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American Journal of Clinical Medicine® Owned and Published by the American Association of Physician Specialists, Inc. Peer Reviewed. Listed in Google Scholar and BioMedLib

Fall 2011 • Volume Eight, Number Three

Featured in this issue 24 Why Train Physicians in Disaster Medicine? 1 Management of 1,000 Injuries Following an F5 Tornado in Tuscaloosa, Alabama

1 26

Disaster Preparedness for the Medical Professional at Home and in the Workplace

1 29

Damage Control Resuscitation: The Case For Early Use of Blood Products and Hypertonic Saline in Exsanguinating Trauma Victims

1 34

Bombings and Blast Injuries: A Primer for Physicians

1 41

Disaster Medicine: Every Physician’s Second Specialty Twenty-First Century Fears

1 44 1 53

Epidemics After Natural Disasters

United States Air Force Aeromedical Evacuation – A Critical Disaster Response Resource


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Primary Ma of the Liv ture Cystic Ter er: Rep ort of a atoma Rare Cas e The Rol e in Pelvic of Physician Exp Examin ation Acc erience uracy

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The American Journal of Clinical Medicine® (AJCM®) is the official, peer-reviewed journal of the American Association of Physician Specialists, Inc. (AAPS), an organization dedicated to promoting the highest intellectual, moral, and ethical standards of its members. Its diversity incorporates physicians that represent a broad spectrum of specialties including anesthesiology, dermatology, diagnostic radiology, disaster medicine, emergency medicine, family medicine/OB, family practice, geriatric medicine, hospital medicine, internal medicine, obstetrics and gynecology, ophthalmology, orthopedic surgery, plastic and reconstructive surgery, psychiatry, radiation oncology, general surgery, and urgent care medicine.

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In This Issue PROCEEDINGS FROM The 2011 House of delegates annual scientific meeting Why Train Physicians in Disaster Medicine? Management of 1,000 Injuries Following an F5 Tornado in Tuscaloosa, Alabama

124 158

Daniel M. Avery, Jr., MD, FAASS

Disaster Preparedness for the Medical Professional at Home and in the Workplace

Mark Pastin, PhD

126

160

Geoffrey Simmons, MD

Damage Control Resuscitation: The Case For Early Use of Blood Products and Hypertonic Saline in Exsanguinating Trauma Victims

134

David M. Lemonick, MD, FAAEP, FACEP

Disaster Medicine: Every Physician’s Second Specialty Twenty-First Century Fears

Epidemics After Natural Disasters David M. Lemonick, MD, FAAEP, FACEP

United States Air Force Aeromedical Evacuation – A Critical Disaster Response Resource Bruce R. Guerdan, MD, MPH

166

Binocular Double Vision – A Review

170

Re-Radiation and Casodex in Locally Advanced, Radiation Recurrent, Locally Progressing Prostate Cancer

141

Heidi Cordi, MD, MPH, MS, EMTP, FACEP Debra Cascardo, MA, MPA, CFP

153

Nancy Lutwak, MD

Gary Shultz, DO, FAAR

172 144

A Systematic Approach for the Assessment and Diagnosis of Abdominal Pain in the Premenopausal Female Cornell Calinescu, MD Ilissa Jackson, PA-C Mark Mauriello, MD Ilya Chern, MD E. Robert Schwarz, MD

129

Graeme A. Browne, CAPT MC (FS) USN

Bombings and Blast Injuries: A Primer for Physicians

Medical Ethics: Timmy the Torch

Orthopedic Issues in Family & Emergency Medicine Ben Jones, MS2 Roberto R. Gonzalez, MD


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elcome to the American Journal of Clinical Medicine® (AJCM®). This issue is focused on Emergency Medicine. The Journal is dedicated to improving the practice of clinical medicine by providing up-to-date information for today’s practitioners. The AJCM is the official journal of the American Association of Physician Specialists, Inc. (AAPS), an organization dedicated to promoting the highest intellectual, moral, and ethical standards of its members, and whose diversity incorporates physicians that represent a broad spectrum of specialties including anesthesiology, dermatology, diagnostic radiology, disaster medicine, emergency medicine, family medicine obstetrics, family practice, geriatric medicine, hospital medicine, internal medicine, obstetrics and gynecology, ophthalmology, orthopedic surgery, plastic and reconstructive surgery, psychiatry, radiation oncology, general surgery, and urgent care medicine. Part of the mission of the AAPS is to provide education for its members and to promote study, research, and improvement of its various specialties. In order to further these goals, the AJCM invites submissions of high-quality review articles, clinical reports, case reports, or original research on any topic that has potential to impact the daily practice of medicine. Publication of a peer-reviewed article in the AJCM is one of the criteria needed to qualify for the prestigious Degree of Fellow in the Academies of Medicine of the AAPS. Articles that appear in the AJCM are peer reviewed by members with expertise in their respective specialties. Manuscripts submitted for publication should follow the guidelines in The International Committee of Medical Journal Editors: “Uniform requirements for manuscripts submitted to biomedical journals” (JAMA, 1997; 277:927-934). Studies involving human subjects must adhere to the ethical principals of the Declaration of Helsinki, developed by the World Medical Association. By AJCM policy, all authors are required to disclose any and all commercial, financial, and other relationships in any way related to the subject of their article that might create any potential conflict of interest. More detailed information is included in the AJCM Manuscript Criteria and Information on pages 164 and 165. All articles published, including editorials, letters, and book reviews, represent the opinions of the authors and do not reflect the official policy of the American Association of Physician Specialists, Inc., or the institution with which the author is affiliated, unless this is clearly specified. ©2011 American Journal of Clinical Medicine® is published by the American Association of Physician Specialists, Inc. All rights reserved. Reproduction without permission is prohibited. Although all advertising material is expected to conform to ethical standards, acceptance does not imply endorsement by the American Journal of Clinical Medicine® and the American Association of Physician Specialists, Inc.

Editor-In-Chief

Wm. MacMillan Rodney, MD, FAAFP, FACEP

Senior Editor

Kenneth M. Flowe, MD, FAAEP

Managing Editor

Esther L. Berg, MEd

Editorial Board

Harold M. Bacchus, Jr., MD, FAAFP Gilbert Daniel, MD, FAAR Michael K. Garey, MD Beverly R. Goode-Kanawati, DO Thomas G. Pelz, DO, FAAIM Cyril H. Wecht, MD, JD

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This issue is dedicated to the memory of David G.C. McCann, MD, FAASFP, FAADM, a founding member of the American Academy of Disaster Medicine (AADM) and the American Board of Disaster Medicine (ABODM). Dr. McCann, who passed away in August, was the AAPS incoming President for 2011-2012.

Welcome to the American Journal of Clinical Medicine® (AJCM®)-

The AJCM is committed to improving the practice of clinical medicine by providing up-to-date information for today’s practitioners. The AJCM is continually upgrading its scientific contents to include cutting edge innovations in health services research and educational methodologies. In concordance with our recent Rural Health Association partnership, AJCM is dedicated to excellence in rural and frontier medicine. This is a unique niche in the current scientific literature. This issue includes articles based on the scientific presentations at the 2011 House of Delegates and Annual Scientific Meeting, held at the Ritz-Carlton, Tysons Corner, Virginia, in June. The theme, What Every Physician Should Know about Disasters, included the following topics: GI bleeding in a disaster, damage control resuscitation, ophthalmologic guidelines in disaster response, chemical warfare, bombings and blast injuries, earthquake disaster response/lessons from Haiti, and smoke inhalation. During the President’s Awards Dinner, which concluded the 2011 Annual Meeting, the American Academy of Disaster Medicine presented its first Distinguished Service Award to Rear Admiral Alton L. Stocks, MD, US Navy Medical Corps. Also in attendance was Vice Admiral Regina M. Benjamin, MD, Surgeon General of the US Public Health Service. See the photo feature on pages 122 and 123. The AJCM includes regular features on medical ethics, basic skills, and medical-legal issues. Sounding Board – an open forum in which you can express your thoughts on a subject of interest to you and your colleagues – values your input. Medical Ethics Without the Rhetoric, an informative and stimulating feature, generates interesting responses to the cases that are presented in each issue. Be sure to read the response to Case Nine and email your comments on Case Ten to councile@aol.com. The AJCM offers a regular series on Basic Skills, clinically-focused cases using radiographic, ultrasound, and ECG images as a means of simulating clinical cases commonly used for competency assessment. These Basic Skills cases do not represent material taken from board examinations, which are confidential. We encourage you to submit these types of items as they will be of general interest to physicians among the AAPS specialties. These activities are excellent ways for you – our readers – to participate actively in the AAPS. The Editorial Board would like to thank our many authors for their continuing efforts to provide interesting, thoughtprovoking, informative articles for our readers. In addition, thank you to our peer reviewers, who remain anonymous. We thank you for contributing to the success of the AJCM.

Wm. MacMillan Rodney MD, FAAFP, FACEP Editor, American Journal of Clinical Medicine® Member, American Board of Family Medicine Obstetrics


Tribute to David McCann by William J. Carbone, CEO, AAPS/ABPS Miserere, Misericordia, Magnificat – These were the words imbedded in all emails sent by the late David G.C. McCann, MD, MPH, FAADM, FAASFP. I have literally hundreds of emails since first communicating with Dave in 2004. There may be other readers that recognize these words from Dave’s emails. Who was this man? That’s not an easy question to answer and, even though I knew him very well, it is difficult to adequately describe who Dave McCann was on this earth and who he is in spirit. Myriad thoughts come to mind when I reminisce about Dave. His effect on me is stronger now than it was before his demise.

David G.C. McCann, MD, FAADM, FAASFP 1960-2011

In June Dr. Anthony Russo and I spent several hours with Dave and his family at his home. He greeted us as family with lots of hugs. We presented Dave with the E. O. Martin Award, the highest honor AAPS can bestow. He was stunned and said, “I don’t deserve this,” but he absolutely deserved every scintilla of it. When we left that afternoon, one of his daughters came outside and said, “Thank you for honoring my father.” I said the honor was all ours and will be everlasting in our hearts and minds. I will never forget it.

A week before Dave expired we spoke for 20 minutes. We had had many discussions about the important matters in life, and Dave taught me much about what was important. It was at the end of my last person-to-person conversation with Dave that he said, “Now tell me about my association. How are AAPS and ABPS succeeding?” What kind of man or woman would raise that question knowing that his days and hours are so few? Dave was President of AAPS for only a few weeks, but he epitomized the courage that we all seek in our physician leadership. He would have been an absolutely outstanding and extraordinary President as evidenced by his terms as Membership Officer, Secretary, Treasurer, and President-Elect not to mention chairing the American Board of Disaster Medicine and many other key AAPS and ABPS positions. All those who knew Dave know that what I have written is what Dave was all about. He was a husband, a father, a physician leader – he was a human being. He is sorely missed, but etched in my brain are all those wonderful moments and hours I was given to enjoy his courage and joy. Also etched in memory is his voice. It is a comfort to be able to recall these senses so vividly, but it is also bittersweet. Miserere, Misericordia, Magnificat – Have mercy on me, O God. Let thy mercy, O Lord, be upon us, for we have trusted thee. My soul doth magnify the Lord. These were Dave’s core beliefs. The next time your day doesn’t seem to be going the way you would like, please stop and think about that in view of how Dave lived his last days and what he taught us all. His courage, peacefulness, and love of God should, and I hope, remind us all that our days in comparison aren’t difficult, and we need to place our problems in their proper perspective. It was great knowing you, Dave. Bill

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SPECIAL DISASTER MEDICINE SECTION Including Proceedings from 2011 House of Delegates & Annual Scientific Meeting: What Every Physician Should Know about Disasters 

Why Train Physicians in Disaster Medicine? Management of 1,000 Injuries Following an F5 Tornado in Tuscaloosa, Alabama Daniel M. Avery, Jr., MD, FAASS 

Disaster Preparedness for the Medical Professional at Home and in the Workplace Geoffrey Simmons, MD 

Damage Control Resuscitation: The Case For Early Use of Blood Products and Hypertonic Saline in Exsanguinating Trauma Victims Graeme A. Browne, CAPT MC (FS) USN 

Bombings and Blast Injuries: A Primer for Physicians David M. Lemonick, MD, FAAEP, FACEP 

Disaster Medicine: Every Physician’s Second SpecialtyTwenty-First Century Fears Heidi Cordi, MD, MPH, MS, EMTP, FACEP Debra Cascardo, MA, MPA, CFP 

Epidemics After Natural Disasters David M. Lemonick, MD, FAAEP, FACEP 

United States Air Force Aeromedical Evacuation – A Critical Disaster Response Resource Bruce R. Guerdan, MD, MPH 


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American Journal of Clinical Medicine® • Fall 2011 • Volume Eight, Number Three

