scubadoc Ten Foot Stop

January 30, 2009

DNA Damage from Hyperbaric Oxygen Exposure?

Filed under: Article, Newsscubadoc @ 4:47 pm

DNA damage after long-term repetitive hyperbaric oxygen exposure.   
MED   09-11   200919023023  NDN- 230-0919-4585-0

AUTHORS- Groeger, Michael; Oter, Soukrou; Simkova, Vladislava; Bolten, Markus; Koch, Andreas; Warninghoff, Volker; Georgieff, Michael; Muth, Claus-Martin; Speit, Gounter; Radermacher, Peter

JOURNAL NAME- J Appl Physiol
VOLUME 106
NUMBER 1
PUBLICATION DATE- 2009 Jan
PP 311-5
DOCUMENT TYPE- Journal Article
JOURNAL CODE- 8502536
JOURNAL SUBSET- MEDJSIM
ISSN- 8750-7587
CORPORATE AUTHOR- Sektion Anoasthesiologische Pathopyhsiologie und Verfahrensentwicklung Universitoatsklinikum, Parkstrasse 11, D-89073 Ulm, Germany. peter.radermacher@uni-ulm.de).
PUBLICATION COUNTRY- United States
LANGUAGE- English

A single exposure to hyperbaric oxygen (HBO), i.e., pure oxygen breathing at supra-atmospheric pressures, causes oxidative DNA damage in humans in vivo as well as in isolated lymphocytes of human volunteers. These DNA lesions, however, are rapidly repaired, and an adaptive protection is triggered against further oxidative stress caused by HBO exposure. Therefore, we tested the hypothesis that long-term repetitive exposure to HBO would modify the degree of DNA damage. Combat swimmers and underwater demolition team divers were investigated because their diving practice comprises repetitive long-term exposure to HBO over years. Nondiving volunteers with and without endurance training served as controls. In addition to the measurement of DNA damage in peripheral blood (comet assay), blood antioxidant enzyme activities, and the ratio of oxidized and reduced glutathione content, we assessed the DNA damage and superoxide anion radical (O(2)(*-)) production induced by a single ex vivo HBO exposure of isolated lymphocytes. All parameters of oxidative stress and antioxidative capacity in vivo were comparable in the four different groups. Exposure to HBO increased both the level of DNA damage and O(2)(*-) production in lymphocytes, and this response was significantly more pronounced in the cells obtained from the combat swimmers than in all the other groups. However, in all groups, DNA damage was completely removed within 1 h. We conclude that, at least in healthy volunteers with endurance training, long-term repetitive exposure to HBO does not modify the basal blood antioxidant capacity or the basal level of DNA strand breaks. The increased ex vivo HBO-related DNA damage in isolated lymphocytes from these subjects, however, may reflect enhanced susceptibility to oxidative DNA damage.

===============================================================

January 29, 2009

Decompression illness without gas bubbles!!??

Filed under: Article, Newsscubadoc @ 4:38 pm

Gas bubbles may not be the underlying cause of decompression illness - The at-depth endothelial dysfunction hypothesis.

Madden LA, Laden G.

Postgraduate Medical Institute, University of Hull, Cottingham Road, Hull HU6 7RX, UK.

Med Hypotheses. 2009 Jan 5. [Epub ahead of print]

Gas formed in tissues and the circulating blood due to decompression is thought to be a significant factor in the progression of decompression illness (DCI). DCI is a potential problem for a growing population of professional and recreational divers. We hypothesise that these gas bubbles are not the causative agent in progression of DCI, rather an exacerbating factor. Endothelial dysfunction caused by a temporary loss of haemostasis due to increased total oxidant status is postulated to be the cause in this at-depth endothelial dysfunction hypothesis. Breathing oxygen at any pressure increases the oxidant status in the circulation causing vasoconstriction; this increase can be prevented by antioxidants, such as Vitamin C, maintaining haemostasis and preventing activation of endothelium, leukocyte recruitment and subsequent localised inflammation. Bubbles have the potential to exacerbate the situation on decompression by damaging the vascular endothelium either through ischemia/reperfusio n, physical contact with the endothelium or by an increase in shear stress. Furthermore, this damage may manifest itself in the release of endothelial membrane fragments (microparticles) .

