Undersea and Hyperbaric Medicine Section Newsletter - May 2008, Vol 15, #2
Message from the Chair
Christopher J. Logue, MD
Spring is in the air. It is during this time of year that I find myself reflecting on the future of the sub-specialty of Undersea and Hyperbaric Medicine. I enjoy watching our two fellows evaluate patients and perform complex medical decision making. They are now adept at overseeing both elective and emergency hyperbaric oxygen treatments for our busy hyperbaric medicine service here at the University of Pennsylvania. I think about how much they have learned over the past 10 months and I am excited for them as they prepare to launch their careers as practicing emergency medicine and hyperbaric medicine physicians. I am also excited about our two incoming emergency medicine residency trained fellows and look forward to their first days come July.
Our fellows are in the process of filling out their applications to take the Undersea and Hyperbaric Medicine Boards which will be administered electronically from September 29th through October 10th. I find myself hoping that there will be scores of other physicians also taking the exam this year. Those of us who practice hyperbaric medicine should feel fortunate that the pioneers of our sub-specialty went through the trouble of obtaining recognition from the American Board of Medical Specialties (ABMS) and that the exam is administered by ABEM. The process of board certification is a powerful tool useful in our efforts to improve acceptance and awareness of hyperbaric medicine in the medical community.
I have met many of you who have been practicing hyperbaric medicine and administering hyperbaric oxygen therapy for years but have not yet obtained board certification. Some of the folks I’ve conversed with had mistakenly thought the "Training Plus Practice Pathway" had closed back in 2005. However, at that time there were not enough true fellowship programs and this pathway was extended until 2010. I would like to take the time now to encourage you to look into this option. Please, go to ABEM’s website http://www.abem.org/PUBLIC/portal/alias__Rainbow/lang__en-US/tabID__3359/DesktopDefault.aspx to read more about this pathway. Board certification is within your grasp and will open further doors for your career in Undersea and Hyperbaric Medicine.
The Training Plus Practice Pathway requires completion of a basic course in Undersea and Hyperbaric Medicine. For course options I recommend checking out the website for the Undersea and Hyperbaric Medicine Society (UHMS). http://www.uhms.org/CoursesExams/tabid/58/Default.aspx
In two years the alternative pathway to board certification will close and the demand for formal fellowships will increase dramatically. In an effort to facilitate this transition, we have decided to move forward with a Winter Symposium "The Future of Undersea and Hyperbaric Medicine" during the upcoming winter season. This focus of the symposium will be on fellowship development, fostering research on the use of hyperbaric oxygen therapy for indications not yet approved, and strategies for improving awareness of hyperbaric medicine in the general medical community. We are processing the paperwork to obtain CME credit and are working on a location for the symposium presently. The symposium will be in a warm weather locale and recreational SCUBA diving will be available. Stay tuned for more details in the next issue of the newsletter.
In addition, we are a little over one year away from launching a board review course (in time for those of you considering taking the exam in 2009). Anyone interested in developing and participating in the course should contact me at my e-mail: firstname.lastname@example.org
Spring is in the air. As I get my SCUBA gear ready for my annual trip to the Outer Banks of North Carolina to dive the "Graveyard of the Atlantic," I will be thinking about all of you and the future of Undersea and Hyperbaric Medicine.
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June 26-28, 2008
Undersea and Hyperbaric Medicine Society
Annual Scientific Meeting
Salt Lake City, Utah
August 11-22, 2008
Physicians Training Course in Diving Medicine
NOAA Diving Center, Seattle, Washington
October 27-30, 2008
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David S. Lambert, MD, Co-Secretary
Recently, in Philadelphia, a meeting of regional toxicologists, emergency physicians and hyperbaric specialists was held at the Children’s Hospital of Philadelphia. It was part of the regularly scheduled monthly Grand Rounds of the Philadelphia Regional Poison Control Center. The main topic discussed was Carbon Monoxide poisoning. The aim of the discussion was to review some of the recent literature regarding carbon monoxide poisoning and treatment in order to develop a regional consensus on the proper treatment and disposition of patients who present with acute CO poisoning. The impetus for this talk was born out of a recent Cochrane Report update and ACEP clinical policy regarding acute carbon monoxide poisoning and the use of hyperbaric oxygen therapy for its treatment. In response to the ACEP clinical policy, an editorial from the Hyperbaric Medicine Section was published in the Annals of Emergency Medicine (March 2008, Vol. 51, Issue 3, Pages 339-340).