Scenes From The Presidents Dinner at the 2011 Annual Scientific Meeting


American Journal of Clinical Medicine® • Fall 2011 • Volume Eight, Number Three

Scenes From The Presidents Dinner at the 2011 Annual Scientific Meeting

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American Journal of Clinical MedicineŽ • Fall 2011 • Volume Eight, Number Three

sounding board

Why Train Physicians in Disaster Medicine? Management of 1,000 Injuries Following an F5 Tornado in Tuscaloosa, Alabama Daniel M. Avery, Jr., MD, FAASS

On April 27, 2011, the City of Tuscaloosa, Alabama, suffered the worst natural disaster in its history. A mile-wide F5 tornado with 200 mile an hour winds damaged or completely destroyed a significant portion of Tuscaloosa. There were 43 casualties and more than 1,000 injuries. Hospitals prepare for disasters of all types but often not the large number of injuries sustained in this disaster. Well-developed disaster plans can be adapted to much larger numbers of injuries. A previously well-thought disaster plan, although not rehearsed for a thousand patients, was able to be expanded to that number and implemented quickly. At the time of the tornado, no one had any idea of the number of injuries or casualties. The hospital received only a single complaint during this disaster. Many streets were neither identifiable nor negotiable; subsequently, all roads were closed except to emergency vehicles. There was no electrical power, land line, or cellular telephone service, and the water supply was contaminated. Large neighborhoods were leveled. Complete buildings were relocated to areas where there had been no buildings before, such as the middle of the interstate highway. Portions of buildings were found on the opposite side of the state. Bodies were strewn into streets, yards, and shrubbery. People were blown by the tornado into other cities and counties. A few of these people were even reported to have survived, although most did not. People described having their automobiles picked up by the twister and then falling 150 feet to the ground. Children were found in refrigerators. Cows were reported hanging from the tops of trees. Debris was found in other states. The mayor declared a state of emergency, and the National Guard was called to police the streets and guard neighborhoods. A curfew began at dusk and ended at daybreak. DCH Regional Medical Center is a large 583-bed hospital and trauma center, which serves as the tertiary care referral center

for West Alabama. The Emergency Department can easily accommodate 47 patients in rooms and bays and then another 10-20 on stretchers in the hallways. The hospital was in the direct line of the tornado until the last 60 seconds, when it turned east. The hospital sustained some broken windows on the two top floors and two small internal fires, which were easily extinguished. The two power substations supplying power to the hospital were completely destroyed. The hospital operated on emergency-generated power with no air conditioning. The water supply to the main operating room sterilization area was damaged. Most life-threatening injuries were brought to the hospital by paramedics and ambulances, although emergency travel was hampered by blocked streets. Most less injured patients walked to the hospital from all parts of town, and most of these patients and families were barefoot. Other seriously injured patients were brought to the hospital on make-shift stretchers made of doors from destroyed homes. Some injured never made it to the hospital. The number of injuries and casualties was unknown but estimated to be much greater than the number usually planned for in disaster drills. A regularly rehearsed disaster plan was quickly implemented and expanded to care for many other patients. A smaller general hospital in town was placed on alert. About 200 of the 300 physicians on active staff showed up at the hospital to help care for patients in the first hour following the tornado without even being summoned. This number included every specialty along with most of the residents and many of the medical students. Many retired physicians, medical school faculty, and community physicians not on the hospital staff presented to care for injured patients. At several times, there were almost as many physicians as there were patients. Medical students served as first assistants to surgeons in the


American Journal of Clinical Medicine® • Fall 2011 • Volume Eight, Number Three

sounding board Operating Room. Medical students sewed until their hands were sore. Every surgical specialty that could sew tissue did so. Patients were triaged into two categories: those seriously injured and life-threatening and those injured but not life-threatening. Physicians were divided into two groups to work in the two treatment areas. Those patients with serious, life-threatening injuries, those needing immediate surgery, those with CPR in progress, and seriously injured children were treated in the Emergency Department. This area was staffed by emergency medicine physicians and fellows along with general, trauma, vascular, plastic, orthopedic surgeons, neurosurgeons, and pediatricians. Those less-injured were triaged to make-shift treatment areas including the hospital auditorium, cardiac catheterization laboratory, endoscopy laboratory, outpatient surgery, and the hospital cafeteria. The make-shift treatment areas were staffed by OB/GYNs, ENTs, internists, family physicians, general practitioners, and pediatricians, along with obstetric fellows, family medicine residents, and medical students. Essentially, all hospital employees that were off duty, including administration, housekeeping, and maintenance, found their way to the hospital to help despite closed roads. Even administrative secretaries served as the transport service. Most patients only wanted the worst injuries treated so that others could receive timely care. Common, less serious injuries included lacerations, extremity fractures, contusions, crush injuries, and embedded glass. Dissection of head injuries from the intense wind speed was seen. Many discharged patients had no place to go, no transportation, no clothes, no food, no home, and no relatives. Children could not find their parents; parents could not find children. Babies and very small children could not tell their names or any other identifying information. There was no reason to write prescriptions because drug stores were closed. So, the hospital pharmacy dispensed medications for those leaving the hospital. The hospital cafeteria was opened in the areas not occupied by patients, and free food was available for anyone. Large conference rooms were used to temporarily house those who had no place to go. Additional patient care areas were available at the smaller general hospital in town, the medical school clinics two blocks from the main hospital, University Student Health Service, and the University Recreation Center. Some 127 very seriously injured patients were transferred to University of Alabama in Birmingham Medical Center and The Children’s Hospital in Birmingham 45 miles away. Several psychiatrists cared for psychiatric needs at the hospital, especially for those who had lost family members and those who had lost children. Ninety mental health professionals provided free psychological care at multiple locations for several weeks following the tornado.

Initially, casualties were placed in the DCH Regional Medical Center morgue. When it was filled to capacity, the VA Medical Center morgue was used, and then an elementary school was converted into a temporary morgue. Identification of the deceased was difficult. Body parts were often scattered over large areas including other counties and cities. Only a few of the x-ray machines were on emergency power; thus slowing the wait time for patients who needed x-rays and those awaiting x-ray reports. Other obstacles to care were the lack of power, lack of air conditioning, slow elevators due to limited power, limited or no medical records, compromised sterile technique, inability to get prescriptions filled, and management of families. The cafeteria was not a good location because it was a long distance from the ER and required the use of elevators, since it was on another floor. In retrospect, the cafeteria was not a good choice for patient care. There was only one complaint, and it did not come from a patient. An adult neurosurgeon had to perform an emergency craniotomy on a child. There were two near cardiac arrests in the less-injured areas. OB/GYNs had to run “codes.” Physicians of every specialty ended up having to sew lacerations. Family medicine residents with minimal supervision had to care for patients. Several lessons were learned. There was an incredible outpouring of physician and healthcare professionals. Most physicians saw the funnel cloud, assumed the worst, and headed for the hospital without being summoned. No one knew exactly what instruments were available on emergency power. Disaster plans and drills are everything. Well-rehearsed disaster plans and drills can be expanded to accommodate much larger numbers of injured. Competent physicians trained in emergency medicine and disaster medicine are essential. Organization and planning can be expanded to care for much larger numbers of patients than usually planned for. Physicians and staff trained in disaster medicine and emergency care are essential for any size hospital. Disaster plans and drills are priceless. The entire medical community untiringly rose to the occasion of rendering impeccable assistance to very large numbers of injured patients without hope of reimbursement, recognition, or reward, but rather for the goodness of mankind and the highest personal reward of medicine . . . care of the sick and injured. Daniel M. Avery, Jr., MD, FAASS, is Professor and Chair, Department of Obstetrics and Gynecology, the University of Alabama School of Medicine, Tuscaloosa, AL. Potential Financial Conflicts of Interest: By AJCM policy, all authors are required to disclose any and all commercial, financial, and other relationships in any way related to the subject of this article that might create any potential conflict of interest. The author has stated that no such relationships exist. ®

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American Journal of Clinical Medicine® • Fall 2011 • Volume Eight, Number Three

Disaster Preparedness for the Medical Professional at Home and in the Workplace Geoffrey Simmons, MD

Based on a presentation at the 2011 AAPS Annual Scientific Meeting, Tysons Corner, VA, June 21-22

Dedication I dedicate my article to the late Dr. David McCann, a friend, mentor, and colleague to many as well as myself. A finer humanitarian would be extremely hard to find. His family’s loss is also the world’s loss. He will be greatly missed. Most MDs were trained, in some capacity, to handle victims of disasters. Some are drilled on a regular basis, but very few physicians are truly prepared for a major disaster that directly impacts them and/or their family while at home, in school, in their car, or in a clinic setting (at work). The lack of data in the literature very loudly supports this notion. There appears to be an unstated mindset among some physicians that their hospital will remain an oasis amidst the turmoil, and that they, as physicians, will also be able to reach the hospital to help. Or, that they already know enough about preparedness. These ideas are dead wrong. Just take my Community Emergency Response Team class. There are over 400,000 citizens (overwhelmingly non-medical) who are trained, serving over 3,000 communities. They are our community’s boots on the ground. The 9.2 Alaskan earthquake/tsunami (1964) or the Katrina hurricane and subsequent flooding (2005) are extreme examples, but there are numerous devastating disasters that happen frequently around the world that seriously injure or kill loved ones and isolate victims for extended periods of time. Rescuers may be stuck elsewhere (at home, in the station, along destroyed highways), short-handed, or attending to a much bigger problem, such as a collapsed high-rise building or school. There are several small earthquakes across this country every day. Every city, town, farmland, and forest of our country has

the potential for one or more catastrophic events, and every citizen is at risk every minute of every day of his/her life – note the Oklahoma bombing, the Midwest tornadoes of 2011, the New York Towers, or Columbine. There is a high likelihood the northwest will have another 9.0+ earthquake this century. Forest fires are almost guaranteed in some parts of the western half of the USA every summer. Hurricanes have not missed a fall yet. Terrorists can easily show up in any neighborhood with explosive devices. One might view preparedness as a kind of immunization. It may not protect everyone from every strain (disaster), but it might modify the symptoms – protect one’s life – buy time. The purpose of my presentation was to teach MDs a few of the basics, to challenge some of their outdated knowledge, and to give them ideas to think about and hopefully act upon. Not everything could be covered – that would require a very thick text, a lot more time, and hands-on practice. Many suggestions within this presentation might be considered simply common sense, but one would be surprised to see how many people have not given preparedness the slightest thought. Many people think “it won’t happen to me” or “the government will always take care of us.” Experience says that will not be the case, and help may come in unexpected and limited ways. Some are too poor to plan for the day after tomorrow. Once the disaster strikes, it may be impossible to get help for protracted periods of time. By then, it may be too late to get supplies, to escape, to find safety, to refill medications, to help neighbors, or even to save your own family. A comprehensive talk on this subject could take many hours, but I tried to cover some of the more pressing items in the forty-five minutes allotted me.


American Journal of Clinical Medicine® • Fall 2011 • Volume Eight, Number Three

For example, do you have enough supplies for everyone in your family – the so called 72-hour kit? Do you have enough water? That would be one gallon per person per day, although one can barely make it with two quarts per day. Some families keep several racks of water bottles and rotate them out every six months. Pick holidays, such as July 4th and New Year’s Day, to check your supplies and expiration dates. Remember, your water heater has 40 gallons of safe water. You might close it off so it doesn’t drain backwards. Do you know how/have a way to clarify water? Do you know how to purify water? Some authorities recommend that we keep much more than 72 hours, perhaps a week’s worth of supplies, because three days is not enough for the worst types of disasters. Most of us who are overweight can make it without food for a few days, but not water. Clean water remains critical for one’s survival. Remember, more water might be needed in hot, more humid climates or for those working the hardest. Also, try lifting a five-gallon tank of water and then consider the problems a large family would have moving these if evacuated. Canned foods are probably best. They last for many months and often come with water or juice. There are packaged meals that will heat up on their own and freeze-dried foods that will last years. The Mormons have a technique for storing food for years. If there is a prolonged after-crisis isolation without power, use up your perishable foods in the refrigerator first (do not open the door frequently) and use frozen foods, which should have been packed tightly together, last. At 72 hours you might want to make one giant stew. Disaster preparedness has become huge business. There are scores of different emergency kits, first aid kits, ear plugs, masks, whistles, gloves, helmets, eye wear, tools, tents, flashlights, generators, and protective clothing. Watch out for “easy to carry” kits that last extended periods of time. They often forget to include water (the heaviest item). Know your local threats. Hurricane prep differs in some ways from earthquake prep. A dirty bomb requires another set of reactions. Rehearse now, especially with children. Studies show that their chance of survival will improve. Always have two routes of escape, whether it is a theater, a classroom, an office, or your home. Carry a whistle so responders can find you.

