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Undersea and Hyperbaric Medicine Section Newsletter - March 2010, Vol 17, #1

Hyperbaric Medicine

circle_arrow Message from the Chair
circle_arrow Acute Painless Vision Loss: Time is Vision!
circle_arrow Mark Your Calendars
circle_arrow Necrotizing Soft Tissue Infection of the Foot

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Hyperbaric Medicine Section


Message from the Chair

Tracy Leigh LeGros, MD, PhD, FACEP
Program Director, LSU Undersea and Hyperbaric Medicine Fellowship

Greetings everyone, from New Orleans, where things feel a little bit different now. The Super Bowl is over, and I must say, it was a different viewing experience down here in the Big Easy. The Saints victory certainly was a nice belated holiday gift for all of us. That being said, I hope all of you had joyful and inspiring holidays as well.

Monthly Meeting of Hyperbaric Fellowships:

The Hyperbaric Fellowships of Duke, San Diego, Hennepin, University of Pennsylvania, San Antonio, and LSU have combined resources to partake in a monthly conference. The next newsletter will detail this meeting. However, I bring it up now to encourage all Hyperbaric Fellowships, and other interested parties, to join us. We have set up a teleconference on the 1st Wednesday of each month (3 pm Central Standard Time). Each site dials in, and each Fellowship takes a turn presenting an interesting diving case(s) and / or Fitness to Dive scenarios. It is a very worthwhile and educational endeavor. If you are interested in learning more, please contact this section's Newsletter Editor Raphael Colon-Hernandez, MD, for more information.

Annual Hyperbaric Board Examination Review Course:

Chris Logue, MD, from the University of Pennsylvania, has authored a section on the huge success of this wonderful course. He will fill you in on the tremendously positive effects that this course, along with a course offered by Dr. Paul Sheffield, had on the board examination rates and on the confidence of those taking this difficult examination. This course was the brainchild of Dr. Logue, and it was amazingly successful. I was fortunate enough to be part of a very well rounded, hand-picked faculty from hyperbaric fellowships around the country. Chris's course was a multi-day, collaborative effort that was very well received. It is going to be offered again this year, so please keep your calendars marked.

Academic Association With Council of Emergency Medicine Residency Directors:

Dr. Ian Glover and Dr. Chris Logue have nurtured and developed a significant step in the progression of our academic partnerships. The Council of Emergency Medicine Residency Directors was started as a scientific and educational organization to improve the quality of emergency medical care, and to maintain high standards of excellence and training in emergency medicine residency programs. Moreover, one of its core missions is to improve communications between the faculty of emergency medicine training programs. Toward this end, they have agreed to sponsor us in the Associate Membership Category. All hyperbaric medicine fellowships, and those interested in starting a fellowship, are welcome to join. The qualifications include any established or proposed undersea and hyperbaric medicine fellowship that accepts (or plans to accept) emergency medicine graduates as Fellows. Membership benefits include access to all of the resources of full members, including the SharePoint Members only website, subscription to the Internet Based Test Site for Residents, the CORD all member listserv, the HBOT specific listserv, the HBOT SharePoint work area, and the CORD Academic Assembly. The annual dues are $375 per calendar year per program. Each program is able to designate their Program Director, Administrative Coordinator, and two additional faculty representatives without additional cost. If a program wishes to have additional faculty representatives, the cost is $50 per additional representative. Please contact Barbara A. Mulder, the Executive Director of CORD (901 N. Washington Avenue, Lansing, MI 48906) for further information. You may also call her at 517.485.5484.

ACEP Resolution for Support for Undersea and Hyperbaric Medicine Fellowships:

Presently, I am drafting a formal resolution before the ACEP Council in support of our continuing efforts in providing outstanding clinical care for our patients and educating future hyperbaricists. As you may know, there is some concern on the part of our regulatory agencies as to the value of continued accreditation of fellowships due to the low number of new programs. I have been in touch with Margaret Montgomery, the practice management manager for ACEP, and she has given me some direction, in the form of a similar resolution put forth by our colleagues in Critical Care Medicine. This was an initiative begun by our own Dr. Chris Logue, and I will be running this by him and Dr. Heather Murphy-Lavoie, prior to its submission.