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Reviewer: David S. Lambert, MD
Rockswold SB, Rockswold GL, Defillo A. Hyperbaric oxygen in traumatic brain injury. Neurol Res. 2007; 29(2):162-172.
This is an excellent review of both the historical and current literature of the efficacy and mechanisms of hyperbaric oxygen (HBO) treatment in traumatic brain injury (TBI) from the Division of Neurosurgery at Hennepin County Medical Center in Minneapolis, Minnesota.
The article starts with a brief, yet concise, review of the pathophysiology of TBI, illustrating the fact that ischemia is a major cause of secondary brain injury and death. As aerobic metabolism is converted to anaerobic metabolism an acidosis and depletion of cellular energy occurs, leading to a cascade of events culminating in the impairment of mitochondrial respiratory chain-linked oxidative phosphorylation and dysfunction that can last for days following the initial insult. Immediately following TBI the metabolic needs of the brain are increased, yet paradoxically there is a "flow/metabolism mismatch" with impaired or decreased cerebral blood flow (CBF) and oxygen delivery secondary to both vasogenic and cytotoxic edema.
A historical review of the literature goes dates back to the 1950’s with a study of CBF in humans by Lambertson, et al. From the 1950’s through the mid-1980’s there were many excellent studies and experiments on both human and canine models of TBI with the majority of results favoring HBO in the use of TBI. The most important of these studies was one by Holbach, et al who demonstrated an ideal depth of 1.5 ATA. However, many in many of these studies there was a lack of uniformity in the protocols, a paucity of randomization, as well as too small of sample sizes, which limited their strength. However, in 1988 a well performed study by Contreras et al showed that HBO had a persistent and beneficial effect on cerebral glucose metabolism in rats. In the 1990’s studies by Mink, et al and Siddiqui, et al respectively described the effects of HBO on promoting the blood-brain barrier integrity following global cerebral ischemia and molecular oxygen acting as both a respiratory metabolite and signal transducer to promote healing.
In 1992 the author’s published the first modern prospective RCT on the efficacy of HBO in the treatment of severe TBI in humans. While overall this trial did not show any benefit at one year, there was notable improvement in the subgroup analysis of patients who were severely injured with a GCS between 4-6, had elevated ICP and required surgical evacuation of mass lesions, with a ~50% reduction in mortality compared with controls. Additionally, this study, with a total 1688 HBO treatments, demonstrated the safety and efficacy of using HBO in critically injured patients with no reports of oxygen toxicity or significant complications. In 2001, Rockswold, et al wanted to elucidate and further understand the metabolic effects of HBO in TBI and completed a follow up clinic study on 37 severely injured patients. In this study they noted a shift towards aerobic metabolism up to 6 hours post-HBO when followed by 100% normobaric oxygen by measuring such parameters as cerebral blood flood, CSF lactate levels, and ICP. Finally, in 2004, Daugherty, et al in a basic science article, presented convincing data corroborating the clinical findings of Rockswold, et al on the benefits of HBO in TBI with ex vivo measurements of mitochondrial metabolic activity in rats. They concluded that mitochondrial function may be depressed after TBI, but there is a potential for HBO enhancement of mitochondrial function recovery.
And, more recently, continued studies in the non-human models have demonstrated improved cognitive recovery, increased cerebral ATP levels, and reduced hippocampal neuronal cell loss with HBO following TBI. The authors summarized their findings and completed the article by discussing safety and oxygen toxicity issues confronting the HBO provider. Lastly, the future scope of HBO in TBI was discussed with a mention of ongoing trials.