Have a pair of slip-on shoes and gloves next to your bed. Nighttime earthquakes commonly lead to lacerated bare feet from broken glass and cut hands from climbing through rubble. Have a portable radio with back-up batteries to help insure that you have the latest news to make the best decisions. Your escape route might just be too dangerous or washed out. Do not drive through large pools of water on any highway as there may be a washout beneath, and next thing you know, you are floating (and sinking) downstream. Do you have the right plans? Power and utilities may be down. Police and Fire Departments may not be available. Garbage collection may be nonexistent. Public transportation may be on hold. Commonly traveled roads may not be usable. Previously planned shelters may be too damaged, and new ones need to be set up. A portable radio can tell you where the newer shelters are located and how best to get there. If you’re contaminated with a dirty bomb or nerve gas, undress immediately and hose down with cool water. Do not go inside any buildings, especially hospitals, where you can contaminate others. Being quickly decontaminated trumps modesty. Watch out for looters, sexual predators, con men, and kidnappers. Consider walkie-talkies for every member of your family. If there is an emergency evacuation, plan to have Mom or Dad get the emergency kit while the other partner gets the important papers (hopefully, all stored in one place), and the kids round up the pets. By law, pets can be taken to shelters, but you need to know your state’s requirements and plans. Remember to bring pet food, cleanup materials, and immunization records. Do not bring aggressive dogs or your six-foot alligator. Never forget that the people in shelters might be going through the worst day of their lives. They might not be themselves. Babies cry all night, older men snore, food may be late in coming, and space is limited. Working toilets may be rare. Instead, for bowel movements, carry large, plastic garbage bags to line the inner bowl which can be tied up and discarded rather than lugging five gallon containers of water to flush each time or reuse putrid toilet bowls.

Be sure to accommodate any special needs for your family in your emergency kit; for example, extra medications (prescription and OTC), diapers, extra glasses, formula. If you need dialysis, know where else to report. If you are dependent on oxygen, know distant options.

Have you checked your stored food and water for expiration dates or the presence of vermin lately? Cardboard and cellophane are easily chewed through. Your gas tank should never drop below half. Gas stations may be closed or empty. Carry cash in small bills – ATMs will be down and banks closed. An orange might cost you $20 if the seller claims no change. Credit and debit cards will be useless if lines are down. Don’t count on checks working.

Do you have the right equipment? Can you move or roll your emergency kit into a vehicle at a moment’s notice? A flashlight should easily be found next to every bed (with a flashing pinpoint light on its side or a fluorescent top so as to not waste your time searching). Have back-up batteries. Check your flashlight monthly. Use LED lights – they last much longer and are often brighter, but note they cannot sort out the color red very well.

Has your family memorized emergency options, such as having a meeting place outside the house in case of fire, so no one runs back in to save a life? Have they memorized phone numbers of a faraway relative or friend so everyone can check in to report their location and status? Knowing what to do when the family is separated is different and just as important as knowing the drill at home when together. Does your cell phone have among

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its contact ICE (In Case of Emergency) or MY SPOUSE or MY KID so paramedics know whom to call.

and Disaster Preparedness, 2011) to read. The AMA, the Red Cross, and various community groups have information.

One’s health, indeed, one’s ultimate survival, may totally depend on preparation now. Know that no downed power line is safe until the utility company has deemed it so. Downed stoplights are now four-way stops. Large aftershocks nullify any previous “safe” postings by building inspectors. Never re-light your pilot light without the utility company making sure it is safe.

Among the preparedness planning that is distinctly doctororiented – telling your reliable patients what to do with their medications in case of a disaster. Hold that diuretic if you’re not getting enough fluids or have lots of diarrhea. Slowly wean off Coumadin onto aspirin. Do not stop XXXX medication abruptly but wean down. Give a small prescription for antibiotics, a tranquilizer, and a narcotic pain medication to keep in their emergency supplies. The last statement may be controversial, but then this might be the time when they most need them and cannot get medical help. Perhaps, consider only reliable patients. Be thorough in checking immunizations at all times.

Do you, at a minimum, have a flashlight and a few protein bars in your car? How about flares? Remember to check the expiration dates on flares and reconsider buying electronic, flashing devices as they are safer and will last many more hours. If you really want to be prepared, have a folding bike(s) in your trunk in case traffic cannot move. Take preparedness classes/training. There are many options offered through the Red Cross and city emergency departments. CPR is always good to know but sometimes useless in major catastrophes as a defibrillator probably is not coming and other victims may have a better chance at surviving if given your time. Join one of the volunteer groups under Citizen Corps, which is under FEMA’s umbrella, such as the Medical Reserve Corps (MRC), back-up doctor and nurse groups for hospitals that are down or filled to capacity. Or you can join DMAT, federalized teams of medical personnel who can be transported anywhere, Neighborhood Watch, Volunteers in Police (VIP), Fire Corps. Map Your Neighborhood and/or Community Emergency Response Teams (CERTS) to learn what every neighbor and family member needs to know, as they may be the very first responders. They are “The Boots on the Ground.” More lives have been saved by those at the scene than paramedics and hospitals, which are later participants. Uninformed but well-intentioned bystanders often become victims or get in the way. Whether you can take the training or not, and most of this is not taught in medical school, everyone should go to Ready.gov and drill down to virtually any topic related to Disaster Preparedness, as there is much, much more. Get the booklet “Are You Ready.” There are many texts (including my own book, Common Sense

Before I took my first of eight CERT classes, I foolishly thought I knew it all as might other doctors. That changed within minutes the first night. I now train trainers and train trainers of trainers as well as doing grassroots teaching. It is amazing how much we as MDs do not know. Geoffrey Simmons, MD, Vice President of the Academy of Disaster Medicine, is in group practice with PeaceHealth. He is a FEMA Advisor for Region X Advisory Council and a Volunteer Team Coordinator for the city of Eugene, OR. Potential Financial Conflicts of Interest: By AJCM policy, all authors are required to disclose any and all commercial, financial, and other relationships in any way related to the subject of this article that might create any potential conflict of interest. The author has stated that no such relationships exist. ®

References 1.

FEMA. Are You Ready? An In-Depth Guide to Citizen Preparedness. August 2004.

2.

Hogan D, Burstein J. Disaster Medicine. 2nd edition. Lippincott Williams and Wilkins. 2007.

3.

National CERT Program/FEMA/DHS. Community Emergency Response Team: Basic Instructor Guide. January 2011.

4.

www.redcross.org.

5.

www.fema.gov.


American Journal of Clinical Medicine® • Fall 2011 • Volume Eight, Number Three

Damage Control Resuscitation:

The Case For Early Use of Blood Products and Hypertonic Saline in Exsanguinating Trauma Victims Graeme A. Browne, CAPT MC (FS) USN Based on a presentation at the 2011 AAPS Annual Scientific Meeting, Tysons Corner, VA, June 21-22

Abstract

Background

Resuscitation of massively traumatized patients is physiologically complex, time-dependent, and a significant resource management matter often associated with poor survival rates. Retrospective medical evidence accumulated from combat trauma admissions to the Joint Theater Trauma Registry (JTTR) 20032007 supports swift replacement blood products when total blood volume losses of 30-40% or greater has occurred. Replacement plasma, packed red blood cells, and platelets in a ratio of 1:1:1 significantly reduces trauma-related coagulopathy. Clinical management specifically avoiding acidosis and hypothermia, in conjunction with administration of specific blood products, or fresh whole blood, will blunt the emergence of the ‘lethal triad.’ Limited Level 1Trauma Center prospective evidence based on massive blood transfusion of penetrating torso injuries supports the JTTR data.

Traumatic injuries have a devastating human global impact. In 2000, approximately five million deaths were attributed to crush and penetrating injuries. Major trauma has a death rate of 83 per 100,000 population and accounts for 9% of global deaths. Victims of penetrating traumatic events who arrive alive at trauma centers and who subsequently die do so because of multi-organ failure and sepsis, not due to blood loss exigent to wounds sustained from those traumatic events. These events typically occur in males between the ages of 1-44 years. Trauma is the leading cause of pediatric deaths. Traumatic events within the continental United States account for 37 million emergency department visits annually and 2.6 million hospital admissions and account for one death every three minutes within the US.

Large resuscitative volumes of isotonic crystalloids are detrimental to survival outcomes of trauma patients. Crystalloid associated dilutional coagulopathy and the initiation of multiple cytotoxic cascades results in terminal cyto-pathology, abdominal compartment syndrome, multi-organ failure, sepsis, and death. Limited crystalloid infusion should accompany medical and surgical management of these complex trauma patients, establishing permissive hypotension until damage control surgical interventions are provided. Compelling evidence exists for use of hypertonic saline in resuscitation of acute anemic hypovolemia. FDA has not approved its use in trauma resuscitation.

The monetary impact to the economy in 2000 was $406 billion, of which $80 billion was due to direct medical costs, and $326 billion was calculated as indirect costs to the economy due to lost productivity. Between 01 January and 15 August 2011, the total number of deaths occurring from traumatic injuries has eclipsed 134,792.1 In comparison, during the interval 20022010, the total number of combat deaths recorded for the wars in Afghanistan and Iraq, Operation Enduring Freedom, and Operation Iraqi Freedom respectively, has reached 5,000. The total number of survivable injuries during this same period has reached 34,000, excluding injuries associated with traumatic brain injury (TBI) and posttraumatic stress disorder (PTSD). The process of resuscitating trauma victims who sustain massive blood loss is a multifaceted, time-dependent clini-

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cal challenge. Despite rapid deployment of first responders, rapid transport of trauma victims to established Trauma Units, prompt use of modern interventions, and monitoring techniques in well equipped intensive care units, mortality rates continue to remain high. Advanced Trauma Life Support (ATLS)2 guidelines developed by the American College of Surgeons (ACOS) have emphasized specific practice management interventions for all trauma victims. A pivotal concept that has remained central, and an immutable belief within the ATLS recommendations, has been that optimal hemodynamic function would be restored by rapidly infusing isotonic crystalloid solution in a ratio of 3:1 saline to blood loss, or at a greater ratio up to 1:8 for massive blood loss.3,4 Repletion of deficient intravascular volume and its associated contracted interstitial fluid was considered an essential step to restore physiological function in acutely anemic trauma victims. High volume acute blood loss or persistent on-going blood losses require banked blood products to be transfused using type specific packed red blood cells or universal donor cells (type O) when these would be made available from the blood bank. Women of child-bearing age should be administered Rh negative red cells to avoid complications of antibody formation against Rh positive donor cells. These antibodies, which are responsible for carnicterus and fetal hydrops, will seriously degrade fetal viability in future pregnancies. In the past, surgical specialties have tacitly stated that trauma victims die from increased clotting complications and not because of extensive blood loss, a belief that has been anchored in the reliance upon ligation and not upon scientific evidence. However, current concepts in cell biology provide clarity to defined cascades of dynamic molecular biochemistry and biophysics, permitting an understanding of the properties of intracellular and extracellular inflammatory cascades mediated by epitopic cell signaling. These entities have significantly altered prevailing scientific appreciation of trauma related tissue and organ effects that devolve from near exsanguinations and shock states.5,6,7

The ‘Lethal Triad’ Within the context of severe hemorrhage, anticipated coagulopathy must be expeditiously managed to avoid later manifesting coagulopathic states. The expression of these is seen to be amplified when associated with hypothermia and acidosis. Hypocoagulation, hypothermia, and metabolic acidosis are collectively termed the ‘lethal triad.’8 The mortality rate increases significantly with one or more of these clinical markers. When malignant arrhythmias are included within the triad of extensive blood loss, hypothermia, and metabolic acidosis, the clinical severity becomes profoundly more complex with a decompensating physiologic reserve. Anaerobic metabolism contributes directly to dysrhythmias by down regulation and functional incompetency of cell membrane ionophores. This causes significant disruption to electrical neu-

trality of cell walls and subsequently to the tonicity within cells via transmembrane energy losses. Thus, declining cardio-myofibril competency and critically diminishing cardiac index and reserve leads to end stage malignant rhythms and cardiac standstill. Consequently, attention must be directed toward terminating unabated blood loss and avoiding early coagulopathic states by establishing environmental conditions conducive to maintaining core body temperatures of greater than 35°C. Acidemia due to tissue hypoperfusion corrected by restoring vascular volume will result in increased perfusion pressure, which will then dislodge immature fibrin clots located at sites of intimal vascular injury. This is better managed by permissive hypotension and prompt damage control surgery, thereby avoiding the consequences associated with persistent blood loss, a condition termed ‘the bloody vicious cycle.’9

Basic Science Evidence Comprehension of basic science cell physiology, epitopic cell signaling, and gene function provides credible evidence for permitting recognition of the cytotoxic effects of crystalloids (L-form and racemic lactated Ringer’s solution, normal saline) and colloids, all of which directly impinge upon the coagulation cascade.6 Isotonic crystalloids initiate activity associated with the neutrophil oxidative burst, dilute essential cofactors within the plasma, and are responsible for delayed and deficient clotting, the consequence of which is continued bleeding from injured sites. Additionally, infusing solutions having low pH values, such as normal saline and lactated Ringers, will further augment in vivo hypo-coagulation. This effect is distinct and separate from disseminated intravascular coagulopathy (DIC). Intravascular volume repletion with crystalloids, while improving systemic blood pressure, will cause immature platelet clots to disengage from the point of intimal tear, resulting in continued hemorrhage. Un-warmed crystalloids inherently adversely impact thermogenesis. Additionally, cellular energy, which is normally derived from mitochondrial aerobic metabolism, is lost by the effects of crystalloid cytotoxicity. The mechanism is seen to be from direct inhibition of cell membrane ionophore function. This energy loss, known as metabolic entropy, further degrades the homeostasis of thermogenesis. Isotonic crystalloids prime immunogenic modulation of neutrophilic burst activity and degrade intrinsic metabolic capability to initiate humeral and cell mediated function. Thus, sepsis, acute respiratory distress syndrome (ARDS), and multiple organ failure (MOF) will rapidly evolve. In contradistinction to isotonic saline, hypertonic saline solution suppresses neutrophilic burst activity, minimizes third spacing of intravascular infusates, and offsets apoptosis of various organ cell lines, making this a temporary but effective fluid for resuscitation of trauma victims. NATO countries have authorized 3% and 7.5% saline for military surgical use.5 The FDA has not approved the use of hypertonic saline solutions for


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combat resuscitation nor for civilian surgical conditions related to massive blood loss. Three percent saline is widely used in US intensive care units for medical conditions requiring vascular support and repletion of serum sodium.

