Decompression Illness

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Peter Wilmshurst - One of the best experts on this subject based on the ideXlab platform.

  • the role of persistent foramen ovale and other shunts in Decompression Illness
    Diving and Hyperbaric Medicine, 2015
    Co-Authors: Peter Wilmshurst
    Abstract:

    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. Approximately a quarter of the population have a PFO, but only a small proportion of the population with the largest right-to-left shunts are at high risk of shunt-mediated DCI. 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.

  • Relationship between right-to-left shunts and cutaneous Decompression Illness.
    Clinical science (London England : 1979), 2001
    Co-Authors: Peter Wilmshurst, Matthew Pearson, Kevin P. Walsh, W L Morrison, P. Bryson
    Abstract:

    The presence of a large right-to-left shunt is associated with neurological Decompression Illness after non-provocative dives, as a result of paradoxical gas embolism. A small number of observations suggest that cutaneous Decompression Illness is also associated with a right-to-left shunt, although an embolic aetiology of a diffuse rash is more difficult to explain. We performed a retrospective case-control comparison of the prevalence and sizes of right-to-left shunts determined by contrast echocardiography performed blind to history in 60 divers and one caisson worker with a history of cutaneous Decompression Illness, and 123 historical control divers. We found that 47 (77.0%) of the 61 cases with cutaneous Decompression Illness had a shunt, compared with 34 (27.6%) of 123 control divers (P < 0.001). The size of the shunts in the divers with cutaneous Decompression Illness was significantly greater than in the controls. Thus 30 (49.2%) of the 61 cases with cutaneous Decompression Illness had a large shunt at rest, compared with six (4.9%) of the 123 controls (P < 0.001). During closure procedures in 17 divers who had cutaneous Decompression Illness, the mean diameter of the foramen ovale was 10.9 mm. Cutaneous Decompression Illness occurred after dives that were provocative or deep in subjects without shunts, but after shallower and non-provocative dives in those with shunts. The latter individuals are at increased risk of neurological Decompression Illness. We conclude that cutaneous Decompression Illness has two pathophysiological mechanisms. It is usually associated with a large right-to-left shunt, when the mechanism is likely to be paradoxical gas embolism with peripheral amplification when bubble emboli invade tissues supersaturated with nitrogen. Cutaneous Decompression Illness can also occur in individuals without a shunt. In these subjects, the mechanism might be bubble emboli passing through an 'overloaded' lung filter or autochthonous bubble formation.

  • effect on migraine of closure of cardiac right to left shunts to prevent recurrence of Decompression Illness or stroke or for haemodynamic reasons
    The Lancet, 2000
    Co-Authors: Peter Wilmshurst, Kevin Walsh, Simon Nightingale, W L Morrison
    Abstract:

    Summary Background A relation between migraine with aura and cardiac right-to-left shunts has been reported. Right-to-left shunts are also associated with stroke and certain forms of Decompression Illness. We investigated the effect of closure of right-to-left shunts on migraine symptoms. Methods A consultant neurologist, who was unaware of information about residual shunt, undertook a structured interview with individuals who had had transcatheter closure of an atrial septal defect or patent foramen ovale to assess how the procedure affected migraine symptoms. Findings 37 of 40 consecutive patients who had had a closure procedure (to permit resumption of diving after Decompression Illness in 29, after stroke when paradoxical thromboembolism was suspected in four, or to close a large atrial septal defect in four) could be contacted. 21 (57%) had a history of migraine before the procedure (with aura in 16, without aura in five). 11 individuals had fortification spectra in the period immediately after closure. During long-term follow-up, no migraine symptoms were reported by seven individuals who had previously had migraine with aura and three who had previously had migraine without aura. Eight others who had had migraine with aura before closure reported improvement in frequency and severity of migraines. Three (one migraine with aura, two migraine without aura) reported no alteration in migraine episodes. Interpretation These observations suggest a causal association between right-to-left shunts and migraine with aura. There may be a subgroup of patients who have severe migraine associated with a large right-to-left shunt in whom closure of the atrial defect may improve or abolish migraine.

