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At least 919 records · Page 51Linked to original sources
PubMed2005

Exercise-induced intrapulmonary shunting of venous gas emboli does not occur after open-sea diving.

Paradoxical arterializations of venous gas emboli can lead to neurological damage after diving with compressed air. Recently, significant exercise-induced intrapulmonary anatomical shunts have been reported in healthy humans that result in widening of alveolar-to-arterial oxygen gradient. The aim of this study was to examine whether intrapulmonary shunts can be found following strenuous exercise after diving and, if so, whether exercise should be avoided during that period. Eleven healthy, military male divers performed an open-sea dive to 30 m breathing air, remaining at pressure for 30 min. During the bottom phase of the dive, subjects performed mild exercise at approximately 30% of their maximal oxygen uptake. The ascent rate was 9 m/min. Each diver performed graded upright cycle ergometry up to 80% of the maximal oxygen uptake 40 min after the dive. Monitoring of venous gas emboli was performed in both the right and left heart with an ultrasonic scanner every 20 min for 60 min after reaching the surface pressure during supine rest and following two coughs. The diving profile used in this study produced significant amounts of venous bubbles. No evidence of intrapulmonary shunting was found in any subject during either supine resting posture or any exercise grade. Also, short strenuous exercise after the dive did not result in delayed-onset decompression sickness in any subject, but studies with a greater number of participants are needed to confirm whether divers should be allowed to exercise after diving.

Adaptation, Physiological↗
PubMed1984

Loss of cabin pressure in Canadian Forces ejection seat aircraft, 1962-1982.

A review of all aircraft accidents and incidents in the Canadian Forces over the last 20 years (1962-1982) has been carried out. There have been 47 cases of serious loss of cabin pressurization in ejection seat equipped aircraft. Altitudes varied from 15,000 to 54,000 ft (4,572-16,459 m). No one aircraft appears to be more vulnerable. The most common cause was problems with the canopy seal (25%). There were three cases of hypoxia and two cases of decompression sickness. No deaths or permanent injuries occurred. Loss of pressurization is an extremely low, but definite risk to the pilot and aeromedical training with practical demonstration in the hypobaric chamber should continue.

Accidents, Aviation↗
PubMed1989

[Emergency treatment in decompression accidents in shipyards].

The Comex company has underwater workplaces scattered over the whole world, which are therefore very often far away from a medical center equipped for the treatment of decompression sickness. However, the subsequent evolution of such an event depends mainly on how fast the first aid is given to the patient. Therefore, the scientific and medical departments of our company developed a medical handbook to be used by chiefs of working platforms. The text which has to be easily understandable, mentions: a cursory description of the clinical signs of the different decompression accidents the measures which have to be taken in each case, depending on: the moment of the emergency: after or during decompression, the presence of an insufficient decompression, or a "blow-up". The handbook contains several recompression tables, first aid treatment recommendations and drugs. It has to be stressed that these procedures are only emergency steps. They should be performed before the patient can be transferred to a medical center with expertise in the treatment of decompression accidents.

Accidents↗
PubMed1987

A likelihood analysis of experiments to test altitude decompression protocols for shuttle operations.

The principle of maximum likelihood and the method of linear regression both are used to fit mathematical models to experimental data, but likelihood can be applied to binary data such as the outcome of a decompression, whereas linear regression cannot. Maximum likelihood was applied to 548 individual altitude exposures from 30 experimental pressure profiles tested by NASA and the Air Force. Twelve decompression models were studied including modified Haldane models and models which assume that stationary bubbles cause Type I decompression sickness. The data was best represented by a model in which a bubble in tissue is surrounded by a diffusion barrier, but this representation was statistically indistinguishable from a single tissue Haldane model with a halftime of 508 min. By providing a quantitative measure of the agreement between theory and data, the principle of maximum likelihood offers an opportunity for improving the understanding of decompression mechanisms and for developing safer and faster decompression procedures.

Altitude↗
PubMed1997

Nature and incidence of bubbles in the spinal cord of decompressed goats.