The Basis of JTTR Clinical Practice Guidelines20 Clinical evidence for a paradigm shift in the early management of massive blood loss in trauma victims has been provided by robust retrospective documentation compiled by the JTTR.17 Published JTTR surgical records from 2003-2007, of which 708 trauma records underwent multivariate logistic regression analysis, concluded that at 48 hours, increased survival rates (82% vs. 62% p<0.001) occurred in those casualties receiving fresh whole blood or aphoretic platelets when compared to casualties not receiving either whole blood or platelets. Survival rates at 30 days were sustained (62% vs.50% p= 0.04).18 This analysis suggests the use of whole blood and aphoretic platelets are independent predictors of survival. When administered in a 1:1:1 ratio of PRBCs:plasma:platelets, this resulted in a reduction of long term mortality from 65% to 19%.23 Retrospective data from 466 massively transfused civilian patients appear concordant with the conclusions that emerged from the JTTR analysis. These observations present compelling reasons to reconsider the logic of continuing to follow the principles of ATLS in those situations where penetrating chest injuries are present. Based on JTTR and other limited prospective civilian trauma data19 it would be prudent to carefully monitor how much and how rapidly, or indeed should large volumes of crystalloids be administered as the initial strategy for the resuscitation of complex trauma victims who have lost 30-40% of their blood volume. It seems that keeping the resuscitative crystalloid volume to less then 250 mls is the approach to be undertaken. This would then be closely followed by rapidly infusing red blood cells, plasma, and platelets in high ratio.10,11,12,13,14,15 To date this strategy has not achieved a consensus amongst civilian traumatologists, unlike military surgeons who employ the JTTR clinical practice guidelines (CPG).

Joint Theater Trauma Registry Clinical Practice Guidelines20 Laboratory and clinical parameters are used in management planning for exsanguinating trauma patients. These are: 1) INR greater than 1.5; 2) base deficit greater than 6.0; 3) hemoglobin less than 12; 4) temperature less than 96F; 5) systolic blood pressure less than 90mm Hg. The mortality rate associated with massive blood loss trauma is seen to be 25% with one or more of these markers being present. JTTR CPG requires the administration of six units of cross matched packed red blood cells (PRBCs), six units of plasma,

and six pack platelets (equivalent to 1 pack aphoretic platelets) in a ratio of 1:1:1. In addition, recombinant activated factor VII (rFVIIa)21 is administered as 100mcg/kg intravenously, repeated every 20 minutes for up to four doses when it becomes clinically evident that at least ten units of blood will be required for resuscitation. Fresh whole blood22 may be utilized when the Red Cross supply is depleted.

Discussion Coagulopathic states evolve early following major trauma. This fact has been neglected and generally accepted as a consequence of resuscitation, hemodilution, and hypothermia. Civilian hospitals have limited experience with massive transfusions when compared to that experience obtained by military surgeons managing patients who have sustained extensive penetrating fragmentation wounds. These wounds are frequently accompanied by class III and IV blood losses. Additionally, appreciating the complex role played by pro-inflammatory cascades occurring within the vascular system and within the intracellular chemistry of critical organ systems of exsanguinating trauma patients, ATLS algorithms may actually be deleterious when vascular resuscitation is attempted using large volumes of crystalloids. Data presented suggest that practice management of trauma resuscitation will likely undergo a fundamental change from previously held clinical concepts and algorithms of ATLS in order to decrease morbidity and mortality rates that currently accompany existing practice standards in the management of exsanguinating trauma. New algorithms must be proposed emphasizing ‘minimal use’ resuscitative crystalloid infusions for casualties sustaining massive blood loss if trauma management advances are to improve survivorship and to decrease post-traumatic morbidity. Civilian trauma and emergency medicine specialists to date have given little support to this novel strategy. Effective application of known basic science mechanisms must become rationally integrated within clinical resuscitation strategies and protocols. Aggressive crystalloid repletion of intravascular volume, especially when losses exceed 30-40% total blood volume, fails to support prevailing scientific logic. For example, plasma clotting co-factors are diluted by crystalloid volume infusion. Isotonic crystalloid cytotoxicity augments hemorrhagic diathesis. In contra distinction, hypertonic saline has not been associated with any discernable cytotoxic effects that are readily seen when large volume isotonic crystalloids are administered. Hypertonic saline is available and approved outside the US as 3% and 7.5% concentrations for trauma resuscitation. FDA approval for hypertonic saline use in trauma is under consideration. Extensive retrospective studies generated from Combat Support Hospitals during Operation Iraqi Freedom and Operation Enduring Freedom provide encouraging data when damage

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control surgery is integrated with class 4 (over 40% total blood volume) blood loss trauma victims and with the following specific actions and agents: 1) permissive hypotension is utilized; 2) fresh whole blood or packed red blood cells are promptly infused; 3) plasma volume is rapidly replaced; 4) platelets administered to replete those lost; 5) recombinant Factor VII activated (rFVIIa) administered when ten units or more of blood are required; and 6) minimal crystalloid infusion not to exceed 250 mls. Integration of these actions has contributed to measurably better survival rates (65% vs. 19%). Retrospective Joint Theater Trauma Registry studies reveal improved survivability, less complications, earlier ventilator extubation, decreased incidence of abdominal compartment syndrome, clinically relevant reduction in post-resuscitation edema, and evidence for decreased 3rd spacing, including a quantifiable reduction in the use of blood products when high ratio PRBCs:plasma:platelets are utilized in 1:1:1 ratio. This cannot be stated for the clinical results of similar trauma injury severity situations where receiving transfusions at customary 1:3 ratio of plasma: RBC as is standard practice in the majority of US civilian hospitals. An opinion consensus among civilian traumatologists has not been achieved regarding optimal plasma, platelet, and red blood cell ratios in massive transfusion damage control resuscitation. Recent civilian small prospective trials using a high ratio transfusion regimen, the same as those established by JTTR CPG, are consistent with outcomes reported by JTTR. Recognizing and appreciating the existence of the early presence of coagulopathy in exsanguinating casualties will result in rational transfusion strategies and resuscitation management that employ early use of blood products and very sparing use of isotonic crystalloids. Avoidance of the ‘lethal triad’ (coagulopathy, hypothermia, and acidosis) will substantially improve the rate of successful resuscitative outcomes.

Damage Control Anesthesia23 During damage control resuscitation, anesthesia management is uniquely different from procedural sedation and rapid sequence intubation as performed on hemo-dynamically stable patients in whom intravascular volume is not a critical factor. In hypovolemic anemic shock anesthesia management requires close management to avoid precipitous fluctuations of systemic blood pressure. Variations in blood pressure will occur early during induction, sedation, and when neuromuscular blockade agents are administered for acquisition of mechanical airway control. Pain control and achieving dissociative anesthesia especially sensitize the vascular system to wide oscillations of systemic blood pressure. The loss of vasoconstrictive reflexes characteristic of shock states, or when using induction agents in conjunction with massive hypovolemia, will significantly impact the potential for the

clinical expression of the magnitude of residual catecholamine load and the subsequent catechole surge is expectantly severely attenuated, resulting in profound hypotension. Hypertensive episodes seen under these unstable physiological conditions are believed to disrupt polymerizing collagen found within immature fibrin clots that are localizing at sites of vascular injury. To manage these critical blood pressure oscillations, blood products consisting of PRBCs, plasma, and platelets must be administered rapidly while incrementally titrating small doses of Fentanyl in amounts not exceeding about one-fifth of that commonly used during RSI. The goal is to establish a mean arterial pressure of 65mmHg, which is approximately equal to a systolic pressure of 70mmHg. Limited infusion of 250 mls of crystalloid is permitted during this phase of the damage control resuscitation.

Summary Understanding relevant biochemical cascades associated with cell function and their epitopic triggers operating diverse gene functions that impact interleukin, bradykinin, neutrophil burst oxidation, intravascular coagulation functions, and their relationship with infusible crystalloid toxicity together with their apparent close relationship with trauma related coagulopathy, provides a viable scientific basis for recommending a substantial practice change in how complex trauma resuscitation should be managed. An extensive retrospective series of critically wounded combat personnel during Operation Iraqi Freedom and Operation Enduring Freedom admitted to the JTTR 2003-2007, in whom massive blood loss had occurred, show strong clinical concordance with currently available basic science cell physiology and the justifiable use of plasma, platelets, and RBCs in the ratio of 1:1:1. Recent limited civilian prospective studies have provided similar improved survival outcomes in trauma victims sustaining massive blood loss. Avoidance of coagulopathy, prevention or reversal of hypothermia, and acidosis (lethal triad) in casualties who have sustained massive blood loss who require salvage resuscitation, are best managed by applying new key concepts that reflect improved comprehension of the intrinsic pathophysiology of trauma resuscitation. Applying interventions that are concordant within both basic science and emerging clinical evidence unique to trauma resuscitation will reduce morbidity and mortality within a subgroup of exsanguinating trauma victims. These changes must be appreciated and managed in a longitudinally consistent manner by paramedics, Emergency Medicine, critical-care transport, and Trauma Teams, if improved survivability is to materialize. Permissive hypotension, prompt use of blood products, and hypertonic crystalloid solutions, the latter when approved by the FDA, appear likely to optimize the survivability of the mas-


American Journal of Clinical Medicine® • Fall 2011 • Volume Eight, Number Three

sively injured patient. Avoiding large volumes of isotonic crystalloids, preventing hypothermia and acidosis have been shown to decrease morbidity and mortality. ATLS algorithms should now reflect these recent encouraging trends in trauma stabilization and its subsequent definitive management. Graeme A. Browne, MD CAPT MC (FS) USN, MD, is certified in both Emergency Medicine and Disaster Medicine. He is an Emergency Medicine Physician at Mayo Health System, Austin, Minnesota, and a Flight Surgeon, United States Navy. Potential Financial Conflicts of Interest: By AJCM policy, all authors are required to disclose any and all commercial, financial, and other relationships in any way related to the subject of this article that might create any potential conflict of interest. The author has stated that no such relationships exist. ®

References

be given earlier to patients requiring massive transfusion. J Trauma. 2007;67:112-119. 11. Holcomb JB, Mahoney P, Beilman GJ, et al. Damage Control Resuscitation: Directly Assessing the Early Coagulopathy of Trauma. J Trauma. 2007;62:307-310. 12. Beekley AC. Damage Control Resuscitation: A Sensible Approach to the Exsanguinating Surgical Patient. Critical Care Med. 2008;36(7):S267-S274. 13. Jansen JO, Thomas R, Loundon MA, Brooks A. Damage Control Resuscitation for Patients with Major Trauma. BMJ 2009; 338:1436-1440. 14. MacLeod JBA, Lyn M, McKinney MG, et al. Early Coagulopathy Predicts Mortality in Trauma. J Trauma. 2003;55:39-44. 15. Niles SE, McLaughlin DF, Perkins. JG, et al. Increased Mortality Associated with Early Coagulopathy of Trauma in Combat Casualties. J Trauma. 2008;64(6):1459-1465. 16. Rotondo MF, Schwab CW, McGonigal MD, et al. Damage Control: An Approach for Improved Survival in Exsanguinating Penetrating Abdominal Injury. J Trauma. 1993;35(3): 375-82. 17. Joint Theater Trauma Registry 2011.

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National Trauma Inst. 15 Aug 2011.

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ATLS Manual 8th Ed. p 63.

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Shires T, Coln D, Carrico J, et al. Fluid Therapy in Hemorrhagic Shock. Arch Surg. 1964;88:688-93.

18. Zink KA, Sambasivian CN, Holcomb JB, et al. A high ratio of plasma and platelets to packed red blood cells in the first 6 hours of massive transfusion improves outcomes in a large multi-center study. Am J Surg. 2009;197:565-570.

