scubadoc Ten Foot Stop

October 13, 2006

FREE PSDIVER ISSUE #31 IS NOW AVAILABLE

Filed under: Uncategorizedscubadoc @ 11:45 am

PSDiver Monthly Issue 31 Is Now Available - ALWAYS FREE October 12, 2006 GREETINGS

  

Issue 31 of PSDiver Monthly is now available for download. Click here to go to the download site.

Mark Phillips

Editor / Publisher

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MONOPLACE CHAMBER INFUSION PUMPS

Filed under: Uncategorizedscubadoc @ 11:10 am

Dear Hyperbaric Colleague:

I am making contact with you regarding the issue of monoplace chamber infusion pumps.

You are likely aware that something of a crisis exists in this regard. Production has ceased as a result of decreased consumer interest. A trend over the past several years is to limit hyperbaric access to outpatients. As these patients rarely have concurrent fluid and drug requirements there is little need in infusion pumps in this business model.

This has made it very difficult for those who are committed to treat the full range of patients states. Existing supplies have been exhausted so newly introduced programs are unable to provide care to sick patients, some of whom are likely to benefit most from hyperbaric oxygen therapy.

We have been asked to seek out alternative sources by several hospitals. The purpose for my contact, then, is to see if your program has any infusion pumps surplus to your needs. If this is the case, I would very much like to hear from you.

Best regards, Dick Clarke

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CARBON MONOXIDE REPORTING SYSTEM

Filed under: Uncategorizedscubadoc @ 11:08 am
 

To UHMS Member:

I am writing to determine the level of interest with regard to the development of an online, real time, web-based reporting system for cases of carbon monoxide poisoning treated with hyperbaric oxygen in the US. If the idea moves forward, it would be developed as a joint UHMS/CDC project.

Please take 1-2 minutes to answer the questions on the brief survey

at:

http://www.surveymonkey.com/s.asp?u=755622696910

Thank you. Neil B. Hampson, MD

Past President, UHMS

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October 12, 2006

2006 DAN ON-LINE AUCTION GOES LIVE NOV. 1

Filed under: Uncategorizedscubadoc @ 2:22 pm

Dan Leigh writes to send this information:

  
Divers Alert Network® is holding the 2006 DAN On-Line Auction from Nov. 1 through Dec. 1. All money raised from winning bids in this annual auction will support DAN programs.
 
“The auction has been a success for DAN and its Auction Partners over the past four years; everyone, DAN Member or not, has an opportunity to bid on great packages,” said Eileen Sahlin, DAN Chief Development Officer. “This is the fifth auction we have held. It looks better than ever!”
 
“We anticipate having about $100,000 in retail value of trips, liveaboards, clothing, dive equipment, artwork, books and more. Interested in white-water rafting or snow skiing? The DAN Auction has something for everyone!”
 
Bidding happens online at the DAN website at www.DiversAlertNetwork.org, for both DAN Members and nonmembers. The auction starts on Nov. 1 at noon Eastern Time and closes Dec. 1 at noon ET. This year the preview of items begins on Oct. 25. No bids will be accepted during the preview.
 
The name and contact information of each of the auction donors appear with each item up for auction, with a description and picture of the item, its suggested retail price, its current bid price and whether the reserve has been met. There is a live link to the donor¹s website during the auction.
 
Winning bidders will be notified by Dec. 5. Items will be delivered to winning bidders through their local dive shop, from the auction donor or from DAN with the items slated to arrive no later than Dec. 15.
 
For more details about the 2006 DAN On-Line Auction, visit www.DiversAlertNetwork.org/development, call DAN Development at 1-800-446-2671 ext. 444 or 445 or email development@dan.duke.edu.

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October 10, 2006

HYPERHOMOCYSTEINEAEMIA AND DIVING?

Filed under: Questions From Newslettersscubadoc @ 2:59 pm

Dear DIVE DOC

I am a diving instructor and DAN member in South Africa -  requiring some assistance.

One of my students has the following condition:

- Hyperhomocysteinaemia

- Presently homocysteine level not high

- The diver is currently taking Vit BCo

Not 100% sure if this is a contraindication?

I am sending him for a medical but not sure the Dr will know exaclty if it is a contrainidcation or not?

Please would you lend some advice.

