Section Activities at ACEP13 - Undersea and Hyperbaric Medicine Section Newsletter, October 2013
ACEP13 (Scientific Assembly) Seattle, WA - October 14-17
Monday, October 14th, 12:30pm -1:50 pm
“The Great Debate: Hyperbarics and Carbon Monoxide Poisioning”
Dr. Tracy LeGros, Dr. Stephen Thom, Dr. Jerome Hoffman, Dr. William Mallon
Wednesday, October 16th, 9am-11 am
Undersea & Hyperbaric Medicine Section Meeting
LOCATION: Sheraton Seattle Hotel, Ballard Room
|Speaker:||Dr. Tracy LeGros will present “Iatrogenic Radiation Injuries”|
|Business meeting:||Review and approval of prior meeting minutes|
Report on collaboration with UHMS
Voting on proposed changes to section operational guidelines
Please review linked document and proposed changes making the terms of all section officers 2 years rather than 1 year.
Attend the Sections Showcase!
Find your niche.
Build your network in Emergency Medicine.
Visit the Sections Showcase!
Exhibit Hall Sky Bridge, Washington State Convention Center
Monday, October 14, 2013
9:30 AM - 11:00 AM
University of Florida, College of Medicine /
Network for Pancreatic Organ Donors with Diabetes (nPOD)
Fellow’s Diving Medicine eConference - Undersea and Hyperbaric Medicine Section Newsletter, October 2013
We’ve had outstanding turnout for the “Fellow’s Diving Medicine eConference” over the past few months and we hope to keep this going. Current Duke fellows, Dr. Marlon Medford and Dr. Jude Viola are the organizers of the internet-based video conference which is held on the first Tuesday of every month. Please contact them if you are interested in participating. We request that everyone who joins the conference be prepared to participate in productive, open discussion about the cases. We also ask that you enable your webcams!
|Conference dates:||Tuesday 11/5, 3 PM Eastern:||Hennepin fellows presenting|
| ||Tuesday 12/3, 3 PM Eastern: ||Duke (Salt Lake fellows) presenting|
Greetings from the UHMS!! - Undersea and Hyperbaric Medicine Section Newsletter, October 2013
Tracy Leigh LeGros, MD, PhD, UHM, FACEP
We had a wonderful meeting in Orlando, Florida last month, and I have to tell you, the meeting was intense!! I was very fortunate to be named to the Board of Directors, and I know that both this group and the therapy committee had a lot of important work to go through. However, we also had some fun, and it is my pleasure to report the highlights of this great meeting.
The first pre-course was “Hyperbaric Oxygen Safety: Technical and Clinical Considerations.” The second one was “How to Prepare for Accreditation.” Both courses were very well-received and highly informative.
THE PRESIDENT’S ADDRESS
John J. Feldmeier, DO, FACRP, FUHM gave an inspiring address to the audience and gave a State of the Union for the UHMS that included identification of ongoing challenges to the UHMS and updates regarding current UHMS strategic initiatives.
THE PLENARY SESSIONS: These sessions were very well-attended and well-received!!
- “Rebreathers: Deep Capability or Deep Trouble” was moderated by Dr. Simon Mitchell, MB, ChB, PhD, DipDHM, FUHM, FANZCA.
Dr. Mitchell is the Head of the Department of Anesthesiology at the University of Auckland. He contributes to many works such as Harrison’s Principles of Internal Medicine, Bennett and Elliott’s Physiology and Medicine of Diving, and the American Physiological Society Handbook of Physiology. He is an avid technical diver, was the recipient of the Albert R Behnke Award in 2010 and is an inaugural Fellow in the UHMS. His lecture discussed the use of rebreather devices and their associated benefits and risks. Rebreathers are becoming increasingly popular among the recreational diving community and seem to contribute to a disproportionate number of recreational diving fatalities.
- “International Perspectives on Hyperbaric Oxygen Therapy” was moderated by Dr. Ken LeDez and panel.