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Cervera AL, Moss G. Progressive hypovolemia leading to shock after continuous hemorrhage , and 3:1 crystalloid replacement. Am J Surg. 1975;129:670-74.

19. Duschene JG, Barbeau JM, Islam TM, et al. Damage Control Resuscitation: from emergency department to the operating room. Am J Surg. 2011;77(2):201-6.

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Alam HB. An Update on Fluid Resuscitation. Scand J Surg. 2006;95:136145.

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Alam. HB, Rhee. P. New Developments in Fluid Resuscitation. Surg Clin N Am. 2007;87:55-72.

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Moore FA, McKinley BA, Moore EE. The Next Generation in Shock Resuscitation. Lancet. 2004;363:1988-1996.

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Rotondo MZM, Zonies D. Damage control sequence , and underlying logic. Surg Clin N AM. 1997(77):761-777.

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Kashuk JL, et al. Major Abdominal Vascular Trauma- a unified approach. J Trauma. 1982; 22(8):672-9.

10. Gonzalez EA, Moore FA , Holcomb JB, et al. Fresh frozen plasma should

20. JTTS CPG Mar 2011. 21. Perkins JG, Schreiber G, Martin A, et al. Early vs Late Recombinant Factor VIIa in Combat Trauma Patients Receiving Massive Transfusion. J Trauma. 2007;62(5):1095-1101. 22. Spinella PC. Warm fresh blood transfusion for some hemorrhages: US Military , and potential civilian applications. Critical Care Med. 2008;36(7)S340-S345. 23. Dutton RP. Damage Control Anesthesia. Int Trauma Care. 2005(15):197201. 24. Borgman MA, Spinella PC, Perkins JG, et al. Ratio of Blood Products Transfused Affects Mortality in Patients Receiving Massive Transfusion at a Combat Support Hospital. J Trauma. 2007;63:805-813.

In Memory of Steven G. Carin, Jr., DO, FAAIM

Dwight M. McGlohon, MD

Endy Chung, MD, PhD, DMD

Richard M. McGrew, Jr., MD

Katherine M. Dillig, MD

Joel M. Messina, DO, FAAOG

Dennis F. Kasza, Sr., DO

Alphonse Salerno, DO, FAASS

David G.C. McCann, MD, FAASFP, FAADM

Vincent J. Strangio, DO, FAASS Franz Vanderpool, MD

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Bombings and Blast Injuries: A Primer for Physicians David M. Lemonick, MD, FAAEP, FACEP

Based on a presentation at the 2011 AAPS Annual Scientific Meeting, Tysons Corner, VA, June 21-22

Abstract Conventional weapons and explosives continue to be the most commonly employed instruments of destruction by terrorists worldwide. Such attacks are occurring with increasing frequency and ferocity. The effects of bombings and blast injuries are both physically and psychologically devastating. Explosions combine four mechanisms of injury. In addition to these causes of injury and death, crush injury, entrapment, and compartment syndrome magnify the devastation of blast trauma. By recognizing the unique features of blast injuries and by prioritizing mass casualties to provide maximal benefit for the greatest number of patients, the physician will be better equipped to triage and stabilize these victims.

Bombings and Blast Injuries: A Primer for Physicians

Worldwide, bombings are an increasingly effective and frequent terrorism tool. Explosions are the most common cause of casualties associated with terrorism.1-5 The 1995 Oklahoma City bombing, the 2004 Madrid train bombing, and the explosions of September 11, 2001, in New York City and Washington, DC, and the 2005 London subway bombings have demonstrated the capacity of bombings and blast injuries to kill and to terrify. According to Dennis C. Blair, Director of National Intelligence, “Conventional weapons and explosives will continue to be the most often used instruments of destruction in terrorist attacks.”6 While biological and chemical weapons are often mentioned and are much feared as terror tools, it is bombs that have actually produced the majority of injuries, deaths, and societal disruptions in the modern era.1 In addition to deliberately detonated explosions, there are also industrial accidental explosions that occur with regularity at factory and mining operations, in fuel transportation and storage, and in grain elevators.

Bombings and blasts have the potential to inflict multiple and devastating injuries to a large number of victims simultaneously and without warning. Because of the variety of circumstances involved in such an event (e.g., indoor vs. outdoor, size of the explosive charge, distance of victims from the explosion, presence of secondary debris and of biological or radiological contaminants, structural collapse), each bombing event is unique.

Because of the constant risk of civilian incidents and the increasing risk of terrorist attacks, health care providers must become familiar with the characteristics of explosives and of explosions and of the nature of the injuries they may inflict.

Also unique to blasts is the range of potential physiological consequences to different human organs and organ systems, ranging from tympanic membrane rupture to impalement, and from burns to traumatic amputations.

Explosives cause the rapid conversion of a solid or liquid to a gas, resulting in a sudden release of energy. Explosives are categorized as either high-order explosives (HE) or low-order explosives (LE).2

Blast Physics


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HE produce a supersonic over-pressurization shock wave. Examples of HE include ammonium nitrate fuel oil (ANFO), TNT, C-4, semtex, nitroglycerin, and dynamite. Air is rapidly compressed, and then, as the blast wave passes, the air is temporarily under-pressurized before returning to the ambient pressure level. The characteristic HE blast wave is presented graphically in Figure 1. HE detonate quickly, producing a blast wave that rapidly expands from the detonation point, filling the involved space within a fraction of a second with the supersonic over-pressurization wave. Figure 1: Blast Overpressure Wave

work, and this is currently being researched as the most likely of all of these mechanisms of injury in blasts. In contrast, LE produce a subsonic explosion without an overpressurization wave. Examples of LE are gunpowder, pipe bombs, and petroleum-based bombs such as Molotov cocktails, or aircraft improvised as guided missiles. Rather than detonating, LE release energy more slowly, by the process of deflagration. In deflagration, a substance is heated until it burns away rapidly. Thus, LE are generally less destructive than are HE. Incendiary thermal effects differ between HE and LE: while HE produce higher temperatures for a shorter period of time resulting in a fireball at the time of detonation, LE have a longer thermal effect and can cause secondary fires.

Categories of Blast Injuries HE blast injuries are categorized as primary, secondary, tertiary, and quaternary injuries, and these may occur individually or in any combination.4,5 The characteristics of blast injury are described in Table 1. Table 1: Characteristics of blast injury Category

Characteristics

Body Part Affected

Primary

Unique to HE, results from the impact of the overpressurization wave with body surfaces.

Gas filled structures are most susceptible - lungs, GI tract, and middle ear.

Secondary

Results from flying debris and bomb fragments.

Any body part may be affected.

Tertiary

Results from individuals being thrown by blast wind

Any body part may be affected.

Quarternary

All explosion-related injuries, illnesses, or diseases not due to primary, secondary, or tertiary mechanisms.

Any body part may be affected.

TIME

HE exert their destruction by several mechanisms: 1) the blast pressure wave, 2) fragmentation, 3) blast wind, 4) incendiary thermal effect, 5) secondary blast pressure, and 6) ground and water shocks for explosions that occur under ground or water. Fragmentation effect occurs from projectiles that are either included within the container, projectiles that are created by the destruction of the container itself, or from those propelled objects from the surrounding environment and target. The motion of air generated by the blast waves creates blast wind. Secondary blast pressure effects result from the reflection of blast waves off surfaces, magnifying their effect, especially in enclosed spaces. Because ground and water are relatively noncompressible media, underground and underwater explosions transfer more energy to the body than do explosions in the air. Four effects produce injuries from blasts: spalling, implosion, shearing, and irreversible work.2 Spalling is the result of a shock wave moving through tissues of different densities, leading to molecular disruption. Entrapped gases in hollow organs compressing and then expanding result in visceral disruption by implosion. Shearing is due to tissues of different densities moving at different speeds and leading to visceral tearing. Forces exceeding the tensile strength of the tissue cause irreversible

Includes exacerbation or complications of existing conditions.

A primary blast injury is caused by the direct effect on tissue of the blast overpressure wave. A primary blast injury affects air-filled structures most importantly, such as the lung, ear, and hollow viscus of the gastrointestinal tract.6,7 Flying objects that strike victims cause a secondary blast injury. Such injuries are penetrating trauma and fragmentation injuries. Tertiary blast injuries are a feature of high-energy explosions only and occur when people fly through the air and strike other objects. Miscellaneous or quaternary blast injuries encompass all other injuries caused by explosions. This includes burns, crush injuries, toxic inhalations, asphyxia, and exacerbations of victims’ underlying medical conditions. The four categories of blast injuries are depicted graphically in Figure 2.

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Figure 2: Categories of Blast Injuries

Primary Blast Injuries The tympanic membrane (TM) is the organ that is most often damaged by blast injuries, sustaining injury at as low as five pounds per square inch (psi) above atmospheric pressure (1 atm is equal to 14.7 psi, or 760 mm Hg).3,6 At higher pressures, the ossicles of the middle ear can be dislocated. As can be seen in Figure 3, pressures gradients of 56 to 76 psi (3.8 to 5.2 atm) are needed to cause damage to other organs. Thus, in the absence of rupture of the TM, primary blast injuries on other air-containing organs are less likely. For example, in the Madrid train bombings, of 17 critically ill victims with lung injuries from the blast, 13 had ruptured TMs and four did not.3,7,8 A graphic depiction of TM rupture is shown in Figure 4. Figure 3: Effect of peak pressure

The lung is the second most common organ that is injured by overpressure.2,4,5 Injury results in hemorrhage, pulmonary contusion, pneumothorax, hemothorax, pneumomediastinum, and subcutaneous emphysema. Pulmonary contusion results in the classic “butterfly” pattern of bilateral hilar pulmonary edema seen on x-ray, Figure 5. Acute gas embolism (AGE) is also a form of pulmonary barotraumas that requires special attention. Air emboli most commonly occlude blood vessels in the brain or spinal cord. While body armor protects personnel from most ballistic projectiles to the torso, it does not prevent the lung barotrauma of primary blast injury.6

Figure 4: Tympanic membrane perforation

The colon is the hollow viscus most frequently injured by a primary blast injury.5 Rupture of the colon and mesenteric ischemia or infarct leading to delayed rupture of the large or the small bowel may occur. Eye injuries from the primary blast include globe rupture, retinitis, and hyphema.9 Primary blast injuries to the brain include concussion and barotrauma caused by AGE. The extent of injury from an explosion is affected by the magnitude of the device, the distance from the explosion, whether the medium transmitting the over-pressure is air, water, or solid, and the environment (i.e., open or closed). Figure 5: Blast lung x-ray


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Secondary Blast Injuries The most common cause of death in a blast event is secondary blast injuries, which result from the effects of projectiles.1 Projectiles may include objects that were intentionally included in the device or those that were propelled as part of the blast effect. Such objects include nails, bolts, nuts included in the blast mixture, military shrapnel, flying glass, and human parts. Flying debris may injure individuals far from the blast. In the 1998 terrorist bombing of the U.S. Embassy in Nairobi, Kenya, for example, victims up to two kilometers away were injured by flying glass.6 Penetrating injuries are much more common than primary blast injuries, and they represent the leading cause of death in blast victims, except in the case of major building collapse.4 The most common types of secondary blast injuries are trauma to the head, neck, chest, abdomen, and extremities in the form of penetrating and blunt trauma, fractures, traumatic amputations, and soft tissue injuries. Foreign bodies follow unpredictable paths through the body and may have only mild external signs. Thus, there should be a low threshold for imaging studies in such injuries. All of these wounds are considered to be contaminated, and they should not be closed primarily.

attention. In civilian settings, terrorist attacks tend to have a bimodal distribution of mortality — high immediate death rates followed by low early and late rates. Those victims with lesser injuries receive delayed care, and those with a poor prognosis receive minimal care. Up to 75% of victims self-refer to hospital, arriving by private transportation.6 Several factors contribute to the blast victims’ needs exceeding available resources. Large numbers of patients may make rapid triage impossible and may exceed responder treatment capabilities and cause delay in transport to hospitals. Patients are divided into urgent and non-urgent categories, and they receive initial resuscitation while other victims continue to arrive. Definitive, optimal care is delayed until victims stop arriving.3 Expectant management is appropriate for those who are unlikely to survive, such as patients with 100% body surface area (BSA) burns and those in cardiac arrest.4,11 Figure 6: Algorithm for the evaluation of blast injuries

Approximately 10% of blast survivors will have significant eye injuries, often perforations from high-velocity projectiles, especially glass. Secondary eye injuries include blindness and ruptured globes.5,8

Tertiary Blast Injuries Tertiary blast injuries are caused when the victim’s body is thrown into another object by the blast winds of the explosion. Victims may also tumble along the ground, resulting in blunt and penetrating injuries. The most common tertiary injuries are fractures and closed head injuries.1-6 Other injuries include broken, dislocated, or even amputated extremities. The extent of injuries from this mechanism also depends on what the victim strikes in the environment; injuries can range from simple bruises and abrasions to impalements.