PMID: 19128890 [PubMed - as supplied by publisher]

 

Editor’s comment: The chicken before the egg - or vice versa??

January 25, 2009

Several Articles on the Benefits of Exercise on Scuba Diving

Filed under: Articlescubadoc @ 12:37 pm

Exerc Sport Sci Rev. 2008 Jan;36(1):38-42.

Beneficial role of exercise on scuba diving.

Department of Physiology, University of Split School of Medicine, Split, Croatia. zdujic@bsb.mefst.hr

Exercising before, during, or after diving is proscribed because of the assumption that it would increase incidence of decompression sickness. Our findings show that exercise performed in a timely fashion before diving or during decompression will reduce the number of venous gas bubbles formed. Exercise after diving did not increase the number of bubbles. Nitric oxide seems to play a protective role.

 ==========================================================

Aviat Space Environ Med. 2006 Jun;77(6):592-6

Venous bubble count declines during strenuous exercise after an open sea dive to 30 m.

Dujić Z, Obad A, Palada I, Ivancev V, Valic Z.

Department of Physiology, University of Split School of Medicine, Croatia. zdujic@bsb.mefst.hr

INTRODUCTION: The effect of post-dive exercise on bubble formation remains controversial, although the current practice of divers and aviators is to avoid strenuous exercise after diving. Previously, we have shown that exercising 24 h before a dive, or during a decompression stop, significantly reduces bubble formation in man. The objective of this study was to determine whether a short period of strenuous post-dive exercise promotes venous bubble formation. METHODS: Seven male military divers performed an open-sea field dive to a maximum depth of 30 m for 30 min. At maximum depth, subjects performed mild underwater fin swimming, followed by standard decompression. Diving was followed by a post-dive exercise session consisting of short, strenuous incremental upright cycle ergometry, up to 85% of maximal oxygen uptake, for about 10 min. Subjects were monitored for venous gas bubbles in the right heart with an echo-imaging system starting 20 min post-dive while in the supine position, during cycle ergometry in the seated upright position, and immediately after exercise in a supine position. RESULTS: The average number of bubbles was 1.5 +/- 1.4 bubbles x cm(-2) 20 min after diving. Changes in posture from supine to seated upright resulted in significant reduction of bubbles to 0.6 +/- 1.3 bubbles x cm(-2) (p = 0.043), with further reduction to 0.2 +/- 0.3 bubbles x cm(-2) at the end of exercise (p = 0.02). No cases of DCS or intra-pulmonary shunt were observed during or following post-dive exercise. DISCUSSION: These results suggest that post-dive strenuous exercise after a single field dive reduces post-dive gas bubble formation in well-trained military divers. Additional findings are needed for normal sports divers.

=======================================================

J Physiol. 2004 Mar 16;555(Pt 3):637-42. Epub 2004 Jan 30.Click here to read Click here to read

Comment in:
J Physiol. 2004 Mar 16;555(Pt 3):588.

Aerobic exercise before diving reduces venous gas bubble formation in humans.

Dujic Z, Duplancic D, Marinovic-Terzic I, Bakovic D, Ivancev V, Valic Z, Eterovic D, Petri NM, Wisløff U, Brubakk AO.

Department of Physiology and Biophysics, University of Split School of Medicine, Split, Croatia. zdujic@bsb.mefst.hr

