Diving Hyperb Med
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Methaemoglobinaemia results from exposure to oxidizing substances such as nitrates or nitrites. Iron within haemoglobin is oxidized from the ferrous to the ferric state, which blocks the transport of oxygen and carbon dioxide, with subsequent inhibition of the respiratory chain. We describe the case of a 23-year-old male suffering from severe methaemoglobinaemia of 68% after consumption of nitrites ('poppers') in association with considerable ethanol consumption. ⋯ HBOT resulted in enhanced reduction of methaemoglobin, and rapid tissue re-oxygenation by the oxygen dissolved in plasma was provided, independent of the degree of methaemoglobinaemia. The patient recovered uneventfully and was discharged three days later. This case illustrates the potential of supportive HBOT as a time-saving therapeutic tool in this unusual situation, enabling a quick and sustained reduction in methaemoglobinaemia.
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Comparative Study
Comparison of the size of persistent foramen ovale and atrial septal defects in divers with shunt-related decompression illness and in the general population.
Decompression illness (DCI) is associated with a right-to-left shunt, such as persistent foramen ovale (PFO), atrial septal defect (ASD) and pulmonary arteriovenous malformations. About one-quarter of the population have a PFO, but considerably less than one-quarter of divers suffer DCI. Our aim was to determine whether shunt-related DCI occurs mainly or entirely in divers with the largest diameter atrial defects. ⋯ The risk of a diver suffering DCI is related to the size of the atrial defect rather than just the presence of a defect.
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Diving medicine is a peculiar specialty. There are physicians and scientists from a wide variety of disciplines with an interest in diving and who all practice 'diving medicine': the study of the complex whole-body physiological changes and interactions upon immersion and emersion. To understand these, the science of physics and molecular gas and fluid movements comes into play. ⋯ A significant relationship between PFO and cerebral damage, in the absence of high-risk diving or DCI, has yet to be confirmed. Studying PFO-related DCI provides us with unique opportunities to learn more about the effect of gas bubbles in various tissues, including the central vascular bed and neurological tissue. It may also serve to educate divers that safe diving is something that needs to be learned, not something that can be implanted.
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A persistent foramen ovale (PFO) and other types of right-to-left shunts are associated with neurological, cutaneous and cardiovascular decompression illness (DCI). A right-to-left shunt is particularly likely to be implicated in causation when these types of DCI occur after dives that are not provocative. It is believed that venous nitrogen bubbles that form after decompression pass through the shunt to circumvent the lung filter and invade systemic tissues supersaturated with nitrogen (or other inert gas) and as a result there is peripheral amplification of bubble emboli in those tissues. ⋯ The increased risk of DCI in people with migraine with aura is because migraine with aura is also associated with right-to-left shunts and this increased risk of DCI appears to be confi ned to those with a large PFO or other large shunt. Various ultrasound techniques can be used to detect and assess the size of right-to-left shunts by imaging the appearance of bubble contrast in the systemic circulation after intravenous injection. In divers with a history of shunt-mediated DCI, methods to reduce the risk of recurrence include cessation of diving, modification of future dives to prevent venous bubble liberation and transcatheter closure of a PFO.
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Review
Pathophysiology of inner ear decompression sickness: potential role of the persistent foramen ovale.
Inner-ear decompression sickness (inner ear DCS) may occur in isolation ('pure' inner-ear DCS), or as part of a multisystem DCS presentation. Symptoms may develop during decompression from deep, mixed-gas dives or after surfacing from recreational air dives. Modelling of inner-ear inert gas kinetics suggests that onset during decompression results from supersaturation of the inner-ear tissue and in-situ bubble formation. ⋯ A similar difference in gas kinetics may explain the different susceptibilities of cochlear and vestibular tissue within the inner-ear itself. The cochlea has greater perfusion and a smaller tissue volume, implying faster inert gas washout. It may be susceptible to injury by incoming arterial bubbles for a shorter time after surfacing than the vestibular organ.