The nature of so-called autochthonous bubbles was investigated. Their presence in compressed/decompressed goats was compared with that in animals killed before decompression and in controls. Ten goats (group 1) were subjected to compression/decompression in air. Clinical signs of spinal decompression sickness usually occurred. Within 35 min of surfacing, the animals were given a lethal dose of thiopentone sodium, i.v.. Spinal cords were fixed by immersion in 10% formol saline. Histologically autochthonous bubbles appeared to arise from rupture of over-distended blood vessels. The incidence of grossly dilated empty vessels (GDEV) was recorded. Seven goats (group 2) were similarly compressed but killed before decompression. In five animals of group 1 there was a greater number of GDEV than in controls (group 3, seven animals) but in the other five animals the incidence was similar to the controls. The incidence of GDEV in group 2 was greater than in the controls (P < 0.05). The percentage of sections of spinal cord in which the meninges also contained GDEV was assessed. In all except two animals in group 1, the percentage was higher than in the controls, whereas in group 2 the percentage was higher than in the controls. The experiments show that autochthonous bubbles arise as an artifact and that intravascular bubbles arise in situ.

Animals↗
PubMed2001

Neurologic complications of scuba diving.

Recreational scuba diving has become a popular sport in the United States, with almost 9 million certified divers. When severe diving injury occurs, the nervous system is frequently involved. In dive-related barotrauma, compressed or expanding gas within the ears, sinuses and lungs causes various forms of neurologic injury. Otic barotrauma often induces pain, vertigo and hearing loss. In pulmonary barotrauma of ascent, lung damage can precipitate arterial gas embolism, causing blockage of cerebral blood vessels and alterations of consciousness, seizures and focal neurologic deficits. In patients with decompression sickness, the vestibular system, spinal cord and brain are affected by the formation of nitrogen bubbles. Common signs and symptoms include vertigo, thoracic myelopathy with leg weakness, confusion, headache and hemiparesis. Other diving-related neurologic complications include headache and oxygen toxicity.

Barotrauma↗
PubMed1992

Initial evaluation of the diving accident victim.

Diving accidents include air embolism and decompression sickness. Both require early stabilization and initiation of therapy before transfer to a definitive medical center for recompression therapy. Initial treatment consists of hydration, oxygen therapy and often steroids and antithrombosis therapy. Symptoms must be separated from other related conditions including myocardial infarction.

Accidents↗
PubMed1997

Spinal cord myelin is vulnerable to decompression.

Spinal cord white matter is the major site of tissue damage resulting from decompression sickness (DCS or "the bends"). Damage is thought to result from bubble nucleation within the tissue. Why DCS occurs predominantly in the spinal cord and not in the brain is not known; neither is the exact pathological mechanism by which the spinal cord is damaged, nor how multiple sclerosis (MS)-like symptoms may ensue. To investigate the molecular basis of white matter damage, we subjected myelinated mouse tissues to varying durations of decompression, and then after recompression to one atmosphere, examined them for changes in myelin structure and composition. X-ray diffraction showed that the myelin period in spinal cord decreased by 4%, whereas those of optic and sciatic nerves were stable. The change in period was accompanied by a change in membrane bilayer profile--i.e., relative to control, the width of the bilayer decreased by approximately 6 A, whereas the interbilayer spaces each increased by approximately 3 A. The changes in electron density levels suggested a redistribution of matter from the interbilayer spaces into the lipid headgroup layers. By contrast with these structural changes, sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE) and high-performance thin layer chromatography (HPTLC) revealed no noticeable change in myelin composition--i.e., there was no release of myelin-specific proteins or lipids. Our findings indicate that spinal cord myelin has an inherent structural vulnerability that may facilitate the targeting of this tissue during pressure changes.

Animals↗
PubMed1993

[The pulmonary manifestations of diving accidents].

Scuba diving is associated with risks of drowning, lung barotrauma and decompression sickness. In case of near-drowning, irreversible neurologic lesions or death may follow an acute hypoxemia or a cardiopulmonary arrest. Therefore, victims of drowning should benefit from an immediate and prolonged cardiopulmonary resuscitation. Lung barotrauma are due to the failure of expanding lung gases to escape during ascent; they are likely to be complicated by arterial gas embolism. They can follow a panic ascent even from a shallow depth. Most of decompression procedures induce the formation of asymptomatic venous gas bubbles, normally filtrated and eliminated by the lungs. In case of massive intravenous bubbling, the filtering capacity of the lungs can be overwhelmed and the lung microcirculation damaged up to the point of provoking a cardio-respiratory failure.

Adult↗
PubMed1994

Unexplained muscle swelling in divers.