Answer:

Hello Doctor:

This condition is related to increased risks for thrombosis and really poses
little in the way of threat to divers. Increased pressure should not
increase the risk of thrombosis. However, if the condition is being treated
with anticoagulants - there is an increased risk for hemorrhage from
barotrauma to the ears, sinuses and lungs.

See the article at http://www.htcnevada.org/homocystein.htm for more
information about the condition.

Best regards:

Ern Campbell, MD

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Diving with Pacemakers

Filed under: FAQscubadoc @ 2:54 pm

AUTHORS- Trigano, Alexandre; Lafay, Vincent; Blandeau, Olivier; Levy, Samuel; Gardette, Bernard; Micoli, Christophe   

JOURNAL NAME- J Interv Card Electrophysiol   
VOLUME 15   
NUMBER 3   
PUBLICATION DATE- 2006 Apr   
PP 179-83   
DOCUMENT TYPE- Journal Article   
JOURNAL CODE- 9708966   
JOURNAL SUBSET- MEDJSIM   
ISSN- 1383-875X   
CORPORATE AUTHOR- Department of Cardiology, Centre Hospitalier Universitaire Nord, 13915 cedex 20, Marseille, France, alexandre.trigano@mail.ap-hm.fr.   
PUBLICATION COUNTRY- United States   
LANGUAGE- English   

OBJECTIVES: The aim of this study was to test a variety of currently available activity-based rate-adaptive pacemakers under hyperbaric conditions. BACKGROUND: Sports divers with pacemakers can dive under certain circumstances. The rate response of activity-sensing pacing under hyperbaric conditions has rarely been evaluated. MATERIALS AND METHODS: We manufactured a miniaturized hyperbaric chamber A pacemaker inside was kept close to the corresponding telemetry wand placed on top of the chamber. An inflation device for coronary balloon angioplasty was used to create hydraulic pressure. Group I pacemakers were exposed to a 30 msw/98 fsw/4 ATA and after a 1-month waiting period to 60 msw/197 fsw-depth/7 ATA. Group II was exposed to only one dive to 60 msw. The electrogram and event marker telemetry were used to monitor the pacing stimuli and measurements were made for case distortion. RESULTS: The baseline pacing rate did not change in 27 tests. Return to baseline was shown during 18 tests after transient sensor-driven rate. There was a sensor rate response to manual brief shaking during and following testing. A case distortion was shown in 15 of 29 tests at 60 m. CONCLUSIONS: Modern accelerometers showed no sensitivity to pressure on the pacemaker can at 30 msw/98 fsw and 60 msw/197 fsw but in some devices responded to pressure changes. There was no pacing dysfunction or suppression of the sensor response despite the high incidence of case distortion at 60 msw/197 fsw. As a general rule, diving should not be allowed at depths greater than 20 msw/65 fsw. 

Some references to Dysbaric Osteonecrosis

Filed under: FAQscubadoc @ 2:50 pm

 ’Sunny’ - at Reimers Systems, has provided us with a couple of citations about DON.

Dysbaric osteonecrosis: a consequence of intravascular bubble formation, endothelial damage, and platelet thrombosis.   

Slichter SJ, Stegall P, Smith K, Huang TW, Harker LA.

