Undersea and Hyperbaric Medicine Section Newsletter - May 2010, Vol 17, #2
Tracy Leigh LeGros, MD, PhD, UHM, FACEP
Program Director, LSU Undersea and Hyperbaric Medicine Fellowship
Greetings! It is getting to be the busy part of the year for most of us. The end of the academic year is fast approaching, and with it, all the duties and obligations of ending one year and beginning the next. Here in New Orleans, we are matriculating three fellows and are about to welcome four new fellows in July. But really, all we can think about is Florida! I hope to see everyone next month as UHMS is my favorite conference of the year. Its time to renew and reflect on a busy year. It is truly a joy to be inspired by all of the poster sessions, oral presentations and plenary sessions. I am consistently amazed and motivated by the great scientific presentations I see every year.
Meeting at UHMS for the Hyperbaric Medicine Section of ACEP
Following the lead of Dr. Chris Logue, I have arranged a meeting for our section at UHMS. It will be on Thursday, June 3rd, from 3 pm - 4 pm in the Snowy Egret Room. Lisa Tidd was very accommodating and gave us a time that is during a break between the Kronheim Lecture "20,000 Bytes Under the Sea" by Emory Kristof, and the Session B: HBO2 Therapy Mechanisms. This was very gracious of her. I hope that everyone will take advantage of this break, and please attend. This meeting is open to anyone with an interest in what is occurring with hyperbaric fellowships and with current curriculums and other educational opportunities within the hyperbaric community. However, anyone that would like to attend is more than welcome. You will meet some inspiring young leaders from across the country, all very interested in promoting and advancing the education within our specialty.
Fellowship Forms, Surveys, and Evaluations Available Online
I am in the process of sending Stacy Rupurt a wide array of forms related to Undersea and Hyperbaric Fellowship development. It is easy enough to download the program information form, or PIF, a labor intensive form required by all ACGME accredited programs. However, it is quite another thing to stay on top of the serial evaluations required to run a fellowship. In an effort to ease this load, for all programs, but especially the new ones, my fellowship is making our guidelines and forms available to all. I will relay in a separate posting the exact location of these files. They will be in a word format. I invite everyone to peruse them and please use anything that may be helpful. The RRC and ACGME require a lot of fellows signatures of understanding and continual evaluations for a wide variety of things. The forms available to you will include: patient satisfaction surveys, multiple fellow evaluations (inclusive of duty hours and all the core competencies), multiple attending evaluations, rotation evaluations, multiple ways to continually monitor and assess your fellowship as a whole, and even ways to measure the effectiveness of your program director. An updated PIF from our institution will be made available to new programs, as well as tips to help any new program navigate these academic waters.
Annual Undersea and Hyperbaric Medicine Board Examination Review Courses
It is that time of year again. Time for those of you preparing for the written board examination in our specialty to think about taking a review course. You have several to choose from. There is a one day course available in San Antonio on August 5th, 2010. The faculty are nationally known for their exemplary lecturing skills and this course is always well received. Additionally, there is a three day course available in Philadelphia on August 20 - 22nd. It is presented by hyperbaric medicine faculty from the University of Pennsylvania, USCD, Ohio State, LSU, and Syracuse. It has also been very well received. This examination can be difficult. I urge you, if you are preparing for this test, to seriously consider taking one of these fine courses.
Cases of the Month - Wound Care and Hyperbaric Medicine
I invite you to please review our two cases of the month. They are very interesting and informative presentations related to patients at high risk for morbidity and mortality. The wound care case is one of an orphan disease with very few treatment options and usually a grim prognosis. The hyperbaric medicine case concerns a patient of ours that I truly thought was going to die right in front of me. I would truly value your insights as to what you think his initial disease process could have been. He was a wonderful patient who has become a friend and a true fan of hyperbaric medicine. He is the type of patient who makes all the hassles of modern medicine truly worthwhile. I hope you enjoy both cases.
Undersea and Hyperbaric Medicine Fellowship Survey Results
I would like to thank all of you who participated in our survey of the academic landscape in hyperbaric medicine. Our survey response rate was 76% and some very useful information was garnered. My Fellow, Dr. Marina Wilder, will be presenting these findings at her poster presentation. Additionally, as this is a hot topic, she has been granted an oral presentation session as well. We would love as many participants as possible during this presentation. As the practice pathway is closing in our specialty, accredited fellowships will be the single pathway to board certification. Now, more than ever, an informative survey of what is occurring with the fellowships in your specialty, is essential.