Dr. LeDez is the first President of the Canadian Chapter of the UHMS. He is a recognized specialist in Diving and Hyperbaric Medicine by Canada’s offshore petroleum industry. He was the academic chair of anesthesiology at memorial University in Newfoundland, and on the editorial Board of the Canadian Journal of Anesthesia for nine years. He was also a member of the Executive Board of the Canadian Anesthesiologists Society. He continues on the Standards of Practice Committee and Research Committee for the Canadian Anesthesiologists Society. He is the current Vice President of UHMS and serves on the UHMS Board of Directors in this capacity.
- “New Pearls of Wisdom in the Diving and Hyperbaric Medicine Literature” was very well presented by the UHM Fellows from San Diego (see below)
“Hyperbaric Oxygen for Diabetic Foot Ulcers: A Need for Clinical Practice Guidelines” was presented by Dr. Enoch Huang, MD, MPH & TM, FACEP, UHM/ABEM, CWSP, FACCWS, FUHM.
- Dr. Jose Evangelista received his medical degree from Tufts and completed his internal medicine residency at Yale New Haven Hospital. He also completed a fellowship in Pulmonary and Critical Care Medicine. He is boarded in both of these specialties and will be triple boarded (in UHM as well) very soon! He is an avid SCUBA diver and plans on continuing his work in both hyperbaric medicine and critical care.
- Dr. Davut Savaser is attending in Emergency Medicine in San Diego. He obtained his medical degree from Albert Einstein College of Medicine in the Bronx and attended the Harvard University School of Public Health, receiving a Masters of Public Health in Quantitative Methods with a focus in Decision Sciences. He plans on continuing his work within the UC Sand Diego Health System as a hyperbaricist and an emergency medicine specialist.
Dr. Huang is the medical director of the wound Healing and Hyperbaric Medicine Department at the Adventist Medical Center in Portland, Oregon. He attended Tulane School of medicine and completed an Emergency Medicine residency at the University of California at Irvine. He completed his Undersea and Hyperbaric Medicine fellowship at the University of Pennsylvania. His current positions include: ABEM representative to the ABPM Undersea and Hyperbaric medicine Board Examination Committee, President of the Columbia Wound Care Consortium, Chairman of the Publications Committee of UHMS and the President of the Pacific Chapter of the UHMS. His lecture served as an outstanding review of HBOT in the treatment of diabetic foot ulcers and thoroughly reviewed current literature on the topic.
“Department of Defense HBO2 Clinical Trials from Post Concussive Symptoms Due to War and Related Traumatic Brain Injury” was presented by Dr. Lindell Weaver, CTR George Wolf, CPT Brett Hart, Colonel Miller and Colonel McCrary.
THE MODERATED SESSIONS: Six sessions were moderated, and very well I might add!!
Session A: Diving / DCS: Theory and Mechanisms
(moderated by Nick Bird, MD & Kevin C. Buford, MD)
Session B: HBO2 Theory and Mechanisms
(moderated by Jeannie Le, MD and panel)
Session C: Clinical HBO2, CO Poisoning & Wound Healing
(moderated by Heather Murphy-Lavoie, MD, FACEP and Gus Gustavson, ACHRN, CHT
Session D: Diving & Dive Accident Management
(moderated by Robert W. Sanders, MD, FACEP and Kip Posey, CHT)
Session E: HBO2 Therapy, Chambers and Equipment
(moderated by Takkin Lo, MD, MPH, and Sue Churchill, NP)
Session F: Diving Equipment and Decompression Illness
(moderated by Neal W. Pollock, PhD & Laura Josefson)
THE AWARDS CEREMONIES: Below you will find a few of the award recipients. The complete list can be found here:
Best Oral Presentation: Stephen R Thom, MD, FACEP!!!
Best Trainee Presentation: Bruce J. Derrick, MD
The Albert R. Behnke Award: Richard Moon, MD
Craig Hoffman Memorial/Charles W. Shilling Award: James Holm, MD, FACEP and Tracy LeGros, MD, PhD, UHM, FACEP
Young Scientist/Medical Director Award: Bruce J. Derrick, MD and Masaki Horie, PhD
THE KEYNOTE ADDRESSES: These were great lectures that were enjoyed by all!!
The Lambertsen Lecture: Was given by Dave Kenyon and was entitled: “Deep Underground Tunneling: A New Challenge in Manned Hyperbaric Productivity.”
