scubadoc Ten Foot Stop

July 31, 2008

Article on Arterial Gas Embolism

Filed under: Uncategorizedscubadoc @ 9:31 am

Anaesth Intensive Care. 2008 Jan;36(1):60-4
Arterial gas embolism: a review of cases at Prince of Wales Hospital, Sydney, 1996 to 2006.
Trytko BE, Bennett MH.

Department of Diving and Hyperbaric Medicine, Prince of Wales Hospital, Sydney, New South Wales, Australia.

Arterial gas embolism may occur as a complication of diving or certain medical procedures. Although relatively rare, the consequences may be disastrous. Recent articles in the critical care literature suggest the non-hyperbaric medical community may not be aware of the role for hyperbaric oxygen therapy in non-diving related gas embolism. This review is part of an Australian appraisal of experience in the management of arterial gas embolism over the last 10 years. We identified all patients referred to Prince of Wales Hospital Department of Diving and Hyperbaric Medicine with a diagnosis of arterial gas embolism from 1996 to 2006. Twenty-six patient records met our selection criteria, eight iatrogenic and 18 diving related. All patients were treated initially with a 280 kPa compression schedule. At discharge six patients were left with residual symptoms. Four were left with minor symptoms that did not significantly impact quality of life. Two remained severely affected with major neurological injury. Both had non-diving-related arterial gas embolism. There was a good outcome in the majority of patients who presented with arterial gas embolism and were treated with compression.

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From scubadoc Diving Medicine Online:

Pathophysiology

Arterial gas embolism is a major cause of death in diving and the initiating cause (pulmonary barotrauma) usually goes undetected. Caused most often by the expansion of respiratory gases during ascent, it also occurs when the breath is held during ascent from a dive, when there is local pulmonary pathology, when there is dynamic airway collapse in the non-cartilaginous airways and if there is low pulmonary compliance, particularly if this is not distributed evenly throughout the lungs. Boyle’s law is the physical law controlling the event. Experimental evidence indicates that intratracheal pressures of about 10 kPa (4 fsw or 1.22 m. or ascending from 170 feet or 51.82 m. to 120 feet or 36.58 m.) are all that’s needed for it to happen. Distention of the alveoli leads to rupture, alveolar leakage of gas, and extravasation of the gas into the arterial circuit.

Origin of Bubbles

Bubbles in the arterial circulation can arise from basically three sources: venous gas embolism with breach of the pulmonary vascular filter (paradoxic gas embolism), patent foramen ovale (paradoxic gas embolism) and tear of the pulmonary parenchyma with entry of gas into pulmonary venous outflow. Studies show that systemic venous bubbles are trapped in the pulmonary arterial tree and are usually completely eliminated from that site. The lung traps the air and excretes it into alveoli from the arterioles. (RG Presson, J Appl Physiol; 1989;67(5),1898-1902)

The syndrome of paradoxic air embolism (from septal defects) was first described by J. Cohnheim in 1877. (J Cohnheim, ZV Berline, Hirschwald, 1877;1:134). Hagan at the Mayo Clinic reported on 965 normal hearts and showed that more than 25% of patients with a history of cardiac disease have a ‘probe patent’ foramen ovale at autopsy. (PT Hagan, Mayo Clinic Proc, 1984; 59:17-20.).

The other main mechanism for arterial gas embolism is by way of the pulmonary overpressure syndrome or ‘burst lung’. This occurs from baropressure increases as the diver on compressed air ascends with a closed glottis or a free diver takes a breath of compressed air at depth and ascends. Because of Boyle’s law, maximal changes in volume occur in the 4 feet (1.22 m.) closest to the surface and the diver sustains a tear in the pulmonary parenchyma with the escape of air into the pulmonary venous outflow. This can result in several outcomes: pneumothorax (collapsed lung), pneumomediastinum (air in the space around the heart), subcutaneous emphysema (bubbles of air in the fatty tissues under the skin) and air into the pulmonary capillaries.

As the diver takes his first breath after surfacing, the extra-alveolar gas enters the torn blood vessels, migrates to the left side of the heart and is distributed systemically as emboli sent to areas determined by buoyancy.