Monthly Diving Medicine Conference Update
In this newsletter, as previously promised, is Dr. Raphael Colon-Hernandez's update of the monthly diving medical conferences that fellowships from around the country (Duke, San Diego, Hennepin, U Penn, San Antonio, and LSU) have been partaking in during the previous year. The final meeting for this academic year was held last week, and we have some exciting new changes beginning in July. This is a very stimulating and informational meeting that all of you are invited to take part in. I hope you enjoy Dr. Colon's update.
I want to end this message by thanking all of you for belonging to this section. Please remember to join us for our UHMS meeting in Florida next month. I hope you enjoy the case presentations and Dr. Colon's update. See you in sunny Florida!!
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Undersea & Hyperbaric Medicine Fellowship Monthly Seminars: A Distance Learning Experience
Raphael A. Colon-Hernandez, MD
LSU Undersea and Hyperbaric Medicine Fellowship
Video conferencing has become a widely used teaching method in medical schools and residency programs. It allows users to participate in didactic activities even when doing clinical rotations away from the main campus or hospital. Multiple publications have found this method of teaching to be useful and affordable. Markova, et al. published no statistical differences in knowledge gain between face-to-face lectures and distance learning groups while maintaining resident satisfaction.
Recently, the hyperbaric community has benefited from this technology. During the past year, a group of academic centers from around the country have joined in monthly video conferences. This tool has allowed us to discuss different presentations and clinical manifestations of decompression sickness, which is the current focus of discussions. Another advantage that it has given fellows and attending physicians the opportunity to gather input from multiple authorities in our field.
A computer running a high speed internet connection and a telephone line is all the equipment necessary to participate in these meetings. A video camera will be needed if video streaming is desired, but this is not required. Meetings are held the first Wednesday of each month at 3 pm Central Time. Invitations are e-mailed on the scheduled date and include a hyperlink to the Duke Center for Hyperbaric Medicine and Environmental Physiology Website, which hosts our meetings. PowerPoint presentations are given by one of the Undersea and Hyperbaric Medicine fellows from various programs, but attendance and participation is open to any interested physician or group. Lectures are also recorded and available for viewing at later times.
Our plans for the future include widening our discussions to incorporate a lecture on each of the thirteen accepted indications for Hyperbaric Oxygen Therapy. Anyone interested in taking part of this learning experience can contact me by e-mail .
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Marina Wilder, MD
We invite you to review this case presentation. This case involves a disease of high morbidity and mortality that occurs in our diabetic patients. It is, at times, a difficult disease to diagnose, and even more difficult to treat. The well-educated hyperbaricist and wound care specialist can make a world of difference in the care of these patients.
A 43 year old woman presents to the emergency department complaining of extremely painful lesions on her lower extremities. On exam, you note the lesions depicted in the pictures. What is the most likely initial diagnosis?
- Bullous Pemphigoid
- Erythema Nodosum
- Bullous Lupus Erythematosis
- Pyoderma Gangrenosum
|| What co-morbid condition is most likely to be associated with this presentation?
- End Stage Renal Disease (ESRD)
- Disseminated Intravascular Coagulation (DIC)
- Pulmonary Embolus
|| You decide to admit and work-up this patient further. What lab abnormalities might you expect to find?
- Abnormal Protein C or Protein S Levels
- Elevated Serum Phosphate Levels
- Decreased PTH (parathyroid hormone)
- Elevated Albumin Levels
- Decreased Ca++ Levels
|| What definitive test would you recommend to make your final diagnosis?
- Incisional biopsy of the lesions
- Bone scan
- Plain radiographs of lower extremities
- Punch biopsy of the lesions
- D. Calciphylaxis presents with extremely painful lesions, typically on the lower extremities (90%), although it can also be found on the trunk, thighs, and/or buttocks in 44% - 68% of patients.
- B. Calciphylaxis is almost exclusively seen with ESRD. Non-uremic calciphylaxis is extremely rare, and may present with malignancy, alcoholic liver disease, connective tissue disease and primary hyperparathyroidism.
- B. You may also see an elevated PTH level, hypoalbuminemia, and elevated Ca++ levels.
- A. Punch biopsy may not be adequate. A bone scan and plain x-rays may show abnormalities, but would not be diagnostic.