Dave Kenyon is a senior mechanical and systems engineer with decades of experience in engineering, pharmaceutical, medical device design. He has been a colleague of Dr. Bill Hamilton for over 40 years and their joint efforts have yielded decompression systems and procedures used the world over. He is the Principal Engineer for Hamilton Research, Limited.
The Kindwall Lecture: This lecture was given by Dr. George Hart and was entitled: “A Half Century in Hyperbaric Medicine.”
Dr. Hart graduated from the University of Texas School Of Medicine, Galveston, Texas and completed his internship at Rochester General Hospital in New York. He was in the Field Medical service for two years, and then completed his General Surgical Residency at Portsmouth Naval Hospital in Virginia. He then completed a Thoracic Surgery Residency at the Naval Hospital in St Albans, New York and was then named Chief of Surgery at the Naval Hospital at Guantanamo Bay, Cuba. He was also the Chief of Surgery at the Naval Hospital in Long Beach, California. He has also been the Director of Clinical Services and Chief of Surgery at the Naval Hospital in Corpus Christi, Texas and was the Director of Hyperbaric Medicine at the Memorial Medical Center at Long Beach, California.
AND NOW, TO END WITH A LITTLE HISTORY LESSON
To learn more about the men for whom the lectures are named see the links provided.
Christian James Lambertsen: was principally responsible for developing the United States Navy frogman’s rebreather. http://en.wikipedia.org/wiki/Christian_J._Lambertsen
Dr. Eric Kindwall is known as the "Father of Hyperbaric Medicine.” http://membership.uhms.org/?page=ASM_SpecialLectures
Hyperbaric Oxygen, Sepsis and Inflammation - Undersea and Hyperbaric Medicine Section Newsletter, October 2013
Marlon A. Medford, MD
Hyperbaric Medicine Fellow
Hyperbaric oxygen for a headache instead of aspirin? Not exactly, but growing basic science research is pointing toward an anti-inflammatory role for HBO2 particularly in sepsis. It may well be a ways off that HBO2 finds a clinical use for treating septic patients, but emerging laboratory data is suggesting that this might well be possible in future.
During the golden age of HBO2 in 1960’s and 1970’s, HBO2 found got a reputation as a cure all, a magic potion for ailments ranging from diabetes to autism. It was during this time that the earliest work on the effect of HBO2 on bacterial infection was pursued. In a petri dish Ross and McAllister showed that HBO2 was bacteriostatic to a number of gram-positive organisms including Streptococcus and Staphlococcus ssp. In vivo HBO2 improved survival in mice with S. pneumonia septicemia and so HBO2 found itself another magic purpose!. In the years that followed it became clear that HBO2 was finding clinical applications without the rigorous studies to justify such applications. HBO2’s impressive list of uses had to be reorganized into but a handful of evidence based indications that included a number of conditions in which inflammation and/or infection plays a central role such as radiation injury and necrotizing fasciitis. In the basic science realm, work continued on. A variety of animal models using a number of HBO2 protocols were consistently revealing that the effect of HBO2 during sepsis went beyond bacteriostasis and into inflammatory cytokine expression. Such cytokines included Interleukin-6, Tumor Necrosis Factor-α (TNFα) and of particular interest, inducible nitric oxide synthase (iNOS) . These cytokines are transcribed under the control of the transcription factor, NFKB, its genetic commander-in-chief. Interestingly HBO2 suppresses these pro-inflammatory cytokines, designed to wreak havoc on pathogenic microrganisms but which cause collateral damage to healthy host tissue. A good example of this is the lung where a sustained pro-inflammatory response leads to acute lung injury (ALI) and acute respiratory distress syndrome (ARDS). Interestingly HBO2 prevents development of ALI/ARDS in animal models during sepsis . This finding has since been replicated and is felt to be due in part to iNOS suppression by HBO2 [2-7]. Pro-inflammatory suppression is not the whole story. As if by magic, HBO2 simultaneously increases anti-inflammatory cytokines to help protect against tissue injury caused by inflammation. Interleukin 10 for example appears crucial to survival of sepsis in mice treated with HBO2. Buras et al proved this by showing that mice lacking the IL-10 gene showed no survival benefit when treated with HBO2 . More recently HBO2 was found to increase hemeoxygenase 1 (HO-1) levels in the lung during sepsis. HO-1 is a true anti-inflammatory molecule and is particularly protective in the lung where under conditions of heme and oxidative stress is highly induced, scavenging free heme and limiting tissue inflammation. This is particularly exciting since HO-1 has received much attention lately as a novel therapeutic target for anti-inflammatory drug therapy.