Hyperbaric Medicine Fellowship Survey:

You may be receiving a phone call, email, or a letter asking you to participate in a survey being conducted by one of our LSU Fellows, Dr. Marina Wilder. She has undertaken the task of surveying all hyperbaric fellowships (and all potential fellowships) regarding their fellowship needs, difficulties, and future plans. It is part of a collaborative initiative to gather information to bring before our governing bodies in support of the continuation of hyperbaric fellowship training. We have seen a number of facilities put forth applications for new fellowship sites. From the information we have gathered thus far, we seem to have a pretty good idea what the barriers to fellowship development are, for most potential programs. I intend, with help from the other Fellowship Program Directors, to meet with our governing bodies, and present them with our plan not only to develop other fellowship programs, but to strengthen our own programs. Please, if you are contacted by Dr. Wilder, take a minute to fill out her survey. It may help all of us greatly.

And Finally.....

I want to end this message by thanking all of you for belonging to this section. Please take the time to review the excellent article on Central Retinal Artery Occlusion and Hyperbaric Oxygen Therapy by Dr. Heather Murphy-Lavoie and Dr. Frank Butler, as well as the Case Presentation by Dr. Raphael Colon-Hernandez. I think you will find them very enjoyable.  


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Acute Painless Vision Loss: Time is Vision!

Heather Murphy-Lavoie, MD
Frank K. Butler Jr, MD

Ocular complaints comprise a small percentage of annual ED visits per year; however, these ocular pathologies can be some of the most life altering for our patients. One study sites only 2.3 million annual visits to the ED in the United States for problems related to the eye and ocular adnexa.1, 3 Although approximately half of these cases are traumatic1, the morbidity (both physical and psychological) of acute, non-traumatic, painless vision loss deserves special mention. As little as one or two hours of delay may make the difference in whether or not the patients vision is restored. 2, 3, 4, 10, 11 The major differential diagnosis of acute painless vision loss includes: Central Retinal Artery Occlusion (CRAO), Central Retinal Vein Occlusion (CRVO), vitreous hemorrhage, retinal detachment, ischemic optic neuropathies, amaurosis fugax, and posterior circulation cerebral vascular accidents.3 None of these is as crucially time-sensitive as is CRAO, which was recently added to the Undersea and Hyperbaric Medical Society’s list of approved indications for hyperbaric oxygen therapy (HBOT).2

Time is vision and hyperbaric oxygen therapy (HBOT) can save vision if administered before irreversible ischemia has occurred.  

The classic presentation of CRAO is sudden painless loss of vision in the range of light perception to counting fingers. On dilated fundoscopic exam patients with CRAO will classically have a pale yellow/white appearing retina due to ischemia or necrosis. A cherry red spot may develop in the macula but may not always be present. Other physical exam findings may include: an afferent pupillary defect and boxcarring of arterioles. 

Traditional therapeutic regimens for CRAO have been aimed at promoting a downstream movement of the embolus by lowering intraocular pressure and producing vasodilatation. These measures include ocular massage, anterior chamber paracentesis, intraocular pressure lowering medications, vasodilators, and oral diuretics. 3 These treatment modalities have been relatively unsuccessful. 2,3,4,14,15,16 Acute obstruction of the central retinal artery, even when treated promptly, typically results in severe, permanent visual loss. Hayreh stated that no currently used therapy is efficacious for CRAO. 16

Hertzog et al reported a series of 17 patients with CRAO treated with HBO. They retrospectively divided patients into 4 treatment groups based on the time to onset of treatment and noted that HBO seemed most useful in preserving visual function when applied within the first 8 hours from the onset of visual impairment. The authors point out that the colloquialism "Time is Muscle" used in management of myocardial infarctions can be changed to "Time is Vision" in CRAO.2, 11