Calciphylaxis - A Rare but Deadly Systemic Disease
Calciphylaxis is a poorly understood and devastating syndrome of skin necrosis and vascular calcification first reported by Bryant and White in 1898. It's pathophysiology is obscure and multi-factorial. The implicated factors include: chronic renal failure, obesity, diabetes, hypercalcemia, hyperphosphatemia, elevated circulating levels of calcium/phosphate product, and secondary hyperparathyroidism. The conundrum that exists is that these factors are relatively common in those with ESRD, whereas calciphylaxis is relatively rare. Selye's Experimental Hypothesis suggests that calciphylaxis occurs due to a series of events. It starts with hypersensitivity, which is induced by sensitizing agents such as elevated vitamin D or parathyroid hormone (PTH). Calcinosis occurs when those patient who are sensitized, are then challenged by factors such as egg albumin or metallic salts. The bottom line is there is a series of events involving ESRD failure-induced abnormalities in calcium homeostasis that result in systemic calcinosis. However, as elusive as a specific etiology is, in reality calciphylaxis is most likely a common endpoint for patients with the following triggers: long term obesity, malnutrition, sudden weight loss, liver disease, intravenous dextran and / or iron, vitamin D supplementation, patients using calcium based phosphate buffers during medical therapies, patients on immunosuppressive agents, and those taking warfarin.
The frequency of calciphylaxis is 1% - 4% of ESRD patients. This number is increasing, possibly due to widespread use of parenteral vitamin D and iron dextran. It is extremely rare in those without ESRD. The morbidity and mortality is 60% - 80%, with proximal wounds resulting in a higher mortality, and ulcerated wound fairing even worse (two fold increase in mortality). Survival rates are 45% at year one, and 35% at five years. The leading cause of death is wound sepsis. The mean affected age is 48 years, with women affected three times as often as men.
The lesions develop suddenly and progress rapidly. They can occur as a single wound or with numerous eruptions. These wounds usually present on the extremities, but may also occur on the trunk, hands, face, and penis. Uremic calciphylaxis predispositions include elevated levels of phosphate, hyperparathyroidism, and hypoalbuminemia. Non-uremic calciphylaxis predispositions are more broad, including primary hyperparathyroidism, malignancy, alcoholic liver disease, and connective tissue disorders.
The common endpoint in the disrupted cellular milieu of these ESRD patients is a small vessel occlusion that is excruciatingly painful, extremely firm, and occurring in areas of abundant fatty tissues and in areas of subcutaneous injections (IDDM patients). Lesion distribution is proximal in 4% - 68% (thigh, trunk, buttocks), distal extremities in up to 90%, with visceral involvement also occurring. Ulceration is a late finding and associated with very high mortality.
The work-up of these patients should include a CBC, CMP, amylase, lipase, PTH level, coagulation studies (including anti-thrombin III, Protein C & S, Anti-Cardolipin, Lupus Anti-Coagulant Level, Factor V Leiden Level and a Homocysteine Level), Hepatitis C Anti-Body Level, Cryofibrinogen Level, Aluminum Level, ESR, CRP, and a Vasculitis Evaluation (ANA, ANCA).
Plain radiographs will show arborization of vascular calcification within the dermis and the subcutaneous tissue. This is, however, common in those with ESRD and not a specific finding. Bone Scintigraphy studies are non-invasive and will show the protein osteopontin present within the cacliphylaxis lesions. These scans may also be used to monitor disease progress or regression. Punch biopsies are often inadequate if the quantity or depth of tissue is not of high quality. A better biopsy would be one that is incisional in nature and ensures an ample amount of subcutaneous tissue for evaluation. Great caution must be taken, however, when incising a non-ulcerated lesion. This may result in a non-healing wound. The tissue often bleeds freely and ulcerations increase mortality two fold.
Medical care is mainly supportive. Elimination of aggravating conditions is mandatory. This includes discontinuing iron, calcium and vitamin D supplementations. Steroids, although considered by some to be a trigger, may be beneficial systemically, unless ulcerated lesions are present. It is of high importance to aggressively correct the calcium and phosphate balance. This can begin with a change in diet, using non calcium and phosphate binders and low calcium bath dialysis. Additionally, it may be necessary to increase the duration or frequency of dialysis sessions, and begin the use of calcimimetics. Calcimimetics are useful for those with hyperparathyroidism, as they increase the sensitivity of calcium receptors to available calcium (which decreases PTH secretion). Bisphosphonates can be added as well. They work by increasing osteoprotegerin production and inhibiting arterial calcification.