A more coherent pattern of pro-inflammatory suppression and anti-inflammatory up-regulation is beginning to unfold, as the mechanism by which HBO2 mediates sepsis survival animal models becomes better understood and, as with most things, is likely to be more complicated than at first glance. The inflammatory cascade in humans and in mice remains a very sophisticated system with still poorly understood mechanisms of crosstalk and interdependent pathways. Whether patients with sepsis will routinely receive HBO2 therapy to improve outcome is to be seen, but its effect on inflammatory markers during sepsis is a very fascinating field of study and perhaps the clues revealed by work in this area will someday benefit patients in a real world setting.
- Ross RM, McAllister TA. Protective Action of Hyperbaric Oxygen in Mice with Pneumococcal Septicaemia. Lancet. 1965;1(7385):579-81.
- Huang TY, et al. Hyperbaric oxygen attenuation of lipopolysaccharide-induced acute lung injury involves heme oxygenase-1. Acta Anaesthesiol Scand. 2005;49(9):1293-301.
- Pedoto A, et al. Beneficial effect of hyperbaric oxygen pretreatment on lipopolysaccharide-induced shock in rats. Clin Exp Pharmacol Physiol. 2003;30(7):482-8.
- Thom SR, Lauermann MW, Hart GB. Intermittent hyperbaric oxygen therapy for reduction of mortality in experimental polymicrobial sepsis. J Infect Dis. 1986;154(3):504-10.
- Gennari R, Alexander JW. Effects of hyperoxia on bacterial translocation and mortality during gut-derived sepsis. Arch Surg. 1996;131(1):57-62.
- Huang CJ, et al. NF-kappaB involvement in the induction of high affinity CAT-2 in lipopolysaccharide-stimulated rat lungs. Acta Anaesthesiol Scand. 2004;48(8):992-1002.
- Huang CJ, et al. Resuscitation of hemorrhagic shock attenuates intrapulmonary nitric oxide formation. Resuscitation. 2002;55(2):201-9.
- Buras JA, et al. Hyperbaric oxygen protects from sepsis mortality via an interleukin-10-dependent mechanism. Crit Care Med. 2006;34(10):2624-9.
Hyperbaric Oxygen Therapy for Radiation Necrosis of the Brain: What an Emergency Physician Should Know - UHM Section Newsletter, October 2013
Alina D. Hulsey, MD
It isn’t out of the ordinary for emergency physicians to encounter patients with neurological complaints, but what about those patients that previously have had brain cancer treated with radiation therapy? If the MRI or CT of the brain shows a new lesion with edema surrounding an irradiation site (the infamous ‘ring enhancing lesion’), one’s first instinct might be to consult neurology or neurosurgery, then move on to the next patient! But what treatment options are available for these patients? In this article we give an overview of radiation-induced necrosis of the brain, a previously uncommon entity that is becoming more commonplace due to the growing popularity of stereotactic radiosurgery for brain tumors. We explore also how hyperbaric oxygen might be useful for these patients by taking a look back through our published experience in hyperbaric medicine of treating this troublesome complication.
Radiation necrosis (RN) of the brain is on the rise due to greater utilization of stereotactic radiosurgery (SRS) and combined modality therapies for brain tumors. The occurrence of RN is in part a function of radiation dose where the higher the dose, the higher the incidence. Accurate diagnosis of RN remains difficult despite having access to several imaging modalities due largely to the fact that radiographically, a new tumor looks similar to brain necrosis. The problem of RN begins with radiation to the brain that in turn causes vascular injury and initiating necrosis. This leads to vascular endothelial damage, fibrinoid necrosis of small arterial vessels and, in the end, a focal coagulative necrosis characterized by oligodendrocyte damage and demyelination. At the molecular level, radiation damages chromosomes (which alters chromosomes and thus gene expression). Inflammation results in increased vascular and blood brain barrier (BBB) permeability, inflammatory cell recruitment (particularly macrophages) and consequent activation and cytokine release.