We have previously shown in a rat model that a single bout of high-intensity aerobic exercise 20 h before a simulated dive reduces bubble formation and after the dive protects from lethal decompression sickness. The present study investigated the importance of these findings in man. Twelve healthy male divers were compressed in a hyperbaric chamber to 280 kPa at a rate of 100 kPa min(-1) breathing air and remaining at pressure for 80 min. The ascent rate was 9 m min(-1) with a 7 min stop at 130 kPa. Each diver underwent two randomly assigned simulated dives, with or without preceding exercise. A single interval exercise performed 24h before the dive consisted of treadmill running at 90% of maximum heart rate for 3 min, followed by exercise at 50% of maximum heart rate for 2 min; this was repeated eight times for a total exercise period of 40 min. Venous gas bubbles were monitored with an ultrasonic scanner every 20 min for 80 min after reaching surface pressure. The study demonstrated that a single bout of strenuous exercise 24h before a dive to 18 m of seawater significantly reduced the average number of bubbles in the pulmonary artery from 0.98 to 0.22 bubbles cm(-2)(P= 0.006) compared to dives without preceding exercise. The maximum bubble grade was decreased from 3 to 1.5 (P= 0.002) by pre-dive exercise, thereby increasing safety. This is the first report to indicate that pre-dive exercise may form the basis for a new way of preventing serious decompression sickness.

=========================================================

J Appl Physiol. 2005 Sep;99(3):944-9. Epub 2005 Apr 21.

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

Dujić Z, Palada I, Obad A, Duplancić D, Brubakk AO, Valic Z.

Dept. of Physiology and Biophysics, Univ. of Split School of Medicine, Soltanska 2, 21000 Split, Croatia. zdujic@bsb.mefst.hr

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.

========================================================

January 23, 2009

Bubble trouble: a review of diving physiology and disease

Filed under: Uncategorizedscubadoc @ 2:34 pm

I have run across a good review article in the Postgraduate Medicine Journal that is free for all readership. It has a very good list of references and can be seen at http://pmj.bmj.com/cgi/content/full/84/997/571

D Z H Levett 1, I L Millar 2 1 Centre for Altitude, Space and Extreme Environment Medicine, UCL, London, UK
2 Hyperbaric Service, The Alfred Hospital, Melbourne, Australia

Correspondence to:
Dr D Levett, Centre for Altitude, Space and Extreme Environment Medicine, UCL, 1st Floor Charterhouse Building, Archway Campus, Highgate Hill, London N19 5LW, UK; denny.levett@ucl.ac.uk

Submitted 14 May 2008
Accepted 18 August 2008


*    ABSTRACT
 TOP
 ABSTRACT
 TYPES OF DIVING
 PHYSICAL AND PHYSIOLOGICAL…
 DIVING GASES: CHARACTERISTICS…
 DIVING DISEASES: AETIOLOGY AND…
 PREVENTION AND TREATMENT OF…
 NEW DEVELOPMENTS AND POTENTIAL…
 SUMMARY
 REFERENCES

Exposure to the underwater environment for recreational or occupational purposes is increasing. Approximately 7 million divers are active worldwide and 500 000 more are training every year. Diving related illnesses are consequently an increasingly common clinical problem with over 1000 cases of decompression illness reported annually in the USA alone. Divers are exposed to a number of physiological risks as a result of the hyperbaric underwater environment including: the toxic effects of hyperbaric gases, the respiratory effects of increased gas density, drowning, hypothermia and bubble related pathophysiology. Understanding the nature of this pathophysiology provides insight into physiological systems under stress and as such may inform translational research relevant to clinical medicine. We will review current diving practice, the physics and physiology of the hyperbaric environment, and the pathophysiology and treatment of diving related diseases. We will discuss current developments in diving research and some potential translational research areas.


Keywords: barotrauma; decompression sickness; diving; hyperbaric oxygen; scuba

Diving exposes humans to immersion and to elevated ambient pressures, which result in a range of physiological effects and potentially pathophysiological sequelae over and above the risk of drowning. Despite these challenges, recreational scuba diving is popular. The world’s largest diver training agency, PADI, certifies approximately 500 000 new divers annually and it is estimated that around 7 million divers are currently active worldwide. Although modern equipment and training have made diving relatively safe, an average of 100 diving related deaths and 1100 cases of decompression illness are reported annually in the USA alone.1 In addition to recreational diving, many dives are undertaken for scientific, seafood harvesting, construction, maintenance, filming, military, forensic and rescue purposes. Currently, the challenging forms of occupational diving associated with offshore oilfield exploration and construction are undergoing a major resurgence.

