promoção, prevenção e reabilitação da saúde do pescador vítima de lesão medular, além de condições seguras e dignas de trabalho como compromisso das políticas de saúde.

RESUMEN Objetivos: analizar las representaciones sociales de la historia de vida de pescadores artesanales con lesión medular víctimas de accidente de buceo en las playas del litoral Norte de Rio Grande do Norte. Método: estudio descriptivo, de naturaleza cuantitativa, desarrollado con 31 pescadores entre octubre de 2013 y agosto de 2014, mediante entrevista semiestructurada. Se empleó análisis lexicográfico y clasificación jerárquica descendiente en los textos (software ALCESTE), en la visión de las Representaciones Sociales. Resultados: las representaciones sociales de los pescadores con lesión medular expresaron las experiencias de las limitaciones físicas y expectativas de jubilación, configurándose éstas como realidad distante de las exigencias impuestas por la legislación laboral vigente. Conclusión: se requieren medidas de promoción, prevención y rehabilitación de la salud del pescador víctima de lesión medular, además de condiciones laborales seguras y dignas, con compromiso de las políticas de salud.

ABSTRACT Objective: analyze social representations in the life trajectory of artisanal fishermen with spinal cord injury caused by diving on the north coast of Rio Grande do Norte. Method: a descriptive, qualitative study was conducted with 31 fishermen between October 2013 and August 2014, using a semi-structured interview. A lexicographic analysis and descending hierarchical classification of texts were performed (with software ALCESTE), in the perspective of the social representations. Results: social representations of fishermen with spinal cord injury presented experiences with physical limitations and expectations regarding retirement, which appeared as a distant reality from the requirements in Brazilian labor laws. Conclusion: measures are required for the promotion, prevention and rehabilitation of the health of fishermen with spinal cord injury, as well as safe and decent fishing conditions, with the commitment of health authorities.

Cutis marmorata and cerebral arterial gas embolism.

Dr Kemper and colleagues reported that, when air was injected into the cerebral circulation of pigs, they developed a rash that looked very similar to cutis marmorata of cutaneous decompression illness (DCI) and to livido reticularis. They postulated that cutaneous DCI in divers may be centrally mediated as a result of cerebral gas embolism. It would be helpful if Kemper et al. described the distribution of the rash in their pigs. In divers, cutaneous DCI is generally confined to parts of the body with significant amounts of subcutaneous fat, such as the trunk and thighs, and the rash often crosses the midline. Colleagues and I have reported that cutaneous DCI is commonly associated with significant right-to-left shunts and particularly persistent foramen ovale (PFO). We postulated that the manifestations of shunt-related DCI, whether neurological or cutaneous, are in large part determined by peripheral amplification of embolic bubbles in those tissues that are most supersaturated with dissolved nitrogen (or other inert gas) at the time that emboli arrive. Hence we postulated that cutaneous DCI is the result of amplification of gas emboli that invade cutaneous capillaries. Dr Kemper has kindly sent me a number of the publications from his department on which their report of this skin rash in pigs is based. The aim of their experiments was to produce significant brain injury by means of cerebral air embolism. Their pigs had no tissues supersaturated with inert gas. They were ventilated with a FiO2 of 0.4 and anaesthetised with ketamine and midazolam. They were also given pancuronium and atropine, before air was injected into their cerebral circulation. If their findings in pigs and the resulting hypothesis were applicable to man, it would mean that one could get cutaneous DCI without decompression: one would only need cerebral gas embolism. During contrast echocardiography, I have produced arterial gas embolism in many hundreds of patients with right-to-left shunts and it is certain that some bubbles went into their cerebral circulations, but I have never seen and no patient has reported getting a rash. Nor am I aware of any reports of gas embolism causing a rash like cutaneous DCI without there being tissue supersaturation following some form of decompression. Kemper and colleagues injected between 0.25 and 1 ml·kg⁻¹ body weight of air into the ascending pharyngeal artery (roughly equivalent to human internal carotid artery) of pigs weighing 30-40kg. That immediately produced significant elevation of blood pressure and heart rate suggesting a 'sympathetic surge'. This is similar to the haemodynamic effects that can occur with subarachnoid haemorrhage and some other catastrophic brain injuries. That effect may have been potentiated by pre-treatment with atropine. There was also a considerable increase in intracranial pressure and major adverse effects on cerebral metabolism. Some pigs died quickly and the survivors were killed at the end of the experiment. I suspect that no pig would have survived the experiments without major neurological injury if they had not been killed. Most people with cutaneous DCI have no detectable neurological manifestations at the time that they have a rash. In those that do have neurological manifestations, it is rarely catastrophic. The increases in heart rate and blood pressure reported in the pigs are similar to the effects of a phaeochromocytoma, which can cause livido reticularis in man. Therefore, I wonder whether an alternative explanation for these observations might be that the cerebral injury in the pigs was so massive that the sympathetic surge was comparable to the effects of catecholamine release from a phaeochromocytoma and caused a rash similar to that seen in patients with a phaeochromocytoma.