, , , , .Survival and turnover of platelets, fibrinogen, and plasminogen were measured in association with hyperbaric exposure in man. In addition, kinetic and vascular studies were carried out in a hyperbaric swine model to assess the role of vascular injury and thrombosis in the pathogenesis of dysbaric osteonecrosis. In man, significant increases in platelet and fibrinogen consumption were directly associated with dive depth and with repetitive exposure at lesser depths. The increased destruction of platelets and fibrinogen was not accompanied by reduced blood levels because of compensatory shifts in production rats and distribution between circulating and storage compartments. Platelet consumption was substantially greater than fibrinogen destruction with respect to both severity and duration. Platelet function inhibitors decreased platelet consumption. Increased fibrinogen consumption was sometimes associated with reduced plasminogen survival, but levels of fibrinogen/fibrin degradation products were never measurably altered from normal values. The relationships among platelet and fibrinogen consumption, vascular changes, and dysbaric osteonecrosis were studied in hyperbaric swine. Consumption of hemostatic factors was most severe with rapid, uncontrolled decompression, low oxygen concentrations, and deeper or repetitive dives. Platelet consumption induced by hyperbaric exposure resolved spontaneously with time, suggesting a repair process after the simulated diving conditions were discontinued. Interruption of increased platelet and fibrinogen consumption in the swine model required either moderation of the dive profile or a combination of drugs that inhibit platelet function (dipyridamole or sudoxicam) together with an anticoagulant (warfarin or heparin). Repeated hyperbaric exposure under conditions that uniformly produced femoral osteonecrosis and consumption of platelets and fibrinogen was associated with detectable endothelial injury and arterial intimal lesion formation. Since the diving characteristics of increasing depth and inadequate decompression were associated with both the most severe consumption and the highest frequency of intravascular bubble formation, we postulate that intravascular bubbles, formed during hyperbaria, produce osteonecrosis, perhaps through the following sequence: (1) bubble-related endothelial cell damage; (2) platelet thrombus formation with secondary fibrin deposition; (3) microvascular occlusion; and (4) platelet-dependent arterial narrowing through intimal lesion formation. The role of antithrombotic therapy in the prevention of dysbaric osteonecrosis remains to be determined.

, , , , .Survival and turnover of platelets, fibrinogen, and plasminogen were measured in association with hyperbaric exposure in man. In addition, kinetic and vascular studies were carried out in a hyperbaric swine model to assess the role of vascular injury and thrombosis in the pathogenesis of dysbaric osteonecrosis. In man, significant increases in platelet and fibrinogen consumption were directly associated with dive depth and with repetitive exposure at lesser depths. The increased destruction of platelets and fibrinogen was not accompanied by reduced blood levels because of compensatory shifts in production rats and distribution between circulating and storage compartments. Platelet consumption was substantially greater than fibrinogen destruction with respect to both severity and duration. Platelet function inhibitors decreased platelet consumption. Increased fibrinogen consumption was sometimes associated with reduced plasminogen survival, but levels of fibrinogen/fibrin degradation products were never measurably altered from normal values. The relationships among platelet and fibrinogen consumption, vascular changes, and dysbaric osteonecrosis were studied in hyperbaric swine. Consumption of hemostatic factors was most severe with rapid, uncontrolled decompression, low oxygen concentrations, and deeper or repetitive dives. Platelet consumption induced by hyperbaric exposure resolved spontaneously with time, suggesting a repair process after the simulated diving conditions were discontinued. Interruption of increased platelet and fibrinogen consumption in the swine model required either moderation of the dive profile or a combination of drugs that inhibit platelet function (dipyridamole or sudoxicam) together with an anticoagulant (warfarin or heparin). Repeated hyperbaric exposure under conditions that uniformly produced femoral osteonecrosis and consumption of platelets and fibrinogen was associated with detectable endothelial injury and arterial intimal lesion formation. Since the diving characteristics of increasing depth and inadequate decompression were associated with both the most severe consumption and the highest frequency of intravascular bubble formation, we postulate that intravascular bubbles, formed during hyperbaria, produce osteonecrosis, perhaps through the following sequence: (1) bubble-related endothelial cell damage; (2) platelet thrombus formation with secondary fibrin deposition; (3) microvascular occlusion; and (4) platelet-dependent arterial narrowing through intimal lesion formation. The role of antithrombotic therapy in the prevention of dysbaric osteonecrosis remains to be determined.PMID: 7288270 [PubMed - indexed for MEDLINE] 


AJR Am J Roentgenol. 1990 Jul;155(1):95-7. Comment in:

Does dysbaric osteonecrosis progress in the absence of further hyperbaric exposure? A 10-year radiologic follow-up of 15 patients.

Department of Radiology, St. Luke’s Medical Center, Milwaukee, WI 53215.

Progression of dysbaric osteonecrosis of the femoral and humeral heads was evaluated in 15 caisson workers. All patients had dysbaric osteonecrosis but had had no further exposure to hyperbaric pressures for a minimum of 10 years. The original and follow-up radiographs were compared in each case. Of 24 normal articular heads (nine humeral and 15 femoral), one (4%) humeral head developed new subcortical sclerosis. Of the 36 juxta-articular lesions, seven (four humeral and three femoral) showed major changes in the 10-year interval. Of these seven, two (one humeral and one femoral) had new articular fractures and three (two humeral and one femoral) with articular fractures showed progressive osteoarthritis. We conclude that caisson workers can develop lesions in previously normal areas and experience worsening of previously known lesions in the absence of further exposure to hyperbaric pressures.