Quaternary Blast Injuries Quaternary injuries include all those injuries not due to any of the above mechanisms. These include burns, inhalation injuries, toxic exposures, poisoning from carbon monoxide, and crush injuries. Quaternary injuries also include exacerbation of chronic medical conditions, such as asthma, chronic obstructive pulmonary disease, and angina.1,6,10

Management Causes of early mortality due to blast injuries are, in decreasing order: multiple trauma, head trauma, thoracic injury, and abdominal injury.5,6,9 As with any mass casualty incident, effective triage is essential to optimize outcomes. Victims with a reasonable chance for survival receive immediate medical

Management of blast injuries begins with attention to airway, breathing, and circulation. Ventilatory and circulatory support is initiated, and, if possible, a rapid history is obtained. Important historical details of the explosion include whether it occurred in an open, a closed, or a semi-confined space. Blasts in vehicles, mine shafts, buildings, and subways are associated with greater morbidity. Structure collapse also markedly increases mortality. In a military scenario, whether the victim had on body armor is also pertinent, as body armor increases the severity of primary blast injury.5,6 History should assess for the presence of tinnitus, deafness, or earache, nausea, vertigo or

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retrograde amnesia. The patient should be asked about shortness of breath or chest pain. Other important questions regard eye pain, abdominal pain or urge to defecate, nausea, or blood in the stool. Physical examination should evaluate for blood in the external auditory canal and ruptured tympanic membrane. Fluid infusion should be initiated to achieve a palpable pulse at a rate of less than 120 beats per minute, a systolic blood pressure of 100 mmHg, and a return of normal mentation.5 An algorithm for the rapid assessment of blast victims has been proposed, Figure 6.4,5 Cyanosis, hemoptysis, ronchi, or rales are markers for lung injury. The abdominal exam should assess for tenderness, rigidity, or guarding. The presence of any of these history or exam findings should result in a thorough clinical examination and at least eight hours of observation.

Pulmonary Injuries Pulmonary blast injury (PBI) has the highest mortality of primary blast effects. Lung tissue is especially sensitive to barotrauma because of the extensive tissue-air interfaces involved. An over-pressure of 40 ATM will lead to lung damage.6,11 The incidence of pulmonary blast injuries is less than 10% of casualties seen and between 30 and 60% of admitted casualties.5 Pulmonary injury increases with enclosed space events. Injuries include pulmonary contusions, pneumothorax, interstitial emphysema, pneumomediastinum, and subcutaneous emphysema. The most common lung injury associated with a blast wave, pulmonary contusion, is manifested by alveolar hemorrhage and interstitial edema. Such contusions, resulting in micro-hemorrhages and perivascular and peribronchial disruption, may occur as late as 48 hours after the explosion. PBI should be suspected in a patient with the diagnostic triad of dyspnea, bradycardia, and hypotension and with wheezing or hemoptysis following an explosion. Other diagnostic clues to PBI are hypopharyngeal petechia, hypoxia, cyanosis, apnea, decreased breath sounds, and hemodynamic instability. X-ray evidence of PBI may present within hours of the explosion, and it usually resolves within a week. A plain anterior-posterior chest x-ray is usually diagnostic for pulmonary barotraumas, producing a characteristic “butterfly” pattern, Figure 5. Such x-rays must also be inspected for the presence of subcutaneous emphysema, fractured ribs, hemopneumothorax, and pneumomediastinum. Supplemental high-flow oxygen is provided for hypoxemia, either by mask or by endotracheal intubation, if required. Ventilator-associated barotrauma and systemic air embolism are minimized by limiting peak inspiratory pressures (< 40 cm H20), by permissive hypercapnia, and by judicious use of positive pressure ventilation. Chest tubes are inserted as needed for pneumothoraces. Extracorporeal membrane oxygenation (ECMO) has also been used for severe Blast Lung Injury (BLI).2 Arterial gas embolism (AGE) is suggested by sudden blindness, focal neurologic deficit, chest pain, or sudden loss of conscious-

ness. Physical examination may show retinal arterial gas bubbles on fundoscopy, and the victim’s skin may be mottled. Focal neurological deficits and dysrhythmias may also be present. Immediate treatment for AGE is supplemental oxygen and positioning the patient in the left lateral decubitus position with the head down. Definitive care is treatment in a hyperbaric chamber. While BLI results in significant scene mortality, approximately 70% of critically injured patients who are admitted with BLI survive, many with near-normal lung function at one year.

Gastrointestinal Injuries Abdominal injuries include abdominal hemorrhage and abdominal organ perforation and laceration. Blast injury to the gastrointestinal (GI) tract should be suspected in any victim with signs and symptoms that include abdominal pain, rebound, guarding, absent bowel sounds, nausea, vomiting, vomiting blood, rectal pain, testicular pain, or with unexplained hypovolemia.9 The colon is the most common site of hemorrhage and perforation due to blast trauma. The clinical signs of injury may be evident immediately, or they may be delayed up to 48 hours and as late as 14 days after the blast.4 Solid organ lacerations and testicular rupture may also be seen but are less common. Diagnostic peritoneal lavage (DPL), ultrasound, plain x-ray, and CT are all used in imaging of abdominal blast injury. Plain films may show penetrating foreign bodies and free intraperitoneal air. CT may reveal free air, solid organ injury, hemoperitoneum and retroperitoneal injuries, and mesenteric injury, but it has poor sensitivity in identifying hollow viscus injuries.3,5,6,10,11

Neurological Injuries Severe head injury is the chief cause of mortality in blast victims.1 The effect on the central nervous system of an overpressure wave includes diffuse axonal injury, skull fractures, coup- and counter-coup injuries, and subarchnoid and subdural hemorrhage. Primary blast waves can cause concussions or mild traumatic brain injury (MTBI), even without a direct blow to the head. Penetrating brain trauma is also seen. Symptoms of traumatic brain injury (TBI) include headache, nausea, confusion, fatigue, depression, and amnesia, as well as fixed neurological deficits. Patients suspected of sustaining neurological injury should undergo urgent CT of the brain as well as cervical spine imaging. Severe head injuries require ventilatory support and neurocritical care. Attention to cerebral protection includes maintenance of cerebral perfusion pressure, body temperature, neuromuscular blockade and sedation, and cervical spine control. Additionally, glucose and seizure control and DVT prophylaxis are addressed.


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Auditory Injuries The auditory system is most sensitive organ to blast injury.1-7 Overpressure of 5 psi is required to perforate the tympanic membrane, with damage to the cochlea and ossicles occurring at lower pressures.1-3,6 By comparison, pressure gradients of 56 to 76 psi (3.8 to 5.2 atm) are needed to damage to other organs. Thirty-five percent of survivors in the Oklahoma City bombing reported auditory injury.1-4 While TM perforation is considered to be an indicator of other, more serious, injuries, it is neither highly sensitive nor specific; TM perforation may be found in victims with severe pulmonary, intestinal, or other injuries, or it may be found in isolation. Its presence does not indicate that more serious blast injuries exist. In an Israeli study of 11 terrorist attacks that caused 145 fatalities and 647 injuries, 142 had isolated TM perforation, 18 had isolated BLI, and 31 had both. No patient with isolated TM perforation later developed BLI.6 It has been noted that external ear amputation due to primary blast injury is usually associated with other nonsurvivable injuries. Sensorineural and conductive hearing losses are both possible. In addition to hearing loss, symptoms of ear damage include bleeding from the external ear canal, ear pain, tinnitus, and vestibular dysfunction with vertigo. Fifty percent to 80% of ruptured tympanic membranes heal spontaneously, while sensorineural hearing loss is often permanent.6,7,11,12

Eye Injuries Most eye injuries caused by blasts are due to flying debris. While the eye represents only a tiny amount of total body surface area, eye injuries can account for 2% to 16% of bombing injuries.3,9,11 Flying glass was responsible for most of the eye injuries in the Oklahoma City bombing.11 One-half of patients with open globe injuries had head injuries as did one-third of patients with any eye injury.8,9,11 Symptoms of ocular blast injuries include foreign body sensation, pain or irritation, change in vision, and periorbital swelling. Ophthalmology consultation is appropriate for suspected globe injuries, deep corneal foreign bodies, orbital fractures, retinal detachments, hyphemas, intraocular foreign bodies, corneal burns, and deep eyelid burns and lacerations.

Orthopedic Injuries Orthopedic injuries may occur by any of a variety of blast effects: 1) blast waves may lead directly to fractures, 2) projectiles may penetrate and injure extremities, 3) bodies tumble and extremities strike fixed objects in the blast environment, and, finally, 4) extremities are crushed, burned, and neurovascularly compromised. Traumatic amputations due to primary blast injury have a dismal prognosis because victims have been exposed to extreme

overpressure.3 In one series, 11% of blast fatalities had traumatic amputation, and their survival rate was 1%.9,12 In the Oklahoma City bombings, one-third of survivors sustained musculoskeletal injuries, and one-third of these victims had multiple fractures.11 There are several principles that guide the care of orthopedic blast injuries. Significant injuries may result from small entrance wounds, and fragments may not travel in straight lines. Therefore, any victim with entrance wounds in the thighs, perineum, or buttocks should be suspected of harboring an intra-abdominal injury. A hematoma in proximity to an arterial structure may indicate a vascular injury, and compartment syndrome and rhabdomyolysis can complicate musculoskeletal injuries. Tetanus prophylaxis and post-exposure antibiotics are indicated, and these wounds are at high risk for infection and gas gangrene.

Special Situations Pregnant patients, older, and pediatric blast victims require special mention.1,2,6 Direct injury to the fetus is not common due to its protection within amniotic fluid. The blast wave can cause placental abruption, however. For this reason, women in the second or third trimester should have fetal monitoring. A Kleihauer-Betke test is also indicated, and women may require administration of Rh immunoglobulin. A positive test requires mandatory pelvic ultrasound, fetal non-stress test monitoring, and obstetrics/gynecology (OB/GYN) consultation.6 When children are victims of blast injury, the history of the event and of the patient’s complaints may be difficult to obtain. Pulmonary contusion is one of the most common injuries from blunt thoracic trauma in children.2,6  The injury may not be clinically apparent initially and should be suspected when abrasions, contusions, or rib fractures are present.  A chest xray is essential in diagnosis especially when blast lung is suspected. Pediatric blast victims may require specialized resuscitation equipment and transfer to regional pediatric trauma facilities.1,2,6 In the Oklahoma City bombing, which involved a childcare center, there was a high incidence of traumatic amputation, fractures, and head injuries. Experience in Israel has shown that penetrating injuries of the trunk are more common in children who are victims of vehicular bombings than children who have other types of trauma. It has also been noted that children who are victims of terrorism require more ICU resources, have higher Injury Severity Scores, and have longer hospital stays than children who survived traumatic events unrelated to terrorism.11 Like children, the elderly are also at a higher risk of mortality, and their hospital stays may be longer and more complicated than other patients.6  Orthopedic injuries are more prevalent, and blunt chest trauma is of greater significance. Further, decontamination methods may need modification due to limited mobility. Decontamination of medical equipment, such as wheelchairs, walkers, and other walking aides, may also be needed.

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Communications difficulties after blast injuries include language barriers and interaction with hearing-impaired patients. Groups of victims who speak a multitude of different languages may complicate effective triage. Interaction with the deaf, hardof-hearing, newly-deafened, and the deaf-blind are obstacles as well. The history of the event as well as the individual history for the patient may be difficult to obtain. On-scene translation services including medical interpreters, sign language, and telephone translation services should all be available. Because bombings are events that occur with little or no warning, that result in disruptions of unknown duration, and that create a real or potential threat to personal safety, they have the potential to cause profound and lasting emotional impact. Psychological sequelae among victims of an explosive event include anger, frustration, helplessness, and a desire to seek revenge. Responders to bombings are encouraged to promote a sense of safety, calm, connectedness, and hope.1

David Lemonick, MD, is Attending Emergency Physician, Armstrong County Medical Center, Kittanning, PA, and PresidentElect of the American Academy of Emergency Physicians Potential Financial Conflicts of Interest: By AJCM policy, all authors are required to disclose any and all commercial, financial, and other relationships in any way related to the subject of this article that might create any potential conflict of interest. The author has stated that no such relationships exist. ®

References 1.

Halpern P. Bomb, blast and crush injuries. In: Tintinalli JT, Stapczynski J, Ma OJ, et al. Tintinalli’s Emergency Medicine: A Comprehensive Study Guide Edition 7. 2011. McGraw-Hill. p 38-43.

2.

Explosions and blast injuries: a primer for physicians. CDC.gov Web site. Available at: http://www.bt.cdc.gov /masstrauma/explosions.asp. Accessed January 19, 2011.

3.

Sutphen S K. 2005. Blast Injuries: A Review. Medscape. Medical journal online. Available at http://www.medscape.org/viewarticle/516117. Accessed January 19, 2011.

Summary

4.

DePalma RG, Burris DG, Champion HR, et al. Blast Injuries. N Engl J Med. 2005;352:1335-42.