If conservative therapy fails, parathyroidectomy should be considered, but only if hyperparathyroidism is present. A treatment that has shown high promise is intravenous sodium thiosulfate. This potent antioxidant also increase the solubility of calcium deposits. Warning: this is an off label use of this product, however many studies have shown significant benefit. Sodium thiosulfate has been shown beneficial in uremic and non-uremic patients, in both children and adults, and in oral, parenteral or intraperitoneal forms. Improvement is usually seen in two weeks. Adjunctive treatments include the judicious use of antibiotics where applicable, and hyperbaric oxygen therapy. Consultations include those for pain management, dietary consultation, and a surgical consultation for aggressive wound care and appropriate debridements (to avoid wound infection and sepsis). Complications include non-healing lesions, cutaneous gangrene, wound sepsis, internal involvement (GI hemorrhage or infarction, and organ failure), and hypocalcemia (secondary the use of calcimimetics, sodium thiosulfate, and parathyroidectomy). Patient education is mandatory, especially with regard to compliance with dialysis, dietary restrictions and possibly anticoagulation (once a full explanation of the risks and benefits is shared with the patient).
Calciphylaxis - Suggested Readings
- Selye H. Calciphylaxis. Chicago, Ill: University of Chicago Press; 1962.
- Nigwekar SU, Wolf M, Sterns RH, et al. Calciphylaxis from nonuremic causes: a systematic review. Clin J Am Soc Nephrol. 2008;3(4):1139-43.
- Norris B, Vaysman V, Line BR. Bone scintigraphy of calciphylaxis: a syndrome of vascular calcification and skin necrosis. Clin Nucl Med. 2005;30(11):725-7.
- Cosmin A, Soudry G. A case of severe calciphylaxis seen on three-phase bone scan. Clin Nucl Med. 2005;30(11):765-6.
- Robinson MR, Auguesting JJ, Korman NJ. Cinacalcet for the treatment of calciphylaxis.Arch Dermatol. 2007;143(2):152-4.
- Velasco N, MacGregor MS, Innes A, et al. Successful treatment of calciphylaxis with cinacalcet-an alternative to Parathyroidectomy? Nephrol Dial Transplant. 2006;21(7):1999-2004.
- Raymond CB, Wazny LD. Sodium thiosulfate, bisphosphonates, and cinacalcet for treatment of calciphylaxis. Am J Health Syst Pharm. 2008;65(15):1419-29.
- Hanafusa T, Yamaguchi Y, Tani M, et al. Intractable wounds caused by calcific uremic arteriolopathy treated with bisphosphonates.J Am Acad Dermatol. 2007;57(6):1021-5.
- Hackett BC, McAleer MA, Sheehan G, et al. Calciphylaxis in a patient with normal renal function: response to treatment with sodium thiosulfate. Clin Exp Dermatol. 2009;34(1):39-42.
- Hayden MR, Goldsmith D, Sowers Jr, et al. Calciphylaxis: calcific uremic arteriolopathy and the emerging role of sodium thiosulfate. Int Urol Nephrol. 2008;40(2):443-51.
- Meissner M, Kaufmann R, Gille J. Sodium thiosulphate: a new way of treatment for calciphylaxis? Dermatology. 2007;214(4):278-82.
- Vassa N, Twardowski ZJ, Campbell J. Hyperbaric oxygen therapy in calciphylaxis-induced skin necrosis in a peritoneal dialysis patient. Am J Kidney Dis. 1994;23(6):878-81.
- Budisavljevic MN, Cheek D, Ploth DW. Calciphylaxis in chronic renal failure. J Am Soc Nephrol. 1996;7(7):978-82.
- Guerra G, Shah RC, Ross EA. Rapid resolution of calciphylaxis with intravenous sodium thiosulfate and continuous venovenous haemofiltration using low calcium replacement fluid: case report. Nephrol Dial Transplant. 2005;20(6):1260-2.
- Weenig RH, Sewell LD, Davis MD, et al. Calciphylaxis: natural history, risk factor analysis, and outcome. J Am Acad Dermatol. 2007;56(4):569-79.
- Wilmer WA, Magro CM. Calciphylaxis: emerging concepts in prevention, diagnosis, and treatment. Semin Dial. 2002;15(3):172-86.