PMID: 2112875 [PubMed - indexed for MEDLINE]

 Related articles:

Undersea Hyperb Med. 2005 May-Jun;32(3):169-74.
Dysbaric osteonecrosis by X-ray and CT scan in Chinese divers.

Guangzhou Occupational Disease Prevention & Treatment Centre, Guangzhou 510620, China.

OBJECTIVE: To compare the results of X-ray and CT scan for dysbaric osteonecrosis in Chinese divers. METHODS: Both shoulders, hips and knees of 66 asymptomatic divers with diving duration of more than one year were examined by X-ray and CT scan. RESULTS: The most frequent locations of dysbaric osteonecrosis were the upper femurs, followed by the upper humerus, lower femurs and upper tibias, and the most frequent radiographic lesions were calcification spots and cystic changes. Of the lesions detected, 38% (27/71) and 42% (95/229) werejuxta-articular of the femoral and humeral heads by X-ray and CT respectively. The detection rates of dysbaric necrosis (juxta- and/or other lesions) of X-ray and CT scan were 42.4% (95% confidence interval: 30.5%-54.3%) and 81.8% (95% CI: 72.4%-91.2%) respectively (p<0.05). If CT scan was used as the gold standard, the sensitivity of X-ray was 100% and the specificity was 31.6%. CONCLUSION: CT scan showed a higher detection rate of dysbaric necrosis than X-ray. We recommend that CT scan be used for early diagnosis of dysbaric osteonecrosis.

PMID: 16119308 [PubMed - indexed for MEDLINE]

Baillieres Clin Rheumatol. 1989 Apr;3(1):1-23.  

Dysbaric disorders: aseptic bone necrosis in tunnel workers and divers.

Dysbaric osteonecrosis is a serious complication for those exposed to a hyperbaric environment, with prevalence of 17% amongst compressed air workers and 4.2% amongst divers. Bone lesions are characteristically multiple and bilateral, occurring frequently in the shafts of the femora or tibiae and the heads of the humeri or femora. A proportion of the lesions will lie next to the joint surface, the so called juxta-articular lesion, and these may progress to a structural failure and secondary osteoarthritis. These lesions can be severely disabling, especially in a young adult male. When related to the occupational history the prevalence of bone lesions, both in compressed air workers and divers, increases with age, experience and with greater pressures of air or at greater depths. Moreover, acute attacks of decompression sickness, the bends, are more liable to be associated with subsequent bone lesions. Current decompression schedules certainly reduce the bends rate but, no matter how strictly adhered to, will not prevent the development of dysbaric osteonecrosis. It is possible that bone necrosis could result solely from exposure to a high pressure of air, either from work in compressed air or diving. Those men with positive bone lesions should be advised to seek expert medical opinion and probably advised to discontinue work in compressed air or diving if a juxta-articular lesion is present. Detection of bone necrosis depends on good quality radiographs with reliable interpretation, preferably by double observation, especially in the early stages. Lesions, especially when early or doubtful, can be confirmed by CT or bone scintigraphy. MRI promises to detect osteonecrosis in the very early stages but is not yet readily available. To detect dysbaric osteonecrosis at an early stage it is important to monitor both compressed air workers and divers with regular radiological skeletal surveys or bone scintigraphy. In 1987, the Bone Necrosis Working Group of the Decompression Sickness Panel recommended that all divers should have a radiological survey on completion of their initial diving training and that bone scintigraphy should be used for subsequent surveillance for certain groups, including those diving deeper than 30 metres, where the time at depth exceeds 4 hours, when experimental decompression is used and in other situations.

PMID: 2661022 [PubMed - indexed for MEDLINE]

Undersea Hyperb Med. 2001 Summer;28(2):83-8.

Dysbaric osteonecrosis in Turkish sponge divers.

Istanbul University, Istanbul Facility of Medical, Department of Underwater and Hyperbaric Medicine, Turkey.