Conventional weapons and explosives continue to be the most frequently used instruments of disruption and destruction by terrorists worldwide. Such attacks are occurring with increasing frequency and destructive force. The effects of bombings and blast injuries are both physically and psychologically devastating. Explosions combine four mechanisms of injury that may be combined, adding to the complexity and lethality of injury to victims. In addition to the devastating effects of the primary blast wave and the ensuing flying projectiles, crush injury, entrapment, and compartment syndrome magnify the inflicted injuries.

5.

Stewart C. Blast injuries: preparing for the inevitable. Emergency Medicine Practice. April, 2006. Available at http://www.ebmedicine.net/ topics.php?paction=showTopic&topic_id=18. Accessed January 19, 2011.

6.

Sasser SM, Hunt RC. Clinician Outreach and Community Activity (COCA) Conference Call. August 3, 2010 Bombings: Injury patterns, context and care. CDC Training & Continuing Education Online system. Available at: http://www2a.cdc.gov/TCEOnline/. Accessed January 19, 2011.

7.

Leibovici D, Gofrit O, Shapira S. Eardrum perforation in explosion survivors: is it a marker of pulmonary blast injury? Ann Emerg Med. 1999;34:168-172.

8.

de Ceballos J, Fuentes F, Diaz D, Sanchez M, Llorente C, Sanz J. Casualties treated at the closest hospital in the Madrid, March 11, terrorist bombings. Crit Care Med. 2005;33:S107-S112.36.

By recognizing the unique features of blast injuries, the physician will be better equipped to triage these patients rapidly and to stabilize them. By understanding the effects of explosions on each major organ system, the practitioner is ideally prepared to identify and treat these devastating wounds and to save life and limb.

9.

Mines M, Thach A, Mallonee S, Hildebrand L, Shariat S. Ocular injuries sustained by survivors of the Oklahoma City bombing. Ophthalmology. 2000;107:837-843.

10. Stein M, Hirshberg A. Medical consequences of terrorism. The conventional weapon threat. Surg Clin North Am.1999;79:1537-1552). 11. Mallonee S. Physical injuries and fatalities resulting from the Oklahoma City bombing. JAMA. 1996;276:382-387. 12. Arnold J, Halpern P, Ming-Che T, et al. Mass casualty bombings: a comparison of outcomes by bombing type. Ann Emerg Med. 2004;43:263-273.


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sounding board

Disaster Medicine: Every Physician’s Second Specialty Twenty-First Century Fears Heidi Cordi, MD, MPH, MS, EMTP, FACEP Debra Cascardo, MA, MPA, CFP

All one needs to do is turn on the TV news – or log on to the Internet – to see how overwhelming the range and ferociousness of disasters taking place around the world can be. The recent earthquake from Washington, DC, to New York City, as well as the devastation of Hurricane Irene serves as a reminder that potential disasters can strike anywhere, anytime, even in the most of unexpected places. FEMA’s “A Time to Remember, A Time to Prepare” Campaign, running this September during the tenth anniversary of 9/11, and Disaster Preparedness Month should motivate all physicians to action. An executive summary published by the National Academy of Sciences defines disaster as “an event that creates significant, short-term spike in the demand for emergency care services requiring extraordinary measures.”1 Given the one-two punch of the earthquake and cholera outbreak in Haiti and the earthquake, tsunami, and nuclear reactor meltdown in Japan, people are frightened and looking for answers. This fear is nothing new. Ever since September 11 Americans have tried to deal with the myriad of threats from natural disasters, pandemics, bioterrorism, and radiologic events in ways both rational and irrational. Some try to organize to close facilities, such as the Indian Point Nuclear Power Plant in New York. Others stockpile potassium iodide or Cipro, unsure of how to handle the scope and severity of life in the twenty-first century. In trying times, citizens turn to their medical professionals for answers. According to the American Medical Association,

physicians need to provide medical expertise and work in tandem with others to create public health policies that improve both the effectiveness and availability of medical care during epidemics, terrorist attacks, and natural disasters. Since 2007, the American Board of Disaster Medicine (ABODM), the nation’s only board of Disaster Medicine, has worked diligently to bring greater awareness to the need of physicians to make this their secondary specialty. ABODM has worked to fulfill a pressing need by developing this area of medical specialization that will undoubtedly result in a significant diminution of morbidity and mortality in all kinds of disasters in future years. President George W. Bush called for the creation of Disaster Medicine as an independent medical specialty on October 18, 2007. ABODM has been working towards fulfilling this need and Presidential directive, as the government needs a mechanism to identify those medical providers who have the requisite knowledge and skill to be involved in planning and preparedness activities.2 One valuable resource in times of an emergency is future physicians. The bad news is that these medical students are not getting adequate training in order to be of help during a disaster. Disasters know no boundaries, making it imperative that all medical students and practicing physicians, regardless of their specialty, be properly trained in disaster medicine. The good news? These future doctors have a strong desire to become knowledgeable about this area of medical expertise.

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sounding board The Role of Medical Students During Times of Emergency

Gaps in Training for Physicians and Other Staff

A survey of 523 students published in 2009 showed that only 26.2% of future doctors thought they were receiving adequate training to deal with a pandemic influenza.3 The numbers for a natural disaster (17.2%) and radiologic event (13.4%) were even worse. Nearly 85% of students did not even know to whom they should report in times of disaster. And only 2.9% were volunteers with the Medical Reserve Corps (MRC), although 81.3% showed an interest in volunteering for the MRC. A few medical schools have started formal MRC units on campus. For example, the University of Minnesota’s Medical Reserve Corps has more than 1,000 members, including staff, faculty, and medical students.

Sadly, it is not only medical students who are lacking in disaster preparedness education. A national study by Chen and colleagues found that regardless of geographic location, the vast majority of physicians (75%) did not feel they had been given adequate training to respond to a bioterrorist attack.4 And less than 30% of family physicians surveyed thought that the United States could respond effectively to a bioterrorist attack. In order to address these urgent issues the American Board of Disaster Medicine believes that the unification of highly skilled physicians sharing best practices in disaster preparedness would greatly assist in ensuring that all are equipped to deal with a myriad of potential dangers to society.

Despite the woefully low numbers of students who feel as if they have been given adequate disaster training, the majority of students believed that they should be involved in public health emergency planning efforts as well as response and recovery efforts. This is not to say that medical students should be on the front lines of clinical care during a state of emergency. Rather, they can provide surge resources, getting involved in the manning of telephone hotlines during a pandemic, for example, or providing prophylaxis or immunizations in response to a biological threat. The findings clearly indicate a worrisome gap in disaster medical education and training given the dangerous state of the world in the twenty-first century. The authors of the survey recommended that organized medicine hold a summit in conjunction with the Uniformed Services University School of Health Sciences, which is the nation’s federal health sciences university. The goal of this summit would be to elevate training in disaster medicine as one of its core competencies. By integrating disaster medicine into the core curricula of medical schools, medical students could become future leaders in disaster preparedness. Such an emphasis on disaster medicine would also underscore the medical community’s role as a leader in any health emergency. Given the myriad problems facing the medical community in times of disaster, there is every reason to utilize the untapped potential of these students, especially since they have such a clear desire to be of service during times of great need. Incorporating a disaster curriculum into medical school training is a necessary step in facilitating the process of preparedness during a natural disaster, pandemic, biological attack, or radiologic event.

Given the volatile state of political systems throughout the world, this is a true cause for alarm. Early detection and reporting by medical professionals is vital during any disaster, be it bioterrorist attack, infectious disease outbreak, or another public health emergency. Yet, despite efforts to train local physicians beginning in 2002, a study of practicing and retired physicians in Tarrant County, Texas, published in 2007 found that the majority of those responding reported no previous bioterrorism preparedness or response training.5 This finding was consistent with other studies showing a lack of preparedness in this vital area of disaster medicine. Equally important, those who did receive training were far more willing to serve in the front lines in the event of a pubic health emergency. Since training correlates so closely with the likelihood of physicians serving during disasters, this highlights the need for more education in this crucial area of medicine. The existence and mission of the American Academy of Disaster Medicine is to ensure just that. Its board, ABODM® was formed by physician leaders from all specialties to meet the myriad needs created by the disaster planning, preparation, education, response and recovery environment, which private and public institutions should tap into.

At the Breaking Point One could make the case that the entire medical system is at the breaking point when it comes to being ready for a catastrophic event. The Institute of Medicine’s (IOM) Committee on the Future of Emergency Care in the United States Health System studied the emergency care system between 2003 and 2006 and concluded that the capacity of the system to respond to even a small-scale disaster was in question. Not only are hospitals in large cities operating at or near full capacity, but also little fund-


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sounding board ing for bioterrorism and other emergency threats goes directly to hospitals.6 On the systems front, information technologies are a critical part of rapid decision making during an emergency. However, emergency physicians are often without the information they need about the patients under their care. The IOM recommends, “hospitals adopt robust information and communications systems to improve the safety and quality of emergency care and enhance hospital efficiency.”6 According to the IOM’s report, training efforts varied widely, an inconsistency that is a cause for great concern. While 92% of hospitals trained their nursing staff to respond to at least one type of threat, only 49% of hospitals gave residents and interns such training. It should be noted that this is an improvement over pre-9/11 standards, yet a situation that hardly inspires confidence given the volatile state of affairs both in this country and worldwide. One area of extraordinary challenge is protecting hospitals and their staff from biological or chemical events. The SARS outbreak in Toronto in 2003 showed how difficult it is to contain even a small outbreak, given that in such a situation health professionals can become both victims and spreaders of disease. Negative pressure rooms that prevent the spread of airborne pathogens could be a huge help during a terrorist event or pandemic, but there are few such rooms available. Without them, a hospital could quickly become overwhelmed during such a disaster, posing a grave threat to both hospital workers and patients.6

Summary There is no denying that this country is inadequately prepared to deal with a catastrophic event. Being the global leader, and being the most advanced in medicine, the American Board of Disaster Medicine and the American Academy of Disaster Medicine believe that the United States should be setting the example in disaster preparedness and make disaster medicine every medical student and physician’s secondary specialty. To handle the lapses in the American medical system’s response system, the IOM Committee recommended that all institutions responsible for the training, continuing education, and credentialing and certification of professionals involved in emergency care incorporate disaster preparedness training into their curricula and competency criteria. When one takes into account how interconnected our world has become and the many dangers that confront us, it is crucial that those in the medical profession receive more training and support in order to manage those dangers effectively. Americans

will always turn to physicians in times of crisis. By making disaster preparedness a vital part of medical education, future physicians will be able to handle the next major emergency from a position of strength. This will have huge payoffs in terms of lives saved, chaos avoided, and a sense that those upon whom the pubic relies are able to perform their duties in a manner that instills trust and a sense of security. Heidi Cordi, MD, MS, MPH, MS, EMTP, is Associate Medical Director, Emergency Medical Services, The New York Presbyterian Hospital, and Medical Director, Cordi Consultants, Inc. Debra Cascardo, MA, MPA, CFP, Principal of the Cascardo Consulting Group, is a management practice consultant and business advisor to healthcare professionals. She is a board member of the American Academy of Disaster Medicine. Potential Financial Conflicts of Interest: By AJCM policy, all authors are required to disclose any and all commercial, financial, and other relationships in any way related to the subject of this article that might create any potential conflict of interest. The author has stated that no such relationships exist. ®

References 1.

Institute of Medicine. Hospital-based Emergency Care: At the Breaking Point. Washington, DC: National Academies Press, 2007.

2.

Opinion 9.067-Physician Obligation in Disaster Preparedness and Response. Chicago: American Medical Association, 2004.

3.

Kaiser HE, Barnett DJ, Hsu EB, et al. Perspectives of future physicians on disaster medicine and public health preparedness: challenges of building a capable and sustainable auxiliary medical workforce. Disaster Medicine and Public Health Preparedness. 2009;3:210-216.

4.

Chen FM, Hickner J, Fink KS, Galliher JM, Burstin H. On the front lines: family physicians’ preparedness for bioterrorism. J Fam Pract. 2002;51:745-50.

5.

Spranger CB, Villegas D, Kazda MJ, et al. Assessment of physician preparedness and response capacity to bioterrorism or other public health emergency event in a major metropolitan area. Disaster Management and Response. 2007;5:82-6.

6.

Institute of Medicine. Hospital-based Emergency Care: At the Breaking Point. Washington, DC: National Academies Press, 2007.

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Epidemics After Natural Disasters David M. Lemonick, MD, FAAEP, FACEP

Based on a presentation at the 2011 AAPS Annual Scientific Meeting, Tysons Corner, VA, June 21-22

Abstract Epidemics of infectious disease are rare following natural disasters, especially in developed countries. Observations from previous natural disasters suggest that skin, diarrheal, and respiratory infections are the most common infectious diseases in survivors. The etiologies of disease outbreaks are usually predictable, reflecting infectious diseases endemic in the affected area before the disaster. Injury and soft tissue infections are expected during the first few days after a disaster. In contrast, airborne, water-borne, and food-borne diseases are anticipated for up to one month after a disaster. A feared consequence of natural disasters is the potential exposure to dead bodies, both human and animal. No evidence exists that exposure to bodies after a disaster leads to infectious disease epidemics. To be discussed are specific epidemics that have followed earthquakes, floods, tornadoes, tsunamis, volcanic eruptions, landslides, and drought. Preventative public health and safety measures aimed at attenuation of such epidemics will be reviewed.