Muscle swelling in divers may represent a previously unreported form of decompression sickness. It shows marked, brawny swelling of skeletal muscle which clinically most suggests muscular lymphedema in its woody texture to palpation and unresponsiveness to recompression. Four episodes of unexplained muscle swelling in commercial divers are presented, none apparently resulting in muscular injury.

Adult↗
PubMed1998

The influence of an arterial and venous air embolism on the hearing level in laboratory mini pigs.

We examined the influence of an experimental venous and arterial air embolism on the hearing level in laboratory mini pigs. Before and after the injection of air a threshold ABR was measured in anaesthetized mini pigs (n=15). A venous air embolism was performed in 6 animals: no changes in the hearing level or in the interpeak latencies Jewett wave V-I were observed in any of the animals before, during or after the application of air. In 9 animals the arterial embolism was done, 2 animals died and had to be excluded. In 6 animals out of 7 a hearing loss was observed starting after the injection of 40 ml air and finally ending in deafness for these 6 animals. The detected hearing loss is probably of cochlear origin, as no prolongations of the interpeak latencies of Jewett wave V-I at 90 dB HL were observed prior to the deafness. Our results show that air bubbles in the arterial circulation lead to cochlear damage ending in deafness. Our research indicates that decompression sickness, which is comparable to the arterial air embolism, is more often the cause of a sensorineural hearing loss after diving than previously believed.

Animals↗
PubMed1999

Electroencephalography and magnetic resonance imaging after diving and decompression incidents: a controlled study.

Electroencephalography and magnetic resonance imaging after diving and decompression incidents: a controlled study. Undersea Hyper Med 1999.; 26(2):61-65.--Diving incidents with symptoms of decompression sickness (DCS) and/or arterial gas emboli (AGE) might increase the degree of pathologic change in the electroencephalogram (EEG) or magnetic resonance imaging (MRI) of the supraspinal central nervous system (CNS). Diving itself, even without known symptoms of DCS and/or AGE, has been proposed to increase the number of CNS lesions using either EEG or MRI. In the first part of a two-part study we examined the effects of recompression treatment on EEG in decompression incidents in a group of sport and professional divers compared with a control group of healthy naval divers. In the second part we recorded brain MRI from three groups of volunteers: 1) divers who were treated for DCS in pressure chamber, 2) divers who had never had symptoms of DCS (and/or AGE), and 3) healthy normal controls who were not divers. Our results indicate that DCS increases the incidence of pathologic EEG recordings, whereas recompression treatment decreases them. The results of MRI do not verify evidence of increased numbers of CNS lesions in normal divers as compared to non-diving, healthy control subjects, whereas some of the divers treated for DCS in a pressure chamber had hyperintense lesions in brain white matter. None of them had any abnormalities in EEG, neurologic performance, or psychologic behavior. Both EEG and MRI are sensitive and non-specific methods for judging suspected evidence of brain lesions from diving or diving accidents.

Adult↗
PubMed1996

[Developing and testing of decompression regimes for caisson operations while constructing Moscow metro].

Decompression regimes for caisson operations at the pressures up to 5 ata exceeding duration of the regimes specified in the caisson regulations have been developed. The regimes were tested and validated in dry altitude chamber with participation of exercising human subjects. Seventeen test-subjects took part in 54 tests. No symptoms of decompression sickness were documented. Air embolism was observed in 28 +/- 6% of cases at rest and in 72 +/- 6% of cases following provocative leg movements. The air embolism expression tended to increase with exposure to pressure.

Adaptation, Physiological↗
PubMed1999

Infraorbital hypesthesia after maxillary sinus barotrauma.

We report a case of a diver who suffered an episode of maxillary sinus barotrauma that presented with decreased sensation over the cutaneous distribution of the infraorbital nerve after an ascent which produced facial pain and crepitus. This case illustrates a potential confusion between a decompression sickness etiology and a barotraumatic etiology for the observed sensory deficit. The clinical features of this case were most consistent with a barotraumatic etiology for the findings noted. The anatomy of the trigeminal nerve and previous reports of cranial nerve deficits following barotrauma are reviewed.

Barotrauma↗
PubMed1991

Visual evoked and brain stem auditory evoked potentials in divers.