In 2001, Beiran published a retrospective controlled trial of 35 patients treated with hyperbaric oxygen therapy compared to 37 matched controls from another facility where hyperbaric oxygen was not available. All patients were treated within 8 hours of symptom onset and none of the patients included in the trial had a cilioretinal artery. The patients in the hyperbaric group received 2.8ATA for 90 minutes BID for the first three days and then once daily until no further improvement for 3 consecutive days. In the hyperbaric group, 82% of the patients improved compared to only 29.7% of patients in the control group. Improvement was defined as reading at least 3 lines better on Snellen chart compared to admission. The mean visual acuity for the hyperbaric group at discharge was 6/20 in metric or about 20/70 in feet.2,12 A variety of other case reports have shown restoration of vision beyond this ideal 8 hour window; however, the majority of positive results have been reported when treatment is instituted within 24 hours of symptom onset.2

Patients presenting within 24 hours of vision loss should be considered for hyperbaric oxygen therapy. While there are a few case reports of patients presenting after this time interval having positive results when treated with hyperbaric oxygen therapy, the majority of cases do not respond when treated beyond this point.2

Table 1 

Emergent HBOT in Patients with
Acute Vision Loss: Selection Criteria4

HBOT is indicated emergently in patients who present with acute vision loss and meet the following criteria:

  •         Presentation within 24 hours of vision loss
  •         Corrected visual acuity 20/200 or worse
  •         Visual acuity still 20/200 or worse with pinhole testing
  •         Age > 40
  •         No pain associated with the vision loss
  •         No history of acute onset of flashes or floaters prior to vision loss
  •         No history of recent eye surgery or eye trauma 


  1. HBOT should be administered in all cases if the loss of vision was associated a recent exposure to a hyperbaric environment or unpressurized high-altitude conditions.
  2. HBOT should be administered in all cases if the history is suggestive of radiation optic neuropathy or for vision loss that occurs during or immediately after hemodialysis.
  3. Patients waking up with vision loss after a surgical procedure during which general anesthesia was administered should be referred for emergent HBOT.
  4. Consultation with an ophthalmologist is desirable if it can be obtained without delaying HBOT.
  5. Patients with acute, painless, severe vision loss not meeting the criteria for emergent HBOT should be referred emergently to an ophthalmologist in all cases so that additional patients may be identified for whom HBOT or other treatment modalities may be undertaken.

(Adapted from Butler FK, Hagan C, Murphy-Lavoie H. Hyperbaric Oxygen Therapy and the Eye. Undersea Hyper Med. 2008. Sep-Oct;35(5):333-87.) 

Patients who present with sudden painless loss of vision should be triaged "Emergent" because of the possible need for immediate oxygen therapy. (See Table 1 above) Visual acuity should be documented as soon as possible. If decreased vision is confirmed with pinhole exam, the emergency physician should immediately perform a fundoscopic exam, using dilation if feasible and not contraindicated. Patients with findings consistent with CRAO should be placed on 100% oxygen immediately and considered for HBOT when available. If vision improves and stabilizes on normobaric oxygen, HBOT may not be necessary.2,4 For patients confirmed to have a CRAO, a ED evaluation for risk factors and concomitant disease should include: Complete blood count, Erythrocyte sedimentation rate (to screen for giant cell arteritis), fibrinogen, prothrombin time/activated partial thromboplastin time, blood glucose, lipid profile, blood cultures (if septic emboli are suspected), and electrocardiogram. (Note: HBOT may be initiated prior to completion of initial work up when it is available) Additional work up that may be completed as an inpatient on an urgent basis may include: carotid ultrasound, fluoroscein angiogram, echocardiogram, electroretinal gram, and magnetic resonance angiography. An ophthalmologist and / or neurologist should be consulted emergently, but oxygen treatment should not be delayed awaiting their arrival. 