  • relationship between the clinical features of neurological Decompression Illness and its causes
    Clinical Science, 2000
    Co-Authors: Peter Wilmshurst, P. Bryson
    Abstract:

    There is dispute as to whether paradoxical gas embolism is an important aetiological factor in neurological Decompression Illness, particularly when the spinal cord is aected. We performed a blind case-controlled study to determine the relationship between manifestations of neurological Decompression Illness and causes in 100 consecutive divers with neurological Decompression Illness and 123 unaected historical control divers. The clinical eects of neurological Decompression Illness (including the sites of lesions and latency of onset) were correlated with the presence of right-to-left shunts, lung disease and a provocative dive profile. The prevalence and size of shunts determined by contrast echocardiography were compared in aected divers and controls. Right-to-left shunts, particularly those which were large and present without a Valsalva manoeuvre, were significantly more common in divers who had neurological Decompression Illness than in controls (P ! 0.001). Shunts graded as large or medium in size were present in 52% of aected divers and 12.2% of controls (P ! 0.001). Spinal Decompression Illness occurred in 26 out of 52 divers with large or medium shunts and in 12 out of 48 without (P ! 0.02). The distribution of latencies of symptoms diered markedly in the 52 divers with a large or medium shunt and in the 30 divers who had lung disease or a provocative dive profile. In most cases of neurological Decompression Illness the cause can be determined by taking a history of the dive profile and latency of onset, and by performing investigations to detect a right-to-left shunt and lung disease. Using this information it is possible to advise divers on the risk of returning to diving and on ways of reducing the risk if diving is resumed. Most cases of spinal Decompression Illness are associated with a right-to-left shunt.

  • transcatheter closure of patent foramen ovale using the amplatzer septal occluder to prevent recurrence of neurological Decompression Illness in divers
    Heart, 1999
    Co-Authors: Kevin Walsh, Peter Wilmshurst, W L Morrison
    Abstract:

    OBJECTIVE—Large flap valve patent foramens may cause paradoxical thromboembolism and neurological Decompression Illness in divers. The ability of a self expanding Nitinol wire mesh device (Amplatzer septal occluder) to produce complete closure of the patent foramen ovale was assessed. PATIENTS—Seven adults, aged 18-60 years, who had experienced neurological Decompression Illness related to diving. Six appeared to have a normal atrial septum on transthoracic echocardiography, while one was found to have an aneurysm of the interatrial septum. METHODS—Right atrial angiography was performed to delineate the morphology of the right to left shunt. The defects were sized bidirectionally with a precalibrated balloon filled with dilute contrast. The largest balloon diameter that could be repeatedly passed across the septum was used to select the occlusion device diameter. Devices were introduced through 7 F long sheaths. All patients underwent transthoracic contrast echocardiography one month after the implant. RESULTS—Device placement was successful in all patients. Device sizes ranged from 9-14 mm. The patient with an aneurysm of the interatrial septum had three defects, which were closed with two devices. Right atrial angiography showed complete immediate closure in all patients. Median (range) fluoroscopy time was 13.7 (6-35) minutes. Follow up contrast echocardiography showed no right to left shunting in six of seven patients and the passage of a few bubbles in one patient. All patients have been allowed to return to diving. CONCLUSION—The Amplatzer septal occluder can close the large flap valve patent foramen ovale in divers who have experienced neurological Decompression Illness. Interatrial septal aneurysms with multiple defects may require more than one device. Keywords: patent foramen ovale; Decompression Illness; Amplatzer septal occluder

Maria Vargas - One of the best experts on this subject based on the ideXlab platform.

  • neuroimaging of diving related Decompression Illness current knowledge and perspectives
    American Journal of Neuroradiology, 2014
    Co-Authors: Kamtchum J. Tatuene, R. Pignel, P. Pollak, K. O. Lovblad, A. Kleinschmidt, Maria Vargas
    Abstract:

    Diving-related Decompression Illness is classified into 2 main categories: arterial gas embolism and Decompression sickness. The latter is further divided into types 1 and 2, depending on the clinical presentation. MR imaging is currently the most accurate neuroimaging technique available for the detection of brain and spinal cord lesions in neurologic type 2 Decompression sickness. Rapid bubble formation in tissues and the bloodstream during ascent is the basic pathophysiologic mechanism in Decompression Illness. These bubbles can damage the central nervous system through different mechanisms, namely arterial occlusion, venous obstruction, or in situ toxicity. Neuroimaging studies of Decompression sickness have reported findings associated with each of these mechanisms: some typical results are summarized and illustrated in this article. We also review the limitations of previous work and make practical methodologic suggestions for future neuroimaging studies.