Arterial gas emboli arise from gas bubbles in the pulmonary capillaries => pulmonary veins to the left side of the heart =>possible coronary artery emboli (rare) or internal carotid and vertebro-basilar arteries to thebrain => cerebral artery embolism (blockage) with the clinical picture of a stroke.

The foam or bubbles block arteries of the 30-60 micron caliber and cause distal ischemia, with astrocyte and neuronal swelling. As the bubble passes over the endothelium, there are direct cellular effects (within 1-2 minutes) causing PMN stimulation. The bubble itself has surface effects causing local swelling, downstream coagulopathy with focal hemorrhages. There is immediate increased permeability of the blood-brain barrier, loss of cerebral auto-regulation, rise in CSF and a rise in the systemic blood pressure. A phenomenon called ‘no-reflow’ occurs with a post-ischemic impairment of microvascular perfusion. This is thought to be the result of FactorVIII interacting with the prostaglandin system and possibly other blood/tissue factors.

Clinical Manifestations

The clinical manifestations of cerebral gas embolism include a sudden onset of unconsciousness associated with a generalized or focal seizure. There is often confusion, vertigo (extreme dizziness) and cardiopulmonary arrest. In a series of 24 USN cases in which the time was known, 9 occurred during ascent in the water, 11 within one minute at the surface and 4 occurred within 3-10 minutes at the surface.

Other clinical manifestations include the sudden onset of hemiplegia (paralysis on one side), focal weakness, focal hypesthesia (loss of feeling), visual field defect (blank areas in vision), blindness, headache and cranial nerve defects (vision, hearing, eye movements, facial muscles and feeling). The operative word here is “sudden”–nearly all of these symptoms can also be caused by neurological decompression sickness. Less common manifestations are chest pain and bloody, frothy sputum.

Management Outline

Recognition *This usually occurs during or immediately after surfacing*

# Symptoms
# Bloody froth from mouth or nose
# Disorientation
# Chest pain
# Paralysis or weakness
# Dizziness
# Blurred vision
# Personality change
# Focal or generalized convulsions
# Other neurological abnormalities
# Hemoptysis (bloody sputum)
# Signs
# Bloody froth from nose or mouth
# Paralysis or weakness
# Unconsciousness
# Convulsions
# Stopped breathing
# Marbling of the skin
# Air bubbles in the retinal vessels of the eye
# Liebermeister’s sign (a sharply defined area of pallor in the tongue).
# Death

Early management

# CPR, if required
# Open airway, prevent aspiration, intubate if trained person available
# Give O2, remove only to open airway or if convulsions ensue.
# If conscious, give nonalcoholic liquids
# Place in horizontal, neutral position
# Restrain convulsing person loosely and resume O2 as soon as airway is open.
# Protect from excessive cold, heat, water or fumes.
# Transport to nearest ER for evaluation and stabilization in preparation for removal to the nearest recompression chamber.
# Call DAN (919-684-8111) or your own preferred emergency number
# Air evacuation should be at sea level pressure or as low as possible in unpressurized aircraft
# Contact hyperbaric chamber, send diver’s profile with the diver,and send all diving equipment for examination or have it examined locally.

Treatment
Recompression as soon as possible
Oxygen
Cautious hydration

July 29, 2008

HBOT Abstracts

Filed under: Uncategorizedscubadoc @ 10:11 am

Most recent abstracts are attached….

Sunny Sonnenrein
www.hyperbaric-clearinghouse.com
www.ReimersSystems.com


9 attachments — Download all attachments

Acute carbon monoxide poisoning, France.doc
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Chamber advances for delivery of HBOT, UT.doc
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HBOT and radiobiology of a C3H mouse mammary carcinoma, TX.doc
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HBOT attenuates apoptosis and decreases inflammation in an ischemic wound model, TX.doc
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HBOT improves rate of return of spontaneous circulation after prolonged normothermic porcine cardiopulmonary arrest, LA.doc
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Resolution of neurological DCI after long treatment delays, USVI.doc
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The effects of HBOT on colonic anastomosis in rats with peritonitis, Turkey.doc
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Therapeutic window of HBOT for hypoxic-ischemic brain damage, China.doc
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Validation of HBOT software for use with monoplace chambers, TX and CA.doc
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July 27, 2008

Patent Foramen Ovale Article in UHMS Journal

Filed under: Article, News, Publicationscubadoc @ 10:47 am

Undersea Hyperb Med. 2008 May-Jun;35(3):207-11

Underutilization of echocardiography for patent foramen ovale in divers with serious decompression sickness.