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Marina Wilder, MD
Hyperbaric oxygen therapy (HBO2) is an approved treatment of gas emboli. It should be considered with presence of neurological and cardiovascular manifestations resulting from venous gas embolism (VGE). HBO2 potential benefits include compression of air bubbles, improved oxygenation of hypoxic tissues, and attenuation of the inflammatory cascade.
A 60 yo man flew from Israel to New York (12 hour flight) 5 days prior to presentation, and from New York to New Orleans (4 hour flight) 3 days prior to presentation. On the day of presentation, the patient was having dinner with his son, when he developed sudden onset of dizziness, global weakness, nausea, and diaphoresis. He denied chest pain, SOB or vomiting. The initial evaluation by EMS revealed a BP of 70/50. His past medical history included DM II, HTN, glaucoma, and GERD. His medications included aspirin, metformin, enalapril, norvasc, glibenelamide, xalatan ophthalmic drops, and cosopt ophthalmic drops.
Emergency Department Evaluation
Initial Vital Signs: BP 70/35, HR 112, RR 14, and afebrile. The patient was diaphoretic with cool, clammy skin, and an intact neurological exam (GSC=15). The remainder of the exam was unremarkable, despite his toxic appearance.
Working Differential Diagnosis
AMI, PE, aortic dissection, pericardial effusion (cardiac tamponade), and sepsis
Laboratory and Radiological Examinations
CXR: enlarged cardiomediastinal silhouette with no acute cardiopulmonary findings.
2D ECHO: moderate pericardial effusion.
Labs: H/H = 17.5/51.3; PT = 11.6 & INR = 1.1; WBC = 11.3; BUN/Cr = 23/1.21; CKMB = 1.9; and Troponin I = 0.02.
Chest CT: no PE, aortic dissection, aneurysm or mural hematoma. Moderate size pericardial effusion with deformity of IV septum, and pericardial constriction. Large amount of air within the main pulmonary artery/thoracic venous system (750 ml - iatrogenic in origin).
Cardiology performed a stat pericardiocentesis with the removal of 10 ml of fluid (transudate). The patient’s pressure then began deteriorating (requiring Levophed, intubation and Propofol drip).
The patient was transferred to a HBO2 facility for emergent treatment. Upon arrival he coded and CPR was performed. Vitals returned, an arterial line was placed, and he underwent a Navy TT6. During his first several air breaks, his TCOMs would show significant tissue hypoxemia and his vital signs would deteriorate. However, toward the end of his treatment, he no longer became hypoxic during air breaks, his vital signs improved (requiring less Levophed), and he began purposeful movements and moving all extremities (when his Propofol drip was reduced).
Intensive Care Evaluation
Upon arrival, the patient was still intubated and received full evaluations from pulmonary, cardiology and neurology. His cardiac ECHO showed left ventricular enlargement and aortic root dilatation. An IV Adenosine Cardiolite Stress test was normal (EF = 59%). He then developed renal insufficiency (resolved). ICU labs revealed a urine myoglobin = 1773, CPK = 884, and Troponin I = 0.42. Within 72 hours the patient was extubated, with a normal neurological exam and an unremarkable brain MRI. The patient recovered completely and returned home to Israel.
VGE can have potentially severe morbidity and mortality. It has been recognized since the 19th century, with increased occurrence in the last three decades (predominantly an iatrogenic complication). Historically it occurred with neurosurgical patients in the sitting position, with an estimated incidence of 10% - 80%. More recently, VGE has been associated with central venous catheterization, thoracocentesis, hemodialysis, high pressure mechanical ventilation, invasive vascular procedures, posterior neck/cervical surgery, gynecologic procedures, laparoscopic surgery, and the mechanical injection of contrast. The degree of morbidity and mortality in VGE is related to the volume of gas that is introduced. In humans, as little as 20 ml of IV air can cause symptoms. Rapid injections also put a large strain on the right ventricle, increasing pulmonary artery pressure, leading to compromised pulmonary venous return to the left ventricle, eventually causing decreased cardiac output and cardiovascular collapse. Symptoms can include dyspnea, persistent cough, dizziness, nausea, vomiting, chest pain, agitation, and disorientation.
High index of suspicion for VGE is required. Immediate management includes hemodynamic support and identification of the air source to reduce amount of further air entry. As the morbidity and mortality of catheter related VGE may be up to 30%, prompt transfer to a hyperbaric facility has been shown to decrease mortality in patients with cerebral air embolism. Immediate treatment is desired, however, therapy may still have good results even when initiated beyond 6 hours of an embolic event.
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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 newsletter.