P. Bryson - One of the best experts on this subject based on the ideXlab platform.

  • Relationship between right-to-left shunts and cutaneous Decompression Illness.
    Clinical science (London England : 1979), 2001
    Co-Authors: Peter Wilmshurst, Matthew Pearson, Kevin P. Walsh, W L Morrison, P. Bryson
    Abstract:

    The presence of a large right-to-left shunt is associated with neurological Decompression Illness after non-provocative dives, as a result of paradoxical gas embolism. A small number of observations suggest that cutaneous Decompression Illness is also associated with a right-to-left shunt, although an embolic aetiology of a diffuse rash is more difficult to explain. We performed a retrospective case-control comparison of the prevalence and sizes of right-to-left shunts determined by contrast echocardiography performed blind to history in 60 divers and one caisson worker with a history of cutaneous Decompression Illness, and 123 historical control divers. We found that 47 (77.0%) of the 61 cases with cutaneous Decompression Illness had a shunt, compared with 34 (27.6%) of 123 control divers (P < 0.001). The size of the shunts in the divers with cutaneous Decompression Illness was significantly greater than in the controls. Thus 30 (49.2%) of the 61 cases with cutaneous Decompression Illness had a large shunt at rest, compared with six (4.9%) of the 123 controls (P < 0.001). During closure procedures in 17 divers who had cutaneous Decompression Illness, the mean diameter of the foramen ovale was 10.9 mm. Cutaneous Decompression Illness occurred after dives that were provocative or deep in subjects without shunts, but after shallower and non-provocative dives in those with shunts. The latter individuals are at increased risk of neurological Decompression Illness. We conclude that cutaneous Decompression Illness has two pathophysiological mechanisms. It is usually associated with a large right-to-left shunt, when the mechanism is likely to be paradoxical gas embolism with peripheral amplification when bubble emboli invade tissues supersaturated with nitrogen. Cutaneous Decompression Illness can also occur in individuals without a shunt. In these subjects, the mechanism might be bubble emboli passing through an 'overloaded' lung filter or autochthonous bubble formation.

  • relationship between the clinical features of neurological Decompression Illness and its causes
    Clinical Science, 2000
    Co-Authors: Peter Wilmshurst, P. Bryson
    Abstract:

    There is dispute as to whether paradoxical gas embolism is an important aetiological factor in neurological Decompression Illness, particularly when the spinal cord is aected. We performed a blind case-controlled study to determine the relationship between manifestations of neurological Decompression Illness and causes in 100 consecutive divers with neurological Decompression Illness and 123 unaected historical control divers. The clinical eects of neurological Decompression Illness (including the sites of lesions and latency of onset) were correlated with the presence of right-to-left shunts, lung disease and a provocative dive profile. The prevalence and size of shunts determined by contrast echocardiography were compared in aected divers and controls. Right-to-left shunts, particularly those which were large and present without a Valsalva manoeuvre, were significantly more common in divers who had neurological Decompression Illness than in controls (P ! 0.001). Shunts graded as large or medium in size were present in 52% of aected divers and 12.2% of controls (P ! 0.001). Spinal Decompression Illness occurred in 26 out of 52 divers with large or medium shunts and in 12 out of 48 without (P ! 0.02). The distribution of latencies of symptoms diered markedly in the 52 divers with a large or medium shunt and in the 30 divers who had lung disease or a provocative dive profile. In most cases of neurological Decompression Illness the cause can be determined by taking a history of the dive profile and latency of onset, and by performing investigations to detect a right-to-left shunt and lung disease. Using this information it is possible to advise divers on the risk of returning to diving and on ways of reducing the risk if diving is resumed. Most cases of spinal Decompression Illness are associated with a right-to-left shunt.