This review will address:

  • the types of diving practised today
  • the physical and physiological effects of the underwater environment
  • the breathing gases used by divers and their toxic effects
  • the aetiology and pathophysiology of diving diseases
  • the management principles of diving diseases
  • current developments in diving research and areas of translational research.

January 22, 2009

From the UK: Divers Open Day, Monday 9th February 2009

Filed under: Uncategorizedscubadoc @ 11:55 am

 Steve McKenna sends us the following valuable information for UK divers subscribing to our Ten Foot Stop weblog:

Divers Open Day

Monday 9th February 2009

Diver trainers from all agencies welcome
Come along, listen to our presentations and visit our chamber

·       DCI signs, symptoms, doctor evaluation and treatments by our specialist hyperbaric doctors

·       Coastguard Presentation

·       Dive tables and Decompression by Mark Ellyott

·       Preventative Measures and Good dive practice by Wayne Ford, Hyperbaric Supervisor

·       Police Divers Talk by Steve McKenna

·       Crisis/Accident Management and Risk Assessments by Lee Griffiths

·       Diver Emergency Service UK and our other services by Jane Stevens

·       Chamber Tour

The open day will take place in the Medical Education Centre, Whipps Cross University Hospital. Leytonstone, London, E11 1NR

Admission is free, but booking is essential to guarantee your place as number are limited due to high update of places already. Please contact our organiser, Jane Stevens, on 020 8539 1222 or email her at mail@londonhyperbaric.com.


January 19, 2009

Interesting Information from UHMS vis a vis BC-BS

Filed under: Uncategorizedscubadoc @ 5:47 pm

BlueCross/BlueShield Information

As you are aware, several of the regional BlueCross BlueShield affiliated insurance companies have responded to a change in the national coverage policy for use of hyperbaric oxygen treatment recommended by the BlueCross BlueShield Association. We do not know the full extent to which local BlueCross BlueShield companies have adopted these recommendations, which are summarized below.

Those conditions moved to the investigational category include:

  • Radiation necrosis (osteoradionecrosis and soft tissue radiation necrosis)
  • Refractory mycoses (mucormycosis, actinomycisis, canidiobolus coronato)
  • Cerebral edema
  • Chronic refractory osteomyelitis and acute osteomyelitis refractory to standard medical management
  • Acute peripheral arterial insufficiency
  • Necrotizing soft tissue infections
  • Carbon monoxide poisoning (see statement below)

Here are the current (03.2005) nationally recommended coverage guidelines for adjunctive hyperbaric oxygen treatment…

Systemic hyperbaric oxygen pressurization may be considered medically necessary in the treatment of the following conditions:

  1. Non-healing diabetic wounds of the lower extremities in patients who meet the following 3 criteria:
    1. Patient has type I or type II diabetes and has a lower extremity wound that is due to diabetes;
    2. Patient has a wound classified as Wagner grade 3 or higher*; and
    3. Patient has no measurable signs of healing after 30 days of an adequate course of standard wound therapy.
  2. Acute traumatic ischemia
  3. Decompression sickness
  4. Gas embolism, acute
  5. Cyanide poisoning, acute
  6. Gas gangrene (i.e., clostridial myonecrosis)
  7. Profound anemia with exceptional blood loss: only when blood transfusion is impossible or must be delayed

* The Wagner classification system of wounds is defined as follows: grade 0 = no open lesion; grade 1 = superficial ulcer without penetration to deeper layers; grade 2 = ulcer penetrates to tendon, bone, or joint; grade 3 = lesion has penetrated deeper than grade 2 and there is abscess, osteomyelitis, pyarthrosis, plantar space abscess, or infection of the tendon and tendon sheaths; grade 4 = wet or dry gangrene in the toes or forefoot; grade 5 = gangrene involves the whole foot or such a percentage that no local procedures are possible and amputation (at least at the below the knee level) is indicated.