Overall, this was an excellent and thorough review of the literature on the subject of HBO in TBI. It is worthwhile for our community to be aware of the subject and to understand that many academic HBO centers have expressed interest in possible multicenter trials in the future.
Reviewer: Christopher J. Logue, MD
Hopkins RO, Weaver LK, Valentine KJ, et al. Apolipoprotein E genotype and response of carbon monoxide poisoning to hyperbaric oxygen treatment. Am J Respir Crit Care Med. 2007; 176(10):1001-1006.
This is another article utilizing data from the large RCCT published in the New England Journal of Medicine from the same group back in 2002. The article looks at a possible link to poor neurological outcome after acute CO poisoning in association with the presence of the apolipoprotein E (APOE) e4 allele.
APOE is a lipid binding protein involved in the distribution of cholesterol in the brain and is important for membrane synthesis and neuritic growth and repair. APOE synthesis is upregulated by astrocytes and oligodendrocytes in response to nervous system injury. Specifically, presence of the APOE e4 allele (expressed in 14-25% of the population) has been linked as a risk factor for the development of Alzheimer’s Disease and poor neurological outcomes following other neurological insults such as traumatic brain injury and hemorrhagic stroke.
The authors tested for APOE genotypes in 86 of the 152 patients from the RCCT. 36% of the patients had at least one e4 allele present. Comparison of six week neurological sequelae following CO poisoning revealed that when the APOE e4 allele was absent, patients who received hyperbaric oxygen (HBO2) treatment had a very low incidence of neurological sequelae (only 11%). When the e4 allele was present, HBO2 was not effective in reducing the incidence of sequelae (35% had sequelae). Interestingly, in the control arm (normobaric group), if the e4 allele was absent the incidence of neurological sequelae was 43%. The reduction in the incidence of neurological sequelae in the group of patients treated with HBO2 where the e4 allele was absent was statistically significant.
The authors conclude that HBO2 therapy reduces the incidence of neurological sequelae following CO poisoning specifically in patients without the APOE e4 allele. Since, at the time of poisoning we do not know which patients do or do not carry this allele, treatment with HBO2 is recommended.
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Case Reports of the Hyperbaric Medicine Section
Marvin Heyboer III, MD, FACEP
A 44-year-old otherwise healthy male recreational SCUBA diver presented with a complaint of left hand pain, swelling, and numbness that developed 2-3 hours after ascending from an open water dive 2 days ago. The symptoms were worst with flexion/extension of the metacarpal-phalangeal (MCP)s (especially the index finger) and wrist with radiation up into the elbow. The paresthesias were present in the dorsum of his hand with radiation into the forearm and at times just proximal to the elbow. The patient was an unreliable historian regarding his dive depth and time. He had a dive computer, but he was unable to access it without the assistance of his wife who was his dive buddy (and not present at time of initial assessment). He reported two morning dives. The first dive started at 0900 to a maximum depth of 50 FSW for a dive time of 40 minutes with a 5 minute safety stop at 15 FSW. He then had a 40 minute surface interval before his second dive to a maximum of 50 FSW for a dive time of 40 minutes. This put him within the Navy Dive Tables no-decompression limits.
The patient further reported a history of previous similar episodes to the dorsum of the right hand after dives three separate times in the past year. The symptoms resolved spontaneously over a week after the event.
He has been recreational diving for the past one year. His past medical & surgical history were unremarkable. He’d had previous orthopedic left shoulder surgery and left knee surgery.
On physical exam, he had stable vital signs. He was a healthy appearing pleasant gentleman resting comfortably. Examination of his left upper extremity showed edema and pain to the dorsum of the hand from the wrist to the MCP’s. There was palpable grinding versus crepitance with active flexion and extension over the 2nd extensor tendon. No redness, warmth, or streaking present. No evidence of deformity. Neurological exam showed subjective finding of paresthesias with palpation over the left radial forearm and dorsum of the hand. He had normal 2-point touch and pain sensation.
Chest X-ray, Wrist and Hand X-rays, EKG, and laboratory studies were unremarkable.