Kamtchum J. Tatuene - One of the best experts on this subject based on the ideXlab platform.

  • REVIEWARTICLE Neuroimaging of Diving-Related Decompression Illness: Current Knowledge and Perspectives
    2016
    Co-Authors: Kamtchum J. Tatuene, R. Pignel, P. Pollak, K. O. Lovblad, A. Kleinschmidt, M. I. Vargas
    Abstract:

    SUMMARY: Diving-related Decompression Illness is classified into 2 main categories: arterial gas embolism and Decompression sickness. The latter is further divided into types 1 and 2, depending on the clinical presentation. MR imaging is currently the most accurate neuroimaging technique available for the detection of brain and spinal cord lesions in neurologic type 2 Decompression sickness. Rapid bubble formation in tissues and the bloodstream during ascent is the basic pathophysiologic mechanism in Decompression Illness. These bubbles can damage the central nervous system through different mechanisms, namely arterial occlusion, venous obstruction, or in situ toxicity. Neuroimaging studies of Decompression sickness have reported findings associated with each of thesemechanisms: some typical results are summarized and illustrated in this article. We also review the limitations of previous work and make practical methodologic suggestions for future neuroimaging studies. The term “Decompression Illness ” encompasses all clinicalmanifestations induced by a rapid decrease of environmental pressure, sufficient to cause the formation of inert gas bubbles previously loaded within tissues or blood as a soluble phase. This can occur in various circumstances, including ascent from diving, flying or climbing mountains immediately after a dive, and exer-cising in hyperbaric/hypobaric chambers.1-3 Diving-related de

  • neuroimaging of diving related Decompression Illness current knowledge and perspectives
    American Journal of Neuroradiology, 2014
    Co-Authors: Kamtchum J. Tatuene, R. Pignel, P. Pollak, K. O. Lovblad, A. Kleinschmidt, Maria Vargas
    Abstract:

    Diving-related Decompression Illness is classified into 2 main categories: arterial gas embolism and Decompression sickness. The latter is further divided into types 1 and 2, depending on the clinical presentation. MR imaging is currently the most accurate neuroimaging technique available for the detection of brain and spinal cord lesions in neurologic type 2 Decompression sickness. Rapid bubble formation in tissues and the bloodstream during ascent is the basic pathophysiologic mechanism in Decompression Illness. These bubbles can damage the central nervous system through different mechanisms, namely arterial occlusion, venous obstruction, or in situ toxicity. Neuroimaging studies of Decompression sickness have reported findings associated with each of these mechanisms: some typical results are summarized and illustrated in this article. We also review the limitations of previous work and make practical methodologic suggestions for future neuroimaging studies.

W L Morrison - One of the best experts on this subject based on the ideXlab platform.

  • Relationship between right-to-left shunts and cutaneous Decompression Illness.
    Clinical science (London England : 1979), 2001
    Co-Authors: Peter Wilmshurst, Matthew Pearson, Kevin P. Walsh, W L Morrison, P. Bryson
    Abstract:

    The presence of a large right-to-left shunt is associated with neurological Decompression Illness after non-provocative dives, as a result of paradoxical gas embolism. A small number of observations suggest that cutaneous Decompression Illness is also associated with a right-to-left shunt, although an embolic aetiology of a diffuse rash is more difficult to explain. We performed a retrospective case-control comparison of the prevalence and sizes of right-to-left shunts determined by contrast echocardiography performed blind to history in 60 divers and one caisson worker with a history of cutaneous Decompression Illness, and 123 historical control divers. We found that 47 (77.0%) of the 61 cases with cutaneous Decompression Illness had a shunt, compared with 34 (27.6%) of 123 control divers (P < 0.001). The size of the shunts in the divers with cutaneous Decompression Illness was significantly greater than in the controls. Thus 30 (49.2%) of the 61 cases with cutaneous Decompression Illness had a large shunt at rest, compared with six (4.9%) of the 123 controls (P < 0.001). During closure procedures in 17 divers who had cutaneous Decompression Illness, the mean diameter of the foramen ovale was 10.9 mm. Cutaneous Decompression Illness occurred after dives that were provocative or deep in subjects without shunts, but after shallower and non-provocative dives in those with shunts. The latter individuals are at increased risk of neurological Decompression Illness. We conclude that cutaneous Decompression Illness has two pathophysiological mechanisms. It is usually associated with a large right-to-left shunt, when the mechanism is likely to be paradoxical gas embolism with peripheral amplification when bubble emboli invade tissues supersaturated with nitrogen. Cutaneous Decompression Illness can also occur in individuals without a shunt. In these subjects, the mechanism might be bubble emboli passing through an 'overloaded' lung filter or autochthonous bubble formation.