Visual evoked potentials (VEP) were examined in 14 divers during dives to 360 metres of seawater (msw). All latencies increased significantly with depth. VEP and brain stem auditory evoked potentials (BAEP) were similarly examined in 18 divers before and after these dives. N75 was significantly increased after compared to before the dive, while there was no significant difference in the P100 and N145 latencies. BAEP I-V latency was significantly decreased after the dives. VEP and BAEP were examined in 156 divers and 99 controls. There was no significant difference in VEP. BAEP I-III interpeak latency was significantly increased for the divers, but with no significant changes in I-V and III-V latencies. VEP and BAEP were examined in 26 divers after treatment for neurological decompression sickness. There was no significant difference compared to the control group. The conclusions are that VEP and BAEP change transitorily with influence of hyperbaric pressure, but do not measure major permanent disturbances in the divers' visual and auditory pathways.

Adult↗
PubMed2004

[Patent foramen ovale: an underrated risk for divers?].

The foramen ovale which is the fetal connection between the right and left atrium persists in about 30 % of the adult population. In the presence of a persistent foramen ovale (PFO) shunting of blood may occur from the right to the left atrium, and bubbles can reach the systemic circulation during or after the decompression phase of a dive with compressed air. Therefore, divers with PFO may have an increased risk to develop ischemic cerebral lesions and neurologic decompression sickness (DCS). Significant right-to-left shunting may be diagnosed using transcranial doppler ultrasound of the medial cerebral artery and echocardiography with echo contrast media and Valsalva provocation. However, there are no official guidelines concerning PFO screening in medical fitness exams for professional or recreational divers in Germany. Therefore, it remains in the diver's choice to be screened for PFO. Divers with a history of DCS should be monitored for PFO, especially when diving strictly adhered to decompression tables. Divers with PFO who refuse to stop diving after DCS should be advised to adhere to very save dive profiles.

Decompression Sickness↗
PubMed2006

Haemodynamic changes induced by submaximal exercise before a dive and its consequences on bubble formation.

OBJECTIVES: To evaluate the effects of a submaximal exercise performed 2 h before a simulated dive on bubble formation and to observe the haemodynamic changes and their influence on bubble formation. PARTICIPANTS AND METHODS: 16 trained divers were compressed in a hyperbaric chamber to 400 kPa for 30 min and decompressed at a rate of 100 kPa/min with a 9 min stop at 130 kPa (French Navy MN90 procedure). Each diver performed two dives 3 days apart, one without exercise and one with exercise before the dive. All participants performed a 40 min constant-load submaximal and calibrated exercise, which consisted of outdoor running 2 h before the dive. Circulating bubbles were detected with a precordial Doppler at 30, 60 and 90 min after surfacing. Haemodynamic changes were evaluated with Doppler echocardiography. RESULTS: A single bout of strenuous exercise 2 h before a simulated dive significantly reduced circulating bubbles. Post-exercise hypotension (PEH) was observed after exercise with reductions in diastolic and mean blood pressure (DBP and MBP), but total peripheral resistance was unchanged. Stroke volume was reduced, whereas cardiac output was unchanged. Simulated diving caused a similar reduction in cardiac output independent of pre-dive exercise, suggesting that pre-dive exercise only changed DBP and MBP caused by reduced stroke volume. CONCLUSION: A single bout of strenuous exercise 2 h before a dive significantly reduced the number of bubbles in the right heart of divers and protected them from decompression sickness. Declining stroke volume and moderate dehydration induced by a pre-dive exercise might influence inert gas load and bubble formation.

Adult↗
PubMed2002

Internal carotid artery dissection in stroke from SCUBA diving: a case report.

Although diving with compressed air is generally safe, neurological problems resulting from infarction in SCUBA diving are well known, including arterial gas embolism and decompression sickness (caisson's disease, bends) involving the brain and spinal cord. While air gas embolism forms the overwhelming majority of causes for stroke in divers, internal carotid artery (ICA) dissection is another potential mechanism for central nervous system infarction in the setting of SCUBA diving. A 38 year-old female, who presented with complaints of headache, nausea, vomiting, and left sided hemiparesis after rapid ascent to the surface from a depth of 120 feet of seawater was initially treated for decompression illness in a hyperbaric chamber. Further neurological workup revealed a right ICA dissection. This case demonstrates the dangers of ICA dissection following rapid ascent to the surface from underwater and emphasizes an interesting presentation of stroke associated with SCUBA diving.

Adult↗