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Results for “Decompression sickness”

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At least 1,603 records · Page 89Linked to original sources
PubMed1999

Treatment of diving emergencies.

Recognition of condition attributable to the environmental changes experienced by divers will facilitate appropriate treatment. The diagnosis of these conditions rarely requires sophisticated imaging or electrophysiologic testing. Divers who have suspected DCI, in addition to general supportive measures, should be administered fluids and oxygen and transported to a recompression chamber. For diving-related conditions, on-line consultation is available from the Divers Alert Network, Durham, NC (919-684-8111).

Algorithms↗
PubMed2001

[Acute respiratory distress syndrome after prolonged hyperbaric oxygen therapy: a case of pulmonary oxygen toxicity?].

A 42-year-old patient was admitted to our ICU for severe decompression illness with tetraplegia. He presented an acute respiratory distress syndrome (ARDS), following a very long hyperbaric oxygen therapy (using a US. Navy Treatment Table 7). The ARDS resulted in pulmonary fibrosis, and the patient died despite maximal support in ICU. The risk of pulmonary toxicity of oxygen must be considered when using a prolonged recompression treatment table.

Acute Disease↗
PubMed2000

[Toxic-metabolic and physically-induced myelopathies].

The differential diagnosis in patients with spinal cord disorders is sometimes very difficult. There is an overview about important toxic-metabolic myelopathies, like drugs, ergotamines, Kichererbsen, avitaminosis, diving accidents and radiation exposition. Beside the cause- and the senso-motoric therapy, disturbances bladder-, bowel-, sexual and cardiovascular disorders needs a specialised therapy.

Decompression Sickness↗
PubMed1989

Memory deficit caused by compressed air equivalent to 36 meters of seawater.

Twenty-four students from a diving school undertook a hyperbaric chamber dive to a pressure equal to 36 m of seawater. Tests of cognitive function and manual dexterity, performed in the chamber during the 35-min bottom time and before, or after, the dive included immediate and delayed free recall of words presented as 7 lists of 15 each, recognition of previously presented words, number identification, and a forceps pickup of ball bearings. Delayed free recall and immediate free recall (primacy region) were significantly impaired, whereas manual dexterity and recognition memory were not. These are in keeping with previously reported findings but indicate that significant impairment of memory may occur in experienced divers at operational depths for air diving. Lack of effect on recognition memory suggests that cueing strategies might be useful for debriefing divers.

Adolescent↗
PubMed1994

Role of cardiorespiratory abnormalities, smoking and dive characteristics in the manifestations of neurological decompression illness.

1. Blind analysis of contrast echocardiograms to detect intracardiac shunts, blind analysis of lung function tests for evidence of small airways disease, smoking history and dive characteristics were examined in an attempt to explain neurological symptoms that occurred within 5 min of surfacing from unprovocative dives. 2. Pulmonary abnormalities were significantly more frequent in those divers without intracardiac shunts (50%) than in those with shunts (0%). Smoking was more common in those divers without shunts (55% versus 15%), although this just failed to reach conventional significance levels. Divers without shunts experienced cerebral rather than spinal symptoms after significantly shallower dives with lower tissue nitrogen loads. Depths of dives, tissue nitrogen loads and clinical manifestations in those divers without shunts were similar to the findings in divers who had symptoms after rapid ascents. Despite conservative dive profiles, clinical manifestations in divers with shunts resembled those observed after missed decompression stops. 3. The findings suggest that occult lung disease, and probably smoking, increase the risk of neurological symptoms, even after unprovocative dives, and the similarity of the dive profiles and clinical manifestations to cases with rapid ascents suggest that pulmonary barotrauma and arterial gas embolism are responsible. In divers with intracardiac shunts the different dive profiles and clinical manifestations imply that there is another mechanism, involving different tissue and bubble nitrogen kinetics resulting in venous gas liberation and peripheral amplification in embolized tissues, rather than paradoxical embolism per se.

Adult↗