Harrah JD, O’Boyle PS, Piantadosi CA.

Center for Hyperbaric Medicine and Environmental Physiology, Department of Anesthesiology, Duke University Medical Center, Durham, NC, USA.

The presence of a patent foramen ovale (PFO) in compressed gas diving has been considered a risk factor for serious decompression illness (DCS) for more than 20 years. We conducted a ten year retrospective chart review aimed at determining if physicians treating DCS in a university medical center setting used echocardiography to assess PFO in patients with severe DCS, and if so whether PFO is over-represented in that population. Over the ten-year period, 113 divers underwent recompression therapy for decompression sickness. Of these patients, 48 had serious DCS defined by at least one objective neurological finding. We reviewed medical records for the presence of agitated saline contrast echocardiogram testing and whether or not PFO was present. Only 12 of 48 patients with serious DCS underwent transthoracic agitated saline contrast echocardiogram testing. Of these 12 patients, 6 (50%) had a resting PFO. Binomial proportion testing yielded 95% confidence limits of 21% and 79%. Given 27% PFO prevalence in the general population, PFO may be over-represented in our group of most seriously injured DCS patients yet 75% of patients with objective neurological signs did not undergo echocardiography.

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PFO (Patent foramen ovale) is a persistent opening in the wall of the heart which did not close completely after birth (opening required before birth for transfer of oxygenated blood via the umbilical cord). This opening can cause a shunt of blood from right to left , but more often there is a movement of blood from the left side of the heart (high pressure) to the right side of the heart (low pressure).

People with shunts are less likely to develop fainting or low blood pressure with diving than are obstructive valve lesions (such as mitral valve stenosis or aortic stenosis), but are more likely to develop fluid accumulation in the lungs from heart failure and severe shortness of breath from the effects of combined exercise and water immersion.

Ordinarily, the left to right shunt will cause no problem; the right to left shunt, if large enough, will cause low arterial O2 tension (hypoxia) and severely limited exercise capacity. In divers there is the risk of paradoxical embolism of gas bubbles (passage of bubbles into the arterial circulation) which occur in just about all divers in the venous circulation during decompression.

Blood can flow in both directions with Intra-atrial shunts at various phases of the cardiac cycle and some experts feel that a large atrial septal defect (PFO) is a contra-indication to diving. In addition, a Valsalva maneuver, used by most divers to equalize their ears during descents and ascents, can increase venous atrial pressure to the point that it forces blood containing bubbles across the PFO into the arterial circulation. Thus the usual filtering process of the lungs is by-passed.

Dr. Fred Bove, a Temple University cardiologist, did a search of the literature for patent foramen ovale in relation to diving and diving risks. His conclusion of a meta analysis of 1400 injured divers in about 2.5 million divers (DAN, 1991) in whom the risk of DCS is about 0.05% in the diving population, was that the risk ratio for decompression sickness is increased by a factor of about three for individuals with PFO, and is reduced by a factor of about 2 in individuals who do not have a PFO. It would appear that the risk is low and the significance of the small differences is questionable.

Echocardiography is the tool of choice in making the diagnosis of PFO. However, it’s probably not a good idea to do an echocardiogram on all divers because of the cost/benefit ratio. If you personally are concerned or are having some of the symptoms of decompression illness that are undeserved,  then a bubble contrast echocardiogram should be done. Bubble contrast echocardiography appears to be the most sensitive method for detecting a shunt while color flow doppler appeared to be a poor means of detecting the shunt in a transthoracic echo.

There have been recent reports of an association between cerebral emboli, migraines with aura and right to left shunts (PFO).

Philip Foster et al, in the Journal of the Aerospace Medical Association, has an elegant article “Patent Foramen  Ovale and paradoxical Systemic Embolism: A Bibliographic Review” in which is presented in a single document a summary of the original findings and views from authors in this field. It is a comprehensive review of 145 peer-reviewed journal articles related to PFO that is intended to encourage reflection on PFO detection methods and on the possible association between PFO and stroke.