Hyperbaric oxygen pressurization is considered investigational in the treatment of acute carbon monoxide poisoning. Note: While evidence for the treatment of acute carbon monoxide poisoning with hyperbaric oxygen pressurization has failed to demonstrate improved health outcomes, this technology is accepted in medical practice as a standard medical therapy for the treatment of carbon monoxide poisoning.

Hyperbaric oxygen pressurization is considered investigational in the treatment of the following conditions:

  • Compromised skin grafts or flaps;
  • Chronic refractory osteomyelitis and acute osteomyelitis, refractory to standard medical management;
  • Necrotizing soft-tissue infections;
  • Acute thermal burns;
  • Spinal cord injury;
  • Traumatic brain injury;
  • Severe or refractory crohn’s disease;
  • Brown recluse spider bites;
  • Bone grafts;
  • Carbon tetrachloride poisoning, acute;
  • Cerebrovascular accident, acute (thrombotic or embolic);
  • Fracture healing;
  • Hydrogen sulfide poisoning;
  • Intra-abdominal and intracranial abscesses;
  • Lepromatous leprosy;
  • Meningitis;
  • Pseudomembranous colitis (antimicrobial agent-induced colitis);
  • Radiation myelitis, cystitis enteritis, or proctitis;
  • Sickle cell crisis and/or hematuria;
  • Demyelinating diseases, e.g., multiple sclerosis, amyotrophic lateral sclerosis;
  • Retinal artery insufficiency, acute;
  • Retinopathy, adjunct to scleral buckling procedures in patients with sickle cell peripheral retinopathy and retinal detachment;
  • Pyoderma gangrenosum
  • Acute arterial peripheral insufficiency
  • Acute coronary syndromes and as an adjunct to percutaneous coronary interventions
  • Acute ischemic stroke
  • Idiopathic sudden sensorineural hearing loss
  • Radiation necrosis (osteoradionecrosis and soft tissue radiation necrosis);
  • Refractory mycoses: mucormycosis, actinomycosis, canidiobolus coronato;
  • Cerebral edema, acute;
  • Migraine;
  • In vitro fertilization; and
  • Cerebral palsy.

The UHMS is taking the following actions regarding this critical issue:

  1. We need to understand the extent of the problem. Since commercial insurance companies are not required to make their internal medical policies public, the only way we will know the extent of the problem is to have our member physicians report to us any notices of policy changes under consideration or actual denials for hyperbaric oxygen treatment based on non-coverage. To do that, we are requesting that you fax any BlueCross BlueShield communication (claim denial letter, etc., after removing patient specific identifying information) to Tom Workman, Director, Quality Assurance & Regulatory Affairs, at 1-210-404-1535. We will tabulate this information to give us a better idea of the scope of this problem. Also, your communication with Tom will help us identify member physician contacts to assist the Society in meeting with individual BlueCross BlueShield medical directors. Please also provide for us the name of your BlueCross BlueShield associated insurance company medical director and his contact information.
  2. The Society will provide you over the next few weeks (on request) a sample letter for each of the primary denied coverage indications summarizing the critical clinical information supporting the use of hyperbaric oxygen treatment and a brief bibliography of pertinent references with commentary if needed.
  3. We will also be providing you with a process outline to follow in submitting your appeal and in working with the UHMS to assist you with additional information as needed.
  4. On the national level, the UHMS is in the process of developing a detailed response to BlueCross BlueShield to be presented at the national and regional level.

The Society will keep you informed of our actions and the responses provided by various BlueCross BlueShield affiliated companies as well as the availability of the resources mentioned above. Watch the UHMS website (www.uhms.org) or your email for these updates.

Dysbaric Osteonecrosis in Dive Masters and Instructors

Filed under: Uncategorizedscubadoc @ 5:40 pm

Aviat Space Environ Med. 2007 Dec;78(12):1150-4.Links

Dysbaric osteonecrosis in experienced dive masters and instructors.

Cimsit M, Ilgezdi S, Cimsit C, Uzun G.

Department of Underwater and Hyperbaric Medicine, Faculty of Medicine, Istanbul University, Istanbul, Turkey.