Osteonecrosis disbárica de cabeza humeral en buzo pesquero tratado con artroplastia de superficie / Dysbaric osteonecrosis of humeral head in a diver treated with resurfacing arthroplasty

Describir osteonecrosis disbárica (ODB) en buzo pesquero y exponer la experiencia inédita de tratamiento con artroplastia de superficie (AS). Introducción ODB, forma de necrosis avascular secundaria a enfermedad por descompresión (EDC), cuyo tratamiento gold standard para estadios avanzados continúa siendo la artroplastia total (AT). Presentación de caso: Paciente de 49 años, buzo pesquero, antecedentes de EDC tratada el 2008 en cámara hiperbárica, con diagnóstico compatible con ODB de cabeza humeral derecha de 6 años de evolución; Constant score=29. Se realiza AS del hombro derecho, y luego de 18 meses de seguimiento se reporta una adecuada evolución clínica con remisión de la sintomatología; Constant score a 18 meses=72. Discusión: El uso de AT en el paciente joven es limitado, por lo que surge la necesidad de implementar nuevas técnicas quirúrgicas en este grupo de pacientes. Conclusión: La AS constituye una alternativa terapéutica en adultos jóvenes y activos con ODB...

Introduce and describe Dysbaric Osteonecrosis (DON) in a fishing diver patient, emphasising clinical features, use of imaging methods, and present a new experience of treatment with Resurfacing Arthroplasty (RA). Introduction: DON, a form of avascular necrosis secondary to Decompression Sickness (DCS). Total Arthroplasty (AT) remains the reference treatment for advanced stages. Case report: Male, 49 years old, fishing diver, with a history of DCS treated in a hyperbaric chamber (2008). Right humeral head DON Compatible with 6 years of onset. Constant Score=29. RA performed on right shoulder. Clinical remission of symptoms was observed after 18 months of follow-up. Constant Score at 18 months=72. Discussion: TA use in young patients is limited, so there is a need to implement new surgical techniques in this group of patients. Conclusion: RA is a therapeutic alternative in young and active subjects with DON...

Dysbaric osteonecrosis: a literature review of pathophysiology, clinical presentation, and management.

OBJECTIVE: To perform a general literature review of dysbaric osteonecrosis (DON) to describe its pathophysiology, prevalence in scuba divers, prognosis, and treatment options. DATA SOURCES: A literature search on PubMed was performed using the term "dysbaric osteonecrosis" yielding 67 results. There was no exclusion based on dates. Articles that mainly dealt with decompression sickness secondary to tunnel work, mining, or airplane travel were not selected. An additional search on PubMed using the terms "(osteonecrosis diving) NOT dysbaric" was performed to identify other publications not picked up in the initial search. MAIN RESULTS: Dysbaric osteonecrosis is associated with prolonged hyperbaric exposure and rapid decompression that cause nitrogen bubbles to enter the fatty marrow-containing shafts of long bones leading to reduction in blood flow and subsequent osteonecrosis. Patients may present asymptomatically, and typical radiographic findings of DON include: decalcification of bone, cystic lesions, osteosclerotic patterns, nontraumatic fractures, bone islands, and a subchondral crescent sign. Surgical treatment options are comprised of core decompression and free vascularized fibular graft, whereas nonsurgical treatment options consist of monitoring, physical therapy, and bisphosphonate therapy. CONCLUSIONS: Although the incidence of DON has decreased significantly over the past 2 decades, the lack of timely diagnosis and optimal management keeps DON relevant in the orthopedic and sport medicine community.