The article abstract and related articles can be seen at this address:
http://snipurl.com/4sao

Patent  Foramen Ovale Closure - A button closure (Amplatzer) is performed trans venously without entering the chest. About four weeks  after the surgery, another echocardiogram is done to verify that the device is still in position.

After two-three weeks there is an overgrowth of endothelial cells covering the device, reducing the risk of infection.

After six to eight weeks the connective tissue has completely filled the spaces in the device and it becomes invisible to ultrasound. Return to diving is usually in six weeks (Wilmshurst), given the full recovery to the satisfaction of the cardiologist/surgeon. Others require a longer wait of twelve weeks.

See article by Wilmshurst, et al at http://heart.bmjjournals.com/cgi/content/full/81/3/257 . Google Links, PFO and Scuba Diving
Other related articles

July 16, 2008

Oxygen Therapy Might be Beneficial for Migraine, Cluster Headaches

Filed under: Article, News, Publicationscubadoc @ 8:19 am

As reported in Newswise < http://www.newswise.com/articles/view/542529/ >  — Two types of oxygen therapy could offer some relief to adults who suffer from disabling migraine and cluster headaches, according to a new research review from Australia.

Migraine headaches are severely painful and usually occur with other symptoms such as nausea, vomiting and painful sensitivity to light. Cluster headaches cause sharp, burning pain on one side of the head.

Physicians commonly rely on a number of drug therapies to both treat and prevent migraine and cluster headaches, but some also prescribe oxygen therapy. The aim of the systematic review — comprising nine small studies involving 201 participants — was to determine whether inhaling oxygen actually helps.

“We wanted to locate and assess any evidence from randomized trials that oxygen administration was a safe and effective treatment for migraine or cluster headaches,” said lead reviewer Michael Bennett, of Diving and Hyperbaric Medicine at Prince of Wales Hospital in Sydney. “We hoped this would assist physicians to make effective treatment decisions in this area.”

The review appears in the current issue of The Cochrane Library, a publication of The Cochrane Collaboration, an international organization that evaluates research in all aspects of health care. Systematic reviews draw evidence-based conclusions about medical practice after considering both the content and quality of existing trials on a topic.

The Cochrane reviewers examined studies that evaluated normobaric oxygen therapy and hyperbaric oxygen therapy. Normobaric therapy consists of patients inhaling pure oxygen at normal room pressure, and hyperbaric therapy involves patients breathing oxygen at higher pressure in a specially designed chamber.

Five studies compared hyperbaric versus sham (placebo) therapy for migraine; two compared hyperbaric versus sham therapy for cluster headache; and two investigated the use of normobaric therapy for cluster headache. Length of treatment varied with each study.

Three studies reported the number of patients who had significant relief from their migraines within 40 to 45 minutes of hyperbaric therapy. Although the studies did not specify each patients’ response to treatment, they reported a significant increase in the proportion of patients who had relief with hyperbaric oxygen compared to sham therapy.

For cluster headaches, two studies (69 patients) found a significantly greater proportion of patients had relief of their headaches after 15 minutes of normobaric compared to sham therapy.

The reviewers concluded that hyperbaric treatment might give some relief for migraine headache and that normobaric therapy might provide similar relief for cluster headache, but there is no evidence that these therapies will prevent future attacks.

“We believe that hyperbaric oxygen is also a reasonable measure for migraineurs who have not responded to other measures to treat an acute attack,” Bennett said. “However, the poor availability of hyperbaric chambers makes this an option only in a minority of health facilities. Most physicians treating headaches will continue to rely on established and emerging pharmacological options for treating and preventing acute attacks.”

Estimates indicate that 6 percent to 7 percent of men and 15 percent to 18 percent of women suffer from severe migraine headaches, and cluster headaches effect about 0.2 percent of the population.

John Kirchner, M.D., of the Kirchner Headache Clinic in Omaha, Neb., has treated thousands of patients suffering from a variety of headaches, including migraine and cluster, and said he does not include oxygen therapy in his patients’ treatment plans.

“This [oxygen therapy] would not be practical as the headache comes on fast and does not last long,” he said. “So there would not be time to get the patient to the chamber.”