INTRODUCTION: Dysbaric osteonecrosis (DON) is a type of aseptic bone necrosis of long bones such as the humerus, femur, and tibia. It is observed in workers who perform in high-pressure environments. METHODS: There were 58 volunteer divers included in this study who had performed at least 500 dives, were working as a dive master or instructor, had never performed industrial and commercial dives, and did not have a diagnosis of osteonecrosis. Radiological evaluation was performed according to the guidelines suggested by The British Research Council Decompression Sickness Panel. A total of eight X-rays were taken per patient. When suspicious lesions were detected, MRI of the region was performed. RESULTS: Of the 58 divers, 2 were eliminated because of inadequate X-ray studies. A total of 18 DON lesions were detected in 14 of 56 (25%) divers. Age was the only variable independently associated with the development of DON (P < 0.05). DISCUSSION: The DON prevalence of 25% in this study is high considering the dive instructors had thorough diving training and strictly practiced the decompression rules. We believe this high prevalence is a result of frequent and sometimes deep dives for many years. Our findings raise the question of whether these divers can be seen as “sports divers” or should be seen as “occupational divers.” If the latter description is approved, dive masters and instructors should be kept under periodic screening for DON lesions just like professional commercial divers to help reduce the morbidity associated with this disease.

UK Diving Deaths Down

Filed under: Uncategorizedscubadoc @ 5:39 pm
   

The number of diving deaths in UK waters has dropped, with only ten fatalities reported in the 2008 BSAC Diving Incidents Report. This compares with 12 diving-related deaths in 2007 and a national average of 17.3 over the previous decade.

Brian Cumming, presenting the report findings at the BSAC Diving Officers’ Conference in London, was cautious, adding that the number of fatalities were still in line with previous years.

‘Although it is good that this number is way below the average of recent years, it hides the sad fact that six of these people were BSAC members,’ Cumming said. ‘The ten-year average for BSAC fatalities in the UK is six per year, and so from a members’ perspective, the year has, unfortunately, been an average one.’

Four of the five overseas fatalities recorded during the report period of October 2007 to October 2008, four were BSAC members. Six cases involved a separation of some kind, but the full details of most cases are not yet known. In one case, a diver was lost in low visibility inside a wreck; in two other cases, divers became separated from their buddies during ascent.

‘Two cases involved divers using rebreathers, and while the role of the rebreather in the incident is not clear, problems with, or misuse of, the system cannot be ruled out,’ he added.

The total number of diving incidents recorded had dropped to a below-average 359 in 2008. Decompression illness (DCI) was the most frequently recorded type of incident, with 132 cases. The number of ascent-related problems has dropped significantly, halting the increase of these problems over the last ten years.

‘It is the first time ascents have trended down, perhaps as a result of all the good work being done to pay more attention to this area,’ Cumming said. ‘I think we can pat ourselves on the back.’

Cumming noted a high number of incidents involving free-flowing regulators where divers have rushed to the surface. He said this was a situation that may have to be looked at in training.

The number of incidents involving dives to depths greater than 50m were in line with previous years. However, Cumming said, the increase in the use of mixed gas for deeper diving indicated a need to look at these cases more closely in future reports.

Boat and surface incidents remained low at 52, which Cumming said continues ‘the remarkable trend of improvement’ in this area. Of the boating incidents recorded, 43 per cent involved lost divers.

The Maritime and Coastguard Agency (MCA) and the RNLI were thanked for providing incident information. The MCA was particularly praised for its new detailed recording system.

 

Material compiled from Dive Magazine

January 7, 2009

MRI and Spinal Cord DCS

Filed under: Article, Publicationscubadoc @ 12:09 pm

MRI Findings and Clinical Outcome in 45 Divers with Spinal Cord Decompression Sickness   
BIO   12-04   PREV200900037177  NDN- 244-0571-5330-0

AUTHORS- Gempp, Emmanuel; Blatteau, Jean-Eric; Stephant, Eric; Pontier, Jean-Michel; Constantin, Pascal; Peny, Christophe