Diving fatality investigations: recent changes.

Modifications to the investigation procedures in diving fatalities have been incorporated into the data acquisition by diving accident investigators. The most germane proposal for investigators assessing diving fatalities is to delay the drawing of conclusions until all relevant diving information is known. This includes: the accumulation and integration of the pathological data; the access to dive computer information; re-enactments of diving incidents; post-mortem CT scans and the interpretation of intravascular and tissue gas detected. These are all discussed, with reference to the established literature and recent publications.

Venous gas embolism as a predictive tool for improving CNS decompression safety.

A key process in the pathophysiological steps leading to decompression sickness (DCS) is the formation of inert gas bubbles. The adverse effects of decompression are still not fully understood, but it seems reasonable to suggest that the formation of venous gas emboli (VGE) and their effects on the endothelium may be the central mechanism leading to central nervous system (CNS) damage. Hence, VGE might also have impact on the long-term health effects of diving. In the present review, we highlight the findings from our laboratory related to the hypothesis that VGE formation is the main mechanism behind serious decompression injuries. In recent studies, we have determined the impact of VGE on endothelial function in both laboratory animals and in humans. We observed that the damage to the endothelium due to VGE was dose dependent, and that the amount of VGE can be affected both by aerobic exercise and exogenous nitric oxide (NO) intervention prior to a dive. We observed that NO reduced VGE during decompression, and pharmacological blocking of NO production increased VGE formation following a dive. The importance of micro-nuclei for the formation of VGE and how it can be possible to manipulate the formation of VGE are discussed together with the effects of VGE on the organism. In the last part of the review we introduce our thoughts for the future, and how the enigma of DCS should be approached.

Cerebral arterial gas embolism with delayed treatment and a fatal outcome in a 14-year-old diver.

In today's recreational diving climate, diving fitness examinations are not mandatory, and even divers who go for these examinations may not have routine chest X-rays (CXR) done in the absence of respiratory symptoms or a past history of respiratory problems. We present a case of an ultimately fatal cerebral arterial gas embolism in a 14-year-old boy with an undiagnosed lung cyst, the contribution of which to his death is uncertain. Various factors such as lack of oxygen first aid at the remote dive site; poor communication; lack of diving medicine expertise, poor oxygen administration and management in a local hospital and long delay to recompression therapy contributed to the poor outcome. It is imperative that dive operators and physicians working in close proximity to popular dive sites be educated on how to recognise and treat diving emergencies and be well-acquainted, as should divers, with the contact numbers of diving medical hotlines that offer timely and appropriate advice in case of emergency.

Suspected arterial gas embolism after glossopharyngeal insufflation in a breath-hold diver.

INTRODUCTION: Many competitive breath-hold divers employ the technique of glossopharyngeal insufflation in order to increase their lung gas volume for a dive. After a maximal inspiration, using the oral and pharyngeal muscles repeatedly, air in the mouth is compressed and forced into the lungs. Such overexpansion of the lungs is associated with a high transpulmonary pressure, which could possibly cause pulmonary barotrauma. CASE REPORT: We report a case of transient neurological signs and symptoms occurring within 1 min after glossopharyngeal insufflation in a breath-hold diver. He complained of paresthesia of the right shoulder and a neurological exam revealed decreased sense of touch on the right side of the neck as compared to the left side. Motor function was normal. The course of events in this case is suggestive of arterial gas embolism. DISCUSSION: Although the diver recovered completely within a few minutes, the perspective of a more serious insult raises concerns in using the glossopharyngeal insufflation technique. In addition to a neurological insult, damage to other organs of the body has to be considered. Both acute and long-term negative health effects are conceivable.