Kirchner’s treatment for migraine includes avoiding triggers, taking preventive and symptomatic medications and undergoing behavior modification.

Bennett MH, et al. Normobaric and hyperbaric oxygen therapy for migraine and cluster headache. Cochrane Database of Systematic Reviews 2008, Issue 3.

The Cochrane Collaboration is an international nonprofit, independent organization that produces and disseminates systematic reviews of health care interventions and promotes the search for evidence in the form of clinical trials and other studies of interventions. Visit http://www.cochrane.org for more information.

July 15, 2008

Astro-diver in Lake that Looks Like Mars

Filed under: Article, News, Publicationscubadoc @ 5:35 pm

For the off-beat commercial diver - here is a series of slides about an interesting phenomenon in a fresh water lake in Canada. From Scientific American.

http://snipurl.com/2z6gp

High Dose HBO Resuscitates Swine Dead for 25 minutes after Cardiac Arrest

Filed under: Article, News, Publicationscubadoc @ 4:58 pm

New Orleans, LA – An interesting study by a research group led by Dr. Keith van Meter at the School of Medicine at LSU Health Sciences Center New Orleans published in the August 2008 issue of Resuscitation has implications for the #1 cause of death of Americans — sudden cardiac arrest. They were able to restart the heart of some swine after 25 minutes of being pronounced dead - well over the limit of 16 minutes set by the American Heart Association for CPR, medications and electric shocks in humans.

“To resuscitate any living organism after 25 minutes of heart stoppage at room temperature has never been reported and suggests that the time to successful resuscitation in humans may be extended beyond the stubborn figure of 16 minutes that has stood for 50 years,” notes Dr. Keith Van Meter, Clinical Professor of Medicine and Chief of the Section of Emergency Medicine at LSU Health Sciences Center New Orleans, who led the study.

The study involved the use of three groups of laboratory swine. All swine underwent cardiac arrest for 25 minutes during which time they received no artificial breathing, CPR, medications, or electric shocks. After 25 minutes the swine were randomly divided into 3 groups. The first group remained at normal pressure. The second group was given standard-dose hyperbaric oxygen, and the third group was given high-dose hyperbaric oxygen, a dose that is nearly 1/3 more than the highest dose currently given to humans. Advanced cardiac life support (ACLS) was started on animals in all groups for a two-hour resuscitation period. After the two-hour resuscitation period, four of the six animals in the high-dose hyperbaric oxygen group could be resuscitated. None of the subjects in the other groups were able to be resuscitated.

“The present study shows that short-term high-dose hyperbaric oxygen is an effective resuscitation tool and is safe in a small multiplace hyperbaric chamber,” concludes Dr. Van Meter. “A rehearsed team can easily load a patient in cardiopulmonary arrest into a small multiplace chamber in the pre-hospital or hospital setting without interrupting CPR or advanced cardiac life support. Successful resuscitation at 25 minutes suggests that if high dose hyperbaric oxygen is used at the current ACLS limit of 16 minutes, a greater survival may be achieved in humans and allow application of more definitive treatment such as clot dissolving drugs.”

The research team also included LSU Health Sciences Center New Orleans faculty Diana Barratt, MD, MPH, Heather Murphy-Lavoie, MD, Paul G. Harch, MD, James Moises, MD, and Nicolas Bazan, MD, PhD.

Future studies are planned to further refine knowledge about this important addition to resuscitation and survival procedures.

Are pulmonary bleb and bullae a contraindication for hyperbaric oxygen treatment?

Filed under: Article, Publicationscubadoc @ 12:41 pm
Respir Med. 2008 Jun 19; [Epub ahead of print] Related Articles, LinkOut
Click here to read
Toklu AS, Korpinar S, Erelel M, Uzun G, Yildiz S.

Department of Underwater and Hyperbaric Medicine, Istanbul University, Istanbul Faculty of Medicine, 34093 Fatih, Istanbul, Turkey.