Typically treatment options for RN of the brain include corticosteroids, NSAIDs, neuromodulators, NO and Calcium-Channel Blockers, agents reducing endothelial permeability, antibodies, Cox-Inhibitors, glutamate channel blockers, and agents blocking apoptosis induction. A seldom utilized option is hyperbaric oxygen (HBO2) treatment.
Within the brain, HBO2 treatment is known to prevent irradiation-induced inflammatory cell infiltration, and by stabilizing microglia and calcium homeostasis, reduces synthesis of neurotoxic cytokines, neutrophilic factors and nitric oxide production (NO) thus reducing CNS inflammation. HBO2 also induces angiogenesis, blocks apoptosis and, counter intuitively, reduces the toxicity of O2-derived free radicals in neural tissue.
There are comparatively few studies that look at HBO2 therapy for RN of the brain; a Pubmed search yields about thirteen peer-reviewed articles and/or abstracts that provide evidence for the use of HBO2 treatment in RN of the brain. Perhaps the first case series on this subject was published in 1976, when Hart and Mainous found one patient with radiation encephalitis out of 56 studied, whose symptoms had resolved with the use of HBO2. This ought to have sparked interest in this area but it wasn’t until 1997 when Chuba et al, in a 10 patient case series, found that HBO2 initially improved or stabilized symptoms in all of his patients. At the time of follow up in this series, six out of ten patients were alive; three out of those six had no evidence of disease. Gesell et al, in 2002 in second case series, published an abstract reporting that 58% of her patients had improvement in neurological exam following HBO2 therapy. In yet another case series by Dear et al, 2002 nine out of twenty patients had improved with HBO2 therapy, although 11 of these 20 had glioblastoma multiforme (GBM). This study used a very short course of therapy (mean of 13 treatments) in patients with the rapidly lethal GBM. The study was published only in abstract form and the details of this series are not available for further analysis. One of the largest studies on the topic however was by Ohguri et al in 2007 who performed a nonrandomized control study of 78 patients who were enrolled within 1 week from receiving SRS. The authors found that among the 32 of 78 patients who received HBO2 therapy, the one-year probability of white matter injury was significantly better in the HBO2 group (2%) when compared to the non-HBO2 group (36%). This suggested that prophylaxis with HBO2 significantly improved outcomes in patients likely to develop brain RN following SRS. In between these studies are a number of case reports of a positive outcome using HBO2 and, as with case reports, are subject to reporting bias. Nonetheless of all available data compiled without sophisticated statistical analysis, overall HBO2 therapy improves neurological outcomes in 69.5% of published cases.
There is growing evidence that HBO2 benefits patients with RN of the brain following radiation exposure, and larger, more rigorous studies will be needed before definitive claims can be made. Short of a large double-blinded randomized control trial, HBO2 remains a promising modality with emerging evidence of its efficacy both in prophylaxis and treatment for patients with RN of the brain.
- Chao ST. Challenges with the diagnosis and treatment of cerebral radiation necrosis. Intern J Radiation Oncol, Biol, Physics. 2013.
- Kuffler DP. Hyperbaric oxygen therapy: can it prevent irradiation-induced necrosis? Experimental Neurol. 2012;235(2):517-27.
- Rahmathulla G, Marko NF, Weil RJ. Cerebral radiation necrosis: a review of the pathobiology, diagnosis and management considerations. J Clin Neuroscience: Official Journal of the Neurosurgical Society of Australasia. 2013;20(4):485-502.
- Hart GB Mainous EG. The treatment of radiation necrosis with hyperbaric oxygen (OHP). Cancer. 1976;37(6):2580-5.
- Chuba PJ et al. Hyperbaric oxygen therapy for radiation-induced brain injury in children. Cancer. 1997;80(10):2005-12.
- Girnius S, et al. Treatment of refractory radiation-induced hemorrhagic proctitis with hyperbaric oxygen therapy. Am J Clin Oncol. 2006;29(6):588-92.
- Ohguri T, et al. Effect of prophylactic hyperbaric oxygen treatment for radiation-induced brain injury after stereotactic radiosurgery of brain metastases. Intern J Radiation Oncol, Biol, Physics. 2007;67(1):248-55.