  1. Nash EA, Margo CE. Patterns of Emergency Department Visits for Disorders of the Eye and Ocular Adnexa Arch Ophthal. 1998;116:1222-1226.
  2. Murphy-Lavoie H, Butler FK, Hagan CE. Hyperbaric oxygen therapy in the management of central retinal artery occlusion. In, Gesell L, ed; Hyperbaric Oxygen Therapy Committee Report 2009; Durham; Undersea and Hyperbaric Medical Society; 2009.
  3.  Beran DL, Murphy-Lavoie H. Acute, Painless Vision Loss. J La State Med Soc. 2009 Jul-Aug;161(4):214-6, 218-23.
  4. Butler FK, Hagan C, Murphy-Lavoie H. Hyperbaric Oxygen Therapy and the Eye. Undersea Hyper Med. 2008. Sep-Oct;35(5):333-87.
  5. Bojic L, et al. Hyperbaric oxygen therapy in two patients with non-arteritic anterior optic neuropathy who did not respond to prednisone. Undersea Hyperb Med. 2002 Summer;29(2):86-92.
  6. Bojic L, et al. Hyperbaric oxygen therapy for the treatment of nonarteritic anterior ischemic optic neuropathy. Acta Med Croatica. 1995;49(3):133-6.
  7. Wright J, et al. Clinical case report: treatment of a central retinal vein occlusion with hyperbaric oxygen. Undersea Hyperb Med. 2007 Sep-Oct;34(5):315-9.
  8. Kiryu J, Ogura Y. Hyperbaric oxygen treatment for macular edema in retinal vein occlusion: relation to severity of retinal leakage. Ophthalmologica. 1996;210(3):168-70.
  9. Johnson GP. Cases from the aerospace medicine residents' teaching file. Case #38. A navigator with nonischemic central retinal vein occlusion progressing to ischemic central retinal vein occlusion. Aviat Space Environ Med. 1990 Oct;61(10):962-5.
  10. Beiran I, et al. Early hyperbaric oxygen therapy for retinal artery occlusion. Eur J Ophthalmol. 2001 Oct-Dec;11(4):345-50.
  11. Hertzog LM, Meyer GW, Carson S, et al. Central retinal artery occlusion treated with hyperbaric oxygen. J Hyperbaric Medicine. 1992;7:33-42.
  12. Beiran I, Rimon I, Weiss G, et al. Hyperbaric oxygenation therapy for ischemic optic neuropathy. Eur J Ophthalmol 1995;5:285-6.
  13. Inoue O, et al. Hyperbaric oxygen therapy (HBO) for central retinal vein occlusion (CRVO) - short term results on seventy eyes. Undersea Hyperb Med. 2008 July-Aug;35(4).
  14. Duker JS, Brown GC. Recovery following acute obstruction of the retinal and choroidal circulations. Retina 1988; 8(4): 257-260.
  15. Neubauer AS, Mueller AJ, Schriever S, et al. Minimally invasive therapy for clinically complete central retinal artery occlusion--results and meta-analysis of literature. Klin Monatsbl Augenheilkd 2000 Jul; 217(1):30-6. German.
  16. Hayreh SS, Zimmerman MB. Central retinal artery occlusion: Visual outcome. Am J Ophthalmol 2005; 140: 376-391. 


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Mark Your Calendars

Christopher J. Logue, MD
Past-Chair, ACEP Undersea and Hyperbaric Medicine Section

2nd Annual - Undersea and Hyperbaric Medicine Board Review Course for Physicians
August 20-22, 2010
Philadelphia, PA

Based on feedback from the members of the ACEP Undersea and Hyperbaric Medicine Section, we organized and ran the first comprehensive multi-day board review course in Undersea and Hyperbaric Medicine in August of last year in Philadelphia. We are pleased to report that the course was a huge success!!  