BACKGROUND: Air cysts or blebs in the lungs may predispose pulmonary barotrauma (PBT) by causing air trapping when there is a change in environmental pressure. The changes in the environmental pressure are also seen during hyperbaric oxygen treatments (HBOT). AIM: The aim of this study was to determine how patients were evaluated for pulmonary blebs or bullae, and PBT prevalence in different HBOT centers. METHODS: HBOT centers were asked to participate in this study and a questionnaire was send via e-mail. A total of 98 centers responded to our questionnaire. RESULTS: Sixty-five HBOT centers (66.3%) reported that they applied HBOT to the patients with air cysts in their lungs. X-ray was the most widely used screening method for patients with a history of a lung disease. The prevalence of PBT in theses centers was calculated as 0.00045%. CONCLUSIONS: Our survey demonstrated that (1) a significant portion of the HBO centers accept patients with pulmonary bleb or bullae, (2) although insufficient, X-ray is the mostly used screening tool for patients with a history of pulmonary disease and (3) the prevalence of pulmonary barotrauma is very low in HBOT.

PMID: 18571913 [PubMed - as supplied by publisher]

Bubble formation after a 20-m dive: deep-stop vs. shallow-stop decompression profiles.

Filed under: Article, Publicationscubadoc @ 12:33 pm
Aviat Space Environ Med. 2008 May;79(5):488-94. Related Articles, LinkOu

Schellart NACorstius JJGermonpre PSterk W.

Department of Medical Physics, Academic Medical Centre, University of Amsterdam, The Netherlands. N.A.Schellart@…

OBJECTIVES: It is claimed that performing a “deep stop,” a stop at about half of maximal diving depth (MDD), can reduce the amount of detectable precordial bubbles after the dive and may thus diminish the risk of decompression sickness. In order to ascertain whether this reduction is caused by the deep stop or by a prolonged decompression time, we wanted to test the “deep stop” theory without increasing the total decompression time. From a modeling point of view, Haldanian theory states that this situation would increase the probability of observable bubbles, because of a longer stay at depth. Under these conditions, we examined whether a “deep-stop dive” (DSD) produces more bubbles or less than a “shallow-stop dive” (SSD). METHODS: Recreational divers performed either a DSD or a SSD. Both groups were matched biometrically. MDD was 20 msw, bottom time 40 min and total diving time 47 min. In DSD, the “deep” stop (10 msw) replaced 3 min of the 7 min stop at 4 msw of SSD. RESULTS: DSD produced significantly more precordial bubbles than SSD after knee bends (P-values ranging from 0.00007 to 0.038). DISCUSSION: Our results indicate that at least for the tested dive profile, the higher supersaturations after surfacing overruled any possible beneficial effects of the deep stop on bubble formation. The usefulness of substituting a shallow stop with a deep stop in dives up to 20 msw can be questioned; at the least, more research is needed.

PMID: 18500045 [PubMed - in process]

Acute ischemic colitis during scuba diving: Report of a unique case.

Filed under: Article, Publicationscubadoc @ 12:28 pm
World J Gastroenterol. 2008 May 28;14(20):3262-5. Related Articles, LinkOut
Click here to read

Goumas K, Poulou A, Tyrmpas I, Dandakis D, Bartzokis S, Tsamouri M, Barbati K, Soutos D.

Department of Gastroenterology, Red Cross Hospital of Athens, Ochis 12, 11522 Athens, Greece. ddandakis@….

The presentation of clinical symptoms due to decompression during diving, varies significantly, as mainly minor disturbances for the gastrointestinal tract in particular have been reported. The following case debates whether diving can cause severe symptoms from the gastrointestinal system. We describe a clinical case of ischemic colitis presented in a 27-year-old male, who manifested abdominal pain while in the process of scuba diving 20 meters undersea, followed by bloody diarrhoea as soon as he ascended to sea level. Taking into account his past medical history, the thorough, impeccable clinical and laboratory examinations and presence of no other factors predisposing to ischemia of the colon, we assume that a possible relationship between diving conditions and the pathogenesis of ischemic colitis may exist. This unusual case might represent a hematologic manifestation of decompression sickness, due to increased coagulability and/or transient air emboli, occurring during a routine scuba diving ascent to sea level.

PMID: 18506937 [PubMed - in process]

July 9, 2008

Undercurrent Online Update

Filed under: Uncategorizedscubadoc @ 10:58 am

U N D E R C U R R E N T   O N L I N E    U P D A T E
F O R    N O N - S U B S C R I B E R S

Undercurrent — Consumer Reporting for
the Scuba Diving Community since 1975
www.undercurrent.org

Dive News

July 8, 2008

You have received this message because you have signed up on our website to receive this email or your are a former subscriber or Online Member of Undercurrent . Removal instructions are below.