JOURNAL NAME- Aviation Space and Environmental Medicine
VOLUME 79
NUMBER 12
PUBLICATION DATE- DEC 2008
PP 1112-1116
RELEASE YEAR OR PUBLICATION YEAR- 2008
DOCUMENT TYPE- Article
ISSN- 0095-6562
ADDRESS- Ecole Plongee, BP 311, F-83800 Toulon, France
EMAIL- gempp@voila.fr
DOCUMENT URL- 10.3357/ASEM.2376.2008
LANGUAGE- English

Background: Decompression sickness (DCS) affecting the spinal cord is the most dangerous form of diving-related injury with potential sequelae. This study was conducted to evaluate the relationship between spinal cord lesions on MRI and clinical findings in divers with spinal DCS.

Methods: We studied 45 cases of DCS that were referred to Our hyperbaric facility with clinical evidence of spinal involvement during the period 2002-2007. The study included only patients who underwent MRI within 10 d of injury. The severity of spinal DCS for each patient was rated numerically for both the acute event and I mo later. The presence or absence of back pain was also noted.

Results: Spinal cord lesions were significantly more frequent in divers with severe DCS, and did not occur in any diver who experienced a favorable Outcome (sensitivity = 67%, specificity 100%, negative predictive value = 77%, positive predictive value = 100%). The presence of vertebral degenerative changes that impinged on the spinal cord was strongly associated with MRI abnormalities, but not with a negative outcome. Acute back pain was associated with hyperintense lesions and persistence of neurological sequelae OR = 14 (95%, Cl, 3.1 to 63.5) .

 Conclusion: The results show that MRI could be helpful in predicting clinical Outcome in divers with spinal cord DCS. The presence of medullary compressive factors and vertebral back pain after surfacing indicate increased likelihood of severe myelopathy with incomplete recovery.

 ==============================================================

 Other related links to spinal cord DCS on Diving Medicine Online at

http://tinyurl.com/7sdq8u

===============================================================

Predive Sauna Decreases Venous Gas Bubbles After Chamber Dives

Filed under: Article, Publicationscubadoc @ 11:58 am

Predive sauna and venous gas bubbles upon decompression from 400 kPa.

Blatteau JE, Gempp E, Balestra C, Mets T, Germonpre P.

Hyperbaric Department, Sainte-Anne Military Hospital, 544 Avenue Ernest Roller, Toulon 83200, France. je.blatteau@ infonie.fr

Aviat Space Environ Med. 2008 Dec;79(12):1100- 5.

INTRODUCTION: This study investigated the influence of a far infrared-ray dry sauna-induced heat exposure before a simulated dive on bubble formation, and examined the concomitant adjustments in hemodynamic parameters. METHODS: There were 16 divers who were compressed in a hyperbaric chamber to 400 kPa (30 msw) for 25 min and decompressed at 100 kPa x min(-1) with a 4-min stop at 130 kPa. Each diver performed two dives 5 d apart, one with and one without a predive sauna session for 30 min at 65 degrees C ending 1 h prior to the dive. Circulating venous bubbles were detected with a precordial Doppler 20, 40, and 60 min after surfacing, at rest, and after flexions. Brachial artery flow mediated dilation (FMD), blood pressure, and bodyweight measurements were taken before and after the sauna session along with blood samples for analysis of plasma volume (PV), protein concentrations, plasma osmolality, and plasma HSP70. RESULTS: A single session of sauna ending 1 h prior to a simulated dive significantly reduced bubble formation [-27.2% (at rest) to 35.4% (after flexions)]. The sauna session led to an extracellular dehydration, resulting in hypovolemia (-2.7% PV) and -0.6% bodyweight loss. A significant rise of FMD and a reduction in systolic blood pressure and pulse pressure were observed. Plasma HSP70 significantly increased 2 h after sauna completion. CONCLUSION: A single predive sauna session significantly decreases circulating bubbles after a chamber dive. This may reduce the risk of decompression sickness. Sweat dehydration, HSP, and the NO pathway could be involved in this protective effect.

PMID: 19070305 [PubMed - in process]

===============================================================

Reactivated and Maintained by Centrum Nurkowe Aquanaut Diving