The course was sponsored by the Continuing Medical Education Office at the University of Pennsylvania and the Diver’s Alert Network (DAN). It was co-sponsored by the Undersea and Hyperbaric Medicine Society (UHMS) and ACEP. Participating physicians were eligible for 16 hours of CME credit through the AMA and 15.75 hours of credit through ACEP.  

The course instructors were all ACEP Undersea and Hyperbaric Medicine section members and included faculty members from the fellowship programs at LSU, UCSD and the University of Pennsylvania. 55 physicians participated and the course was well received. In addition, the American Board of Preventative Medicine (ABPM) reported that the pass rate for the exam improved to 86% last year (it was 65% the previous year) and the number of physicians who became board certified tripled from the previous year. 

For those of you who are not aware, board certification is offered through ABPM and the American Board of Emergency Medicine (ABEM). Also, this is the last year that the "training plus practice" (grandfather) pathway will be offered to eligible physicians. After this year, you must be fellowship trained in Undersea and Hyperbaric Medicine in order to sit for the board exam. 

The application period is March 1st – June 30th of 2010. The exam is electronic and given at a local Pearson-Vue testing center from October 4th – 15th, 2010. For more information about the eligibility criteria and application process go to: 



We are currently processing the paperwork for this years course, if you are interested in taking the course do not hesitate to contact me at:  

More details will follow in the next newsletter and we will send out any updates through the list-serve. 

Enhance your credentials and get board certified in Undersea and Hyperbaric Medicine!! 


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Necrotizing Soft Tissue Infection of the Foot

Raphael Colon-Hernandez, MD

Case Report

The patient is a 58 year old white man who presented to the emergency department complaining of two weeks of progressive shortness of breath. The patient also complained of nausea and emesis for the past three days, as well as subjective fevers, chills, diarrhea, diaphoresis, and a swollen red left foot for the past four days. The patient's medical history is remarkable for DMII, and non-compliance with medicines and treatments. His medications included metformin, glipizide, niacin, and aspirin. He denied any allergies or prior surgeries. His maternal family history is positive for emphysema. He admitted to smoking one pack per day of tobacco for over forty years, but denied any alcohol or illicit drug use. 

The patient's initial vital signs were: BP- 144/79, HR- 105, RR- 22, and O2 Sat 100% on room air. His physical examination revealed mild respiratory distress but with clear lung sounds and symmetrical chest expansion. He was tachycardiac, and had an extremity exam remarkable for a swollen, erythematous left foot with calf tenderness and 2+ dorsalis pedis and tibialis posterior pulses. His laboratory studies results demonstrated a WBC - 30,000, Hg - 12.6, Hct - 37.5, Platelets - clumped. His cardiac markers were not elevated. The initial radiographic studies included an unremarkable chest x-ray, and left foot views revealing soft tissue swelling but without evidence of osteomyelitis. This patient was started on Vancomycin and Piperacillin / Tazobactam and admitted to the internal medicine service for left foot cellulitis and to rule out of pulmonary embolism. 

An ultrasound of the lower extremity showed no evidence of deep vein thrombosis, and the contrasted computed tomography of the chest showed no evidence of pulmonary embolism. The MRI of the left foot, however, demonstrated a large amount of swelling and enhancement within the muscles on the plantar surface of the foot without evidence of osteomyelitis. Over the course of five days, the swelling of the foot increased, and the hyperbaric medicine service was consulted. 

When the patient presented to our clinic, his left foot was swollen with several large sloughed areas and denuded surfaces. Some necrotic eschars, as well as cyanosis and necrosis of the second toe were identified. An incision and drainage obtained 90 mL of purulent material, and samples were sent for culture and sensitivities. A surgical consultation was obtained, and hyperbaric treatments immediately instituted.  