Poseidon’s BCD Recall : Swedish dive gear manufacturer Poseidon recalled a batch of its W50 wings last month because the seam holding the two bladder halves together can easily break, deflating the BCD. The faulty bladders are marked with batch number 5445 and were sold between September 2007 and June 10, 2008. Poseidon W50 wing users can check the batch number by opening the zipper between the two “legs” of the wing to reveal the inner bladder. Between the bladder’s two legs is a tab with article number, batch number and manufacturing year. If you see a ‘5445,’ take it back to your dive shop for a free replacement.

Be A Frequent-Flyer Diver : As a sidebar to our discovery of a dive operation on Belize’s Tobacco Caye, we reported on how to use those frequent-flyer miles. “Plan 10 to 11 months beforehand, because most airlines open frequent flyer reservations about 330 days in advance. I use Northwest miles, which also work on Continental and Delta, two airlines with lots of Caribbean and Latin American flights. When I fly Continental or Delta, I put the miles on my Northwest account so they are concentrated in one pot. By booking close to that opening gate, I’ve been able to get the exact or approximate dates to the Caribbean locations I want, using 35,000 miles. If I have to cancel or change a trip, Northwest charges only $50 to get my miles back. By booking way ahead, I haven’t paid for a ticket to the Caribbean in years.” And if you can travel at the last minute, underbooked flights get freed up for frequent-flyer use about two weeks before takeoff. Undercurrent is filled with great tips like this. Become a subscriber now at https://www.undercurrent.org/secure/UCnow/UserNewSub.php.

Caribbean Flight Alert : If you’re holding tickets to anywhere in the Caribbean, reconfirm those flights right up to your departure day. The rising cost of jet fuel will seriously affect the Caribbean because floundering American Airlines controls much of the market; for example, it will cut daily flights out of San Juan from 93 to 51. Spirit Airlines will close its San Juan hub, and Continental Airlines will soon announce destination and flight cuts. Smaller islands are asking LIAT and Air Jamaica to increase flights and coordinate schedules to fill the gaps. On the bright side, JetBlue plans to add daily flights to Puerto Rico this fall, and Virgin Atlantic may also add extra U.S. flights to the Caribbean.

Buy The Best Fish ID Books Around: If you’re planning your next dive trip, you need some good ID book for fish and corals. We’ve got the best ones, covering the Caribbean, Indonesia, Fiji, Hawaii, Mexico and other points. Go to Undercurrent and click on “Diving Books and Guides.” You’ll get the best price Amazon.com has to offer, and all of our profits go to save those fish and coral reefs you’ll be reading about on your next trip.

The Final Word on Tipping, Whether You’re Diving At a Resort or on a Liveaboard : Go to www.undercurrent.org to read “Last Word on Dive Tipping,” in which I, Ben Davison, the lifelong publisher of Undercurrent (33 years now) sets the rules for tipping on your dive trip. I explain why tipping 15% of a liveaboard trip is often outlandish; where $10 a day for your dive guide is right, and where it’s just throwing money away. You’ll find it in our July 2008 issue, on the Web, free to nonsubscribers.

What Else Is In The July Issue :

* Get a seven-month trial subscription to Undercurrent for only $29.95, and in addition to your seven issues delivered by mail, you’ll receive the all-new 2009 Travelin’ Divers’ Chapbook as soon as it’s off the press;
* In the July issue, you’ll find out about: Nai’a, a top-notch liveaboard in Fiji;
* Why stung divers should use hot water for treatment;
* A lethal air compressor on the Baani Adventure;
* Good and bad diving in the Caribbean, Canada and the South Pacific;
* Three Caribbean hubs notorious for leaving dive bags behind;
* Update on the Shear Water shark death;
* An interview with two divers left adrift on the Great Barrier Reef for 19 hours;
* Five divers who fended off sharks, then lethal lizards;
* The fastest fins for divers; Another diver gets charged with killing his wife on a dive trip; and much, much more;

Ben Davison, editor/publisher
Contact Ben


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