Skeletal radiographs were performed to determine the prevalence of dysbaric osteonecrosis (DON) in 51 Turkish sponge divers. DON was correlated with the diver’s age and experience, maximum diving depth, and decompression sickness (DCS). Thirty-six of the 51 divers had radiographic evidence of one or more lesions, for a prevalence of 70.6% DON. Proximal humerus was the most effected site. Type B (head, neck, and shaft) lesions were most common, comprising 63.6% of all DON lesions. Type A (juxta-articular) lesions were observed in all 10 divers who complained of painful motion of their shoulder or hip joints. DON most commonly affected the proximal humerus. Reportedly, 38 of these 51 (74.5%) divers had experienced DCS. We did not fnd any significant relationship between DON and DCS, maximum diving depth, diving experience, and divers’ age.

PMID: 11908699 [PubMed - indexed for MEDLINE]

 

 

October 9, 2006

Diving and Lyme Disease - ?Herxheimer Reaction?

Filed under: Interesting Linksscubadoc @ 10:53 am

 Here is an article sent to us by Sunny at Reimers Systems about Lyme disease, diving and the possibility of a Herxheimer Reaction.

Meeting Dr. Herx — 46’ Under Water
Sometimes A Panic Attack Is Much More Than Anxiety

By Virginia T. Sherr, MD

“What could have happened?” Conrad’s shaky, urgent voice demanded answers. “What is happening to me?” His phone call to this psychiatrist from Florida sounded desperate. An experienced diver, he had been 46 feet down – a mere recreational depth that was usually easy for him, when, with the suddenness of a blow, bizarre sensations and ideas burst into his mind and body – he felt totally disoriented and disconnected from himself. He was flooded with terror. Trembling, he hurriedly checked hoses and gauges. The fact that everything, including his oxygen supply, was in perfect order did not reassure him. He suddenly felt no self-assurance as the idea occurred to him that he had always been totally inept.

Something disastrous was happening to him, and he couldn’t figure it out or control his rising panic. The day’s status was “Blue,” the water depth 70 feet and calm, the equipment in perfect working order, he had not been worried-yet he suddenly lost all confidence. He needed to surface, which he managed to do correctly with the help of his diving buddy, and now he needed advice. He felt so weird he was sure that he was having a break with reality – thus, the urgent call to me.

 

 

 

Conrad knew me because he previously had sought help for a self-diagnosed depression. Actually, I had never been sure that he was “depressed-depressed” or whether he was just lonely-depressed. He was working on a maritime project that had him away from his beloved Boston, where his good friends and family hoped for his quick return. A young marine biologist, he had always been at home in the water. But not that day-now the sea was filled with dread and doom, sensations that he had never experienced before.   

I urged him to come back to my office to be tested for tick-borne diseases, since what he was experiencing sounded for all the world like an oxygen-prompted Jarisch-Herxheimer [cytokine] excessive immune system reaction to a kill-off of toxic spirochetes—the bacterial cause of Lyme disease. Drs. Jarisch and Herxheimer were scientists who discovered the J-H phenomenon while working with spirochetal infections at the start of the last century. Lyme disease is a tick-borne illness that, if not recognized and treated promptly, can result in serious nervous system infection and chronic, sub-acute encephalitis.

Prior to Conrad’s vacation in Florida, something unusual had occurred. While he was not aware of any tick-bite, he had developed a generalized rash. Referred to his family doctor, he had been told it was “non-specific”, and was given a Med-Pack of gradually descending doses of prednisone designed to eliminate the itching and spots. I had suggested then that he first undergo testing for tick-borne diseases, but his family doctor had brushed aside any such considerations because there had been neither the popularly expected “bull’s eye rash” nor flu-like symptoms. These are now known to be present in only perhaps 50% of Lyme victims.

The location of Conrad’s home address had alerted me at the onset to consider Lyme disease as another possible cause of his depression. This was because some of the most serious cases of previously unsuspected Lyme encephalopathy that I have ever seen came to me from his geographic area north of Philadelphia, Pennsylvania, USA. Reviewing my intake notes at the time of his rash, I had found Conrad related no physical complaints other than an old “football injury” that gave him a knee ache without joint swelling from time to time. With his lack of physical symptoms, I had relaxed about the possibility of his depression being caused by tick-borne diseases. It had seemed to me then that neuro-Lyme disease was only a remote possibility what with his assurances that he felt physically well and was “only depressed.”