The wound cultures grew out E. coli and Group B Streptococcus that was sensitive to Piperacillin/Tazobactam. Antibiotics were adjusted to include ciprofloxacin to cover pseudomonas species, and a short course of antifungals were also administered. Surgical debridement was performed on three occasions, and foot amputation was recommended by surgical team due to poor prognosis. The patient refused foot amputation at that time, but a second toe amputation had to be performed due to necrosis. Surgery recommended continued hyperbaric oxygen treatments and antibiotics. 

Our patient was later discharged home on intravenous antibiotics, and after receiving daily hyperbaric oxygen treatments, as well as standard wound care, he has shown marked improvement. Hyperbaric treatments were discontinued after 58 dives. No further surgical debridements or interventions were required. Figure 1 shows the stages of healing.

Figure 1


Necrotizing fasciitis is a life threatening infection and necrosis of the superficial and deep fascia of the skin and soft tissues. The incidence is estimated at 27 hospital admissions per 100,000 population, with a mortality between 20% - 80% in some studies. At risk individuals include diabetics, obese patients, alcoholics, smokers, and intravenous drug abusers. Most cases present in the lower extremities, but infections in the upper extremities, buttocks, head and neck, and perineum have been reported, as well as on the abdominal wall in neonates, associated with omphalitis. Involvement of the scrotum or perineum is known as Fournier’s Gangrene. 

Mixed aerobes and anaerobes infections make up the majority of cases. Common pathogens include streptococci spp., staphylococcus aureus, E. coli, pseudomonas spp., Enterobacter, Klebsiella, Proteus, Bacteroides, Clostridia, and Peptostreptococcus. Elliot et. al. reported an average of 4.4 organisms per patient, and up to 6 organisms in wound cultures. 

The diagnosis is based on physical examination. The classic presentation is one of pain out of proportion to physical exam findings, but this is may not be present. Fever and chills are common, and skin findings are, at times, minimal. Skin changes can also include erythema and swelling early in the disease process, with a fast progression to blistering, bullae, necrosis, and crepitus. Necrosis results from thrombosis of subcutaneous blood vessels. Abscess formation with purulent drainage is also reported. CT scan findings include asymmetrical fascial thickening with fat stranding, but characteristically not found to include muscle involvement or abscess formation. 

Treatment for necrotizing fasciitis includes a combination of early surgical debridement, goal directed management of sepsis, including early administration of antibiotics, and hyperbaric oxygen as an adjunctive treatment. According to the Undersea and Hyperbaric Medical Society, the recommended hyperbaric oxygen treatment protocol is at 2.0 to 2.4 ATA for 90 minutes given twice daily for the first few days. If clostridial myositis and myonecrosis are being considered, the gas gangrene protocol should be followed. Treatment can be decreased to daily dives, once the patient is stabilized. 


Necrotizing fasciitis is a rare, but potentially life threatening infection of the skin. Risk factors include immunosuppression, obesity, alcoholism, and intravenous drug use, amongst others. It is most commonly caused by mixed aerobic and anaerobic organisms. Even though the classic presentation of pain out of proportion to physical exam, this is sometimes not the case. The presentation can vary from fever, chill, and generalized malaise with minimal skin findings, to rapidly progressive skin necrosis and sepsis. The mortality rate can be as high as 68% if hyperbaric oxygen is not administered. Treatment consists of early surgical debridement, early goal directed treatment of sepsis, including adequate parenteral antibiotics, and hyperbaric oxygen as an adjunct to treatment. 



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This publication is designed to promote communication among emergency physicians of a basic informational nature only. While ACEP provides the support necessary for these newsletters to be produced, the content is provided by volunteers and is in no way an official ACEP communication. ACEP makes no representations as to the content of this newsletter and does not necessarily endorse the specific content or positions contained therein. ACEP does not purport to provide medical, legal, business, or any other professional guidance in this publication. If expert assistance is needed, the services of a competent professional should be sought. ACEP expressly disclaims all liability in respect to the content, positions, or actions taken or not taken based on any or all the contents of this newletter.

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