  • effect on migraine of closure of cardiac right to left shunts to prevent recurrence of Decompression Illness or stroke or for haemodynamic reasons
    The Lancet, 2000
    Co-Authors: Peter Wilmshurst, Kevin Walsh, Simon Nightingale, W L Morrison
    Abstract:

    Summary Background A relation between migraine with aura and cardiac right-to-left shunts has been reported. Right-to-left shunts are also associated with stroke and certain forms of Decompression Illness. We investigated the effect of closure of right-to-left shunts on migraine symptoms. Methods A consultant neurologist, who was unaware of information about residual shunt, undertook a structured interview with individuals who had had transcatheter closure of an atrial septal defect or patent foramen ovale to assess how the procedure affected migraine symptoms. Findings 37 of 40 consecutive patients who had had a closure procedure (to permit resumption of diving after Decompression Illness in 29, after stroke when paradoxical thromboembolism was suspected in four, or to close a large atrial septal defect in four) could be contacted. 21 (57%) had a history of migraine before the procedure (with aura in 16, without aura in five). 11 individuals had fortification spectra in the period immediately after closure. During long-term follow-up, no migraine symptoms were reported by seven individuals who had previously had migraine with aura and three who had previously had migraine without aura. Eight others who had had migraine with aura before closure reported improvement in frequency and severity of migraines. Three (one migraine with aura, two migraine without aura) reported no alteration in migraine episodes. Interpretation These observations suggest a causal association between right-to-left shunts and migraine with aura. There may be a subgroup of patients who have severe migraine associated with a large right-to-left shunt in whom closure of the atrial defect may improve or abolish migraine.

  • transcatheter closure of patent foramen ovale using the amplatzer septal occluder to prevent recurrence of neurological Decompression Illness in divers
    Heart, 1999
    Co-Authors: Kevin Walsh, Peter Wilmshurst, W L Morrison
    Abstract:

    OBJECTIVE—Large flap valve patent foramens may cause paradoxical thromboembolism and neurological Decompression Illness in divers. The ability of a self expanding Nitinol wire mesh device (Amplatzer septal occluder) to produce complete closure of the patent foramen ovale was assessed. PATIENTS—Seven adults, aged 18-60 years, who had experienced neurological Decompression Illness related to diving. Six appeared to have a normal atrial septum on transthoracic echocardiography, while one was found to have an aneurysm of the interatrial septum. METHODS—Right atrial angiography was performed to delineate the morphology of the right to left shunt. The defects were sized bidirectionally with a precalibrated balloon filled with dilute contrast. The largest balloon diameter that could be repeatedly passed across the septum was used to select the occlusion device diameter. Devices were introduced through 7 F long sheaths. All patients underwent transthoracic contrast echocardiography one month after the implant. RESULTS—Device placement was successful in all patients. Device sizes ranged from 9-14 mm. The patient with an aneurysm of the interatrial septum had three defects, which were closed with two devices. Right atrial angiography showed complete immediate closure in all patients. Median (range) fluoroscopy time was 13.7 (6-35) minutes. Follow up contrast echocardiography showed no right to left shunting in six of seven patients and the passage of a few bubbles in one patient. All patients have been allowed to return to diving. CONCLUSION—The Amplatzer septal occluder can close the large flap valve patent foramen ovale in divers who have experienced neurological Decompression Illness. Interatrial septal aneurysms with multiple defects may require more than one device. Keywords: patent foramen ovale; Decompression Illness; Amplatzer septal occluder