Re-interested in considering all options he hurriedly returned from Florida and I tested him for the antibodies and DNA of tick-borne diseases. Results showed considerable evidence of Lyme disease but not the full CDC diagnostic number of “bands” on the Western Blot antibody test. Retesting his blood shortly after initiation of antibiotics clearly substantiated the clinical diagnosis of Lyme disease, however. This timing may have allowed the effectiveness of antibiotics to jump-start his immune system and for the formation of antibodies.

Unfortunately, Conrad’s status continued to deteriorate rapidly. This bright young man was struggling to keep up at work, could barely hold on to one task or one thought at a time (loss of short-term memory), and was actually grinding to a halt cognitively. A SPECT brain scan done at Columbia University in NYC revealed “global heterogeneous hypoperfusion” revealing vascular inflammation in a pattern typical of the cerebral Lyme disease that was impairing blood flow to his brain tissues.

Informed of the facts, Conrad was at once relieved to know the source of his problems and chagrined that he hadn’t told me before about such symptoms of extreme fatigue and migrating muscle and joint pains—symptoms that he considered “signs of weakness.” “It was embarrassing enough to tell someone I was depressed,” he said. He has cooperated with his antibiotic and herbal treatment regime offered by a physician skilled in the treatment of TBD’s and is slowly recovering. His employer has been uniquely considerate of his health problems and has redesigned his job, making it compatible with his overwhelming but temporary disabilities.

Knowledgeable Lyme patients are known to make arrangements for carefully managed scuba diving excursions to reduce their spirochetal burden—air (providing oxygen) under pressure is lethal to the bacteria.

 

 

 

The likelihood of disorienting panic attacks while submerged is predicted to people prior to the dive and therefore reactions are much less frightening. Patients often prefer this therapy to the Hyperbaric Oxygen (HBO) dives that stimulate similar therapeutic experiences. The emotional phenomena that occurred to Conrad and that bears the Herxheimer name bears a strong resemblance to what D. Prater wrote concerning the plight of the poet, R. Marie Rilke in another context:   

“In a sudden onset, the hitherto vague feeling of unease had developed into a brutal shock felt to his very marrow, so powerful that he was terrified. He could not explain this covert onslaught but somehow it had sapped the inner confidence, which, even at his worst moments, had always seemed unshakable, and whose absolute and evermore integrated unity with the body had been the wellspring of his art. He felt then a nameless fear that the defection of this body might destroy that unity, that a rift in his nature had been opened which might never be repaired.”

That Conrad will continue to work in marine biology is not in question. But whether he will come to see diving as an ancillary therapeutic tool in his treatment is problematic. At present, he is not ready to chance another underwater meeting with Dr. Herxheimer.

 

 

 

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Best Publishing Offers 10% Discount on Books

Filed under: Classifiedscubadoc @ 10:34 am
 Lisa Wasdin, UHMS sends the following announcement to UHMS members:

  

Best Publishing Company 
“A complete line of books on hyperbaric medicine and diving medicine”

OUR FAVORITE MONTHLY SPECIAL …

To our favorite customers

10% DISCOUNT ON ALL WEB ORDERS!

This is a great chance to receive a discount on the books you have been waiting to order!

ORDER NOW-LIMITED TIME OFFER (expires 10/31/06)!

IMPORTANT NOTE: To receive the discounted pricing - be sure to select the discount code “EMAIL LIST PROMO” in the ’How did you Hear About Us?’ box during checkout…We will deduct the 10% when we process the order and send your receipt with the books. 

Order Now at:   http://www.bestpub.comBook of Interest:Assessment of Diving Medical Fitness for Scuba Divers and InstructorsDAN Guide to Dive Medical FAQ’s

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Hyperbaric Medicine Practice

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Best Publishing Company PO Box 30100, Flagstaff, AZ   86003-0100
Tele: (800) 468.1055—(928) 527.1055

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Ciguatera Fish Poisoning

Filed under: Interesting Linksscubadoc @ 10:26 am
 Dr. Omar Sanchez, diver/cardiologist from Argentina, sends us this article about Ciguatera revision from the Centers for Disease Control and Prevention.
Ciguatera Fish Poisoning—Texas, 1998, and South Carolina, 2004
JAMA. 2006;296:1581-1582. October 4,
Related link: Ciguatera References
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