What is your differential diagnosis? How would you proceed? Would you treat with hyperbaric oxygen?
To be continued . . . The rest of the case will be presented in the next issue of the newsletter.
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Karen Van Hoesen, MD
UCSD Undersea and Hyperbaric Medicine Fellowship
The UC San Diego (UCSD) Fellowship in Undersea and Hyperbaric Medicine is a 12 month fellowship that incorporates training in all aspects of hyperbaric and diving medicine. The fellowship is associated with the ACGME accredited residency in emergency medicine at UCSD and has a multidisciplinary interaction with the UCSD Wound Center, San Diego Regional Poison Center, UCSD Trauma and Burn Centers, Paradise Valley Hospital Wound and Hyperbaric Center, and Long Beach Memorial Hyperbaric Center. The UCSD Division of Hyperbaric Medicine has had a successful non-ACGME accredited fellowship since 1998 and received ACGME accreditation in 2006.
Fellows gain experience in monoplace and multiplace chamber operations, pediatric and adult treatments, management of critically ill patients in the hyperbaric chamber, indications for hyperbaric oxygen therapy, and evaluation of divers for fitness to dive and diving injuries. Physicians successfully completing the one-year fellowship should obtain sufficient didactic and practical knowledge to work efficiently and competently in a hyperbaric clinical and research environment and to act in a supervisory capacity of a hyperbaric chamber. Our program has been carefully designed to train 2 fellows per year. Each fellow spends 6 months at UCSD on the hyperbaric medicine service, 2 months at Paradise Valley Hospital at the Hyperbaric Medicine and Wound Care Center, 2 weeks at Long Beach Memorial Hyperbaric Center for monoplace chamber experience, 2 months of dedicated research time and 2 weeks at the UHMS/NOAA Dive Physicians Training course. The UCSD hyperbaric chamber is a large multiplace chamber at UCSD Medical Center that is capable of treating the full range of conditions amenable to hyperbaric oxygen therapy. The staff is on call 24 hours per day, 7 days per week.
One unique aspect of our training program is the hands-on experience with diving medicine. The San Diego EMS system and Coast Guard bring all acute diving injuries in the San Diego area to the UCSD emergency department for evaluation. We see 30-40 diving accident cases per year at UCSD. Additionally, the UCSD Diving Medicine Clinic is the largest regional diving medicine clinic in Southern California. Fellows work directly with faculty at the clinic which is held weekly at the UCSD Occupational and Environmental Medicine Clinic. The fellow is responsible for initial and annual physical exams for commercial divers, scientific divers, and sport divers for clearance for diving or problems with diving such as ear barotrauma, asthma or follow-up of decompression illnesses. Our faculty and fellows participate in the San Diego County Coroners committee for the investigation of diving fatalities and attend all autopsies on diving fatalities in San Diego County. Additionally, we participate in the Scripps Institute of Oceanography Diving Program.
The Hyperbaric Center averages 160 new consults per year and over 2500 patient treatments per year. Many outlying hospitals in San Diego County refer patients with gas gangrene and necrotizing infections to UCSD for acute hyperbaric oxygen therapy. The San Diego Regional Poison Center is located at UCSD Medical Center and provides 24-hour on-call services for carbon monoxide poisoning. The UCSD Hyperbaric Medicine service consist of biweekly clinics during which the fellow and attending see all the patients undergoing hyperbaric oxygen treatments and includes examinations and debridement of wounds and dressing changes. The fellow is directly involved in seeing both inpatient and outpatient consults and responsible for seeing all emergency consultations presenting to the emergency department including diving injuries, carbon monoxide poisonings (in conjunction with the toxicology service) and cases of necrotizing fasciitis and gas gangrene. The fellow supervises the hyperbaric oxygen treatments under the direct supervision of the faculty.
The UCSD Hyperbaric Medicine faculty are recognized nationally and internationally as leaders in the field of undersea and hyperbaric medicine. Over 50% of our fellows have stayed in academic medicine and we have a 100% success rate on passing the subspecialty board examination.
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