Introduction A disaster has been defined as “a result of a vast ecological breakdown in the relation between humans and their environment, a serious or sudden event on such a scale that the stricken community needs extraordinary efforts to cope with it, often with outside help or international aid.”1­­­ Such disasters may be natural disasters, transportation disasters, the result of terrorism or technological events, and pandemics. This article will focus on epidemics following natural disasters. Such disasters include earthquakes, floods, tornadoes, tsunamis, volcanic eruptions, landslides, and drought.

Much misunderstanding surrounds the potential for communicable diseases after disasters, with a widely held belief that epidemics are inevitable. This is partially due to an overestimation of the capacity for disease spread from dead bodies.2 In fact, the primary driver of disease spread after natural disasters is population displacement and crowding and its interplay with endemic disease and with a breakdown in infrastructure. If a disease is not endemic to a disaster area and is not introduced after a disaster, then it won’t cause an epidemic after the event.2 Factors contributing to disaster severity include human vulnerability due to poverty and social inequality, environmental degradation, and rapid population growth, especially among the poor. Natural disasters have killed millions of people over the last twenty years, impacting the lives of at least one billion more people, and resulting in enormous economic damages.3 In the decade 1994-2004, there were approximately one million thunderstorms, 100,000 floods, tens of thousands of landslides, earthquakes, wildfires and tornadoes, and several thousand hurricanes, tropical cyclones, tsunamis, and volcanoes.3 Table 1 shows the relative risk of communicable diseases following specific disasters. Because developing countries may lack resources, infrastructure, and disaster-preparedness systems, they may be disproportionately affected by natural disasters.4 Phases of natural disasters include an impact, post-impact, and recovery.5 The impact phase occurs from 0-4 days, during which extrication of victims and treatment of immediate soft tissue infections takes place. Hypothermia, heat, illness, and dehydration are characteristic of this phase. In the post- impact


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phase, which takes place from four days to four weeks post-disaster, airborne, foodborne, waterborne, and vector diseases are seen. Examples of diseases in this phase are cholera, bacterial dysentery, cryptosporidiosis, rotavirus, norovirus, salmonella, typhoid and paratyphoid, giardiasis, hepatitis A and E, and leptospirosis. Communicable respiratory infections in post-disaster settings  include viral (e.g., influenza, RSV, adenoviruses), bacterial (e.g., Strep  pneumoniae, pertussis, tuberculosis, Legionella, Mycoplasma  pneumoniae), and diseases transmitted via the respiratory route (e.g., measles, varicella, nisseria meningitides). Tetanus is also seen in this phase. Table 1: Risk of communicable diseases after disasters, by mode of transmission1 Disaster Type Volcano

Person-toperson* Medium

Waterborne# Medium

Foodborne+ Medium

Earthquake

Medium

Medium

Medium

Hurricane

Medium

High

Medium

Tornado

Low

Low

Low

Heat wave

Low

Low

Low

Cold wave

Low

Low

Low

Flood

Medium

High

Medium

Famine

High

High

Medium

Air pollution

Low

Low

Low

Industrial accident

Low

Low

Low

Fire

Low

Low

Low

Radiation

Low

Low

Low

Civil war/ refugees

High

High

High

*Shigellosis, streptococcal skin infections, scabies, infectious hepatitis, pertussis, measles, diphtheria, other respiratory infections, giardiasis, HIV/AIDS, other sexually-transmitted diseases, meningococcal disease, plague. #Typhoid and paratyphoid fevers, cholera, leptospirosis, infectious hepatitis, shigellosis, campylobacter, salmonella, E. coli, cryptosporidiosis. + Typhoid and paratyphoid fevers, cholera, infectious hepatitis, shigellosis, campylobacter, salmonella, E. coli, amebiasis, giardiasis, cryptosporidium.

The recovery phase begins after four weeks, and diseases with long incubation periods, vectorborne, and chronic diseases manifest in this phase. Examples of organisms with long incubation periods are leishmaniasis and leptospirosis. Vectorborne illnesses include malaria, western/Saint Louis encephalitis, dengue, yellow fever, and West Nile virus. Chronic diseases seen in the recovery phase after hurricane Katrina, for example, included cardiac disease, hypertension, diabetes, and asthma. Special needs for shelters, wheelchairs, oxygen, large cots for the obese, glucometers, access to dialysis, and lacking prescription medications were also seen.5 Wound infections among survivors of the 2004 tsunami in Southeast Asia were polymicrobial, with over 600 organisms ultimately identified. Most prominent among these were Aeromonas species, E.coli, Klebsiella pneumonia, and Pseu-

domonas aeruginosa. Some of these organisms were resistant to all licensed antibiotics.6 Among hurricane evacuees from the New Orleans area, a cluster of infections with methicillin-resistant Staphylococcus aureus (MRSA) was reported in approximately 30 pediatric patients at one evacuee facility in Dallas, Texas.7 Additionally, 24 cases of hurricane-associated Vibrio vulnificus and V. parahaemolyticus wound infections were reported, with six deaths.8 Among the factors that contribute to disease transmission after disasters are environmental considerations, endemic organisms, population characteristics and crowding, the pre-event structure and type of public health systems and facilities and levels of immunization, and the magnitude of the disaster itself.9 Environmental considerations include climate, with cold conditions favoring airborne pathogens and warm conditions favoring waterborne pathogens. In temperate climates, the winter is associated with influenza, while summer is a time for enterovirus infections. Similarly, rainfall during El Nino contributes to malaria, while drought leads to malnutrition-related disease. Geography may play a role in epidemics by isolating victims from needed resources. Organisms endemic to a region will be present after the disaster, while those that are not endemic before the event are unlikely to be present afterwards. On the other hand, as was demonstrated with the appearance of Vibrio infections after hurricane Katrina, the lack of reports of an organism prior to a disaster does not guarantee that the organism is not endemic.8 This phenomenon was also demonstrated by the appearance of enterotoxicogenic Shigella dysenteria type 1, Neisseria meningitidis, and hepatitis E, following disasters in Africa.9 As happened in Haiti with cholera, introduction of non-endemic organisms is possible when relief workers carry it to a disaster area. In fact, cholera has emerged as a serious disease in Latin America only in recent years.2 Examples of endemic disease outbreaks to a region will be present after the disaster, including a nine-fold increase in coccidiomycosis (Valley fever) from January- March 1994 after the Northridge, California, earthquake and the giardiasis outbreak in 1980 after the eruption of Mount St. Helens, Montana.9 Population characteristics include the density and age of victims and the preponderance of chronic diseases. Displaced populations may be crowded in refugee camps. Disease incidence is usually increased in the elderly and in the very young. Baseline immunity to specific diseases is another critical feature of populations. Floods in Nepal in 1973 and in Sudan in 1988 displaced hundreds of thousands of victims. Similarly, the eruption of Mount Pinatubo in the Philippines in 1991 and hurricane Katrina resulted in mass displacement and temporary crowded shelter conditions for victims. Refugees living in crowded, temporary settings, of whom there may currently be over 50 million worldwide, are subject to explosive outbreaks of communicable disease of low endemicity, such as malaria, schistosomiasis, and leishmaniasis. Most recently reported, the human immunodeficiency virus has affected almost 10% of refugee Sudanese men since their forced migration to Ethiopia.10

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Table 2: Waterborne, Vectorborne, and Direct Contact Diseases26

Waterborne Diseases: Summary Disease

Incubation Period

Clinical Features

Diagnosis

Treatment

Cholera

profuse watery diarrhea, vomiting

2 hrs - 5 days

direct microscopic observation of V. cholerae in stool

rehydration therapy; antimicrobials

Leptospirosis

sudden onset fever, headache, chills, vomiting, severe myalgia

2 - 28 days

leptospira- specific IgM serological assay

penicillin, amoxi, doxyxycline, erythromycin, cephalosporins

Hepatitis

jaundice, abdominal pain, nausea, diarrhea, fever, fatigue and loss of appetite

15 - 50 days

serological assay detecting anti- HAV of anti-HEV IgM antibodies

supportive care; hospitalize/ barrier nursing for severe cases; monitoring of pregnant women

Bacillary dysentery

malaise, fever, vomiting, blood and mucous in stool

12 - 96 hrs

suspect if bloody diarrhea, confirm by isolation of organism

nalidixic acid, ampicillin; hospitalize seriously ill or malnourished; rehydration

Typhoid fever

sustained fever, headache, constipation

3 - 14 days

culture from blood, bone marrow, bowel fluids; rapid antibody tests

ampicillin, trimethoprimsulfamethoxazole, ciprofloxacin

Vectorborne Diseases: Summary Malaria

fever, chills, sweats, head and body aches, nausea and vomiting

7 - 30 days

parasites on blood smear observed using a microscope; rapid diagnostic assays if available

chloroquine, sulfadoxinepyrimethamine

Dengue

sudden onset severe flu- like illness, high fever, severe headache, pain behind the eyes, and rash

4 - 7 days

Serum antibody testing with ELISA or rapid dot-blot technique

intensive supportive therapy

Japanese encephalitis

quick onset, headache, high fever, neck stiffness, stupor, disorientation, tremors

5 - 15 days

serological assay for JE virus IgM specific antibodies in CSF or blood (acute phase)

intensive supportive therapy

Yellow fever

fever, backache, headache, nausea, vomiting; toxic phasejaundice, abdominal pain, kidney failure

3 - 6 days

serological assay for yellow fever virus antibodies

intensive supportive therapy

Pneumonia

cough, difficulty breathing, fast breathing, chest indrawing

1 - 3 days

Clinical presentation; culture respiratory secretions

co-trimoxazole, chloramphenicol, ampicillin,

Measles

rash, high fever, cough, runny nose, red and watery eyes; serious postmeasles complications (510% of cases) - diarrhea, pneumonia, croup

10 - 12 days

generally made by clinical observation

supportive care; nutrition/ hydration; vitamin A; control fever; antibiotics in complicated cases

Bacterial meningitis

Sudden onset fever, rash, neck stiffness; altered consciousness; bulging fontanelle in <1 yrs of age

5 - 15 days

Examination of CSF – elevated WCC, protein; gram negative diplococci

Penicillin, ampicillin, chloramphenicol, ceftriaxone, cefotaxime, co-trimoxazole; diazepam (seizures)

Tetanus

difficulty swallowing, lockjaw, muscle rigidity, spasms

3 - 21 days

entirely clinical

immune globulin

Direct Contact Diseases: Summary


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Malnutrition, diabetes, and heart disease among victims also make them more vulnerable to infections. Another important population characteristic includes level of education, with less educated people tending to be less responsive to disaster teams. Religious beliefs may thwart public health efforts as was seen in the polio epidemic in Nigeria in 2004. The underlying health education and hygiene of the public and the types of trauma present (e.g., penetrating, blunt, burns) are also important population characteristics. Critical pre-disaster variables include sanitation, primary health care and nutrition, medical infrastructure, equipment and medications, disaster preparedness, disease surveillance, and roads and transportation. The spread of microorganisms during a natural disaster is facilitated by disruption of public water and sewage systems, crowded living conditions, air borne transmission, lack of immunization, and injury-related infection due to exposure to debris. The type of disaster can determine the variety of trauma and other post-disaster noninfectious illnesses. Earthquake, hurricane, and tsunami can lead to crush injury and other penetrating injuries. Tsunami and floods lead to near-drowning and electrocution. Floods cause about 50% of all deaths from natural disasters in the United States.9 The majority of these are due to vehicle-related drowning during flash floods. Flooding also leads to carbon monoxide exposure and death. According to the World Health Organization (WHO), the most common causes of death in a disaster are diarrhea, acute respiratory infections, measles, malaria, and malnutrition.11

Diseases Associated with Natural Disasters Diseases associated with natural disasters can be divided generally into those associated with overcrowding, waterborne diseases, vectorborne diseases, and other diseases (Table 2). Crowding after disasters has contributed to epidemics of acute respiratory illness and pneumonia, measles, and meningitis. Evacuation to camps following natural disasters is prone to lead to infectious diseases. Camps combine high population density and poor sanitation, synergistic preconditions for fecal-oral and airborne droplet transmission of disease.12 These illnesses are spread person-to-person by airborne droplet transmission. A measles outbreak followed the eruption of Mount Pinatubo, Philippines, in 1991. Most of the more than 100,000 displaced persons were members of the Aeta tribe that lived on the slopes of the volcano. More than 18,000 cases of measles were reported within two months of the eruption, with a 25% mortality rate. Since that time, fewer cases of measles have followed natural disasters, as immunization has been more widespread. Acute respiratory infections (ARI) are a significant contributor to death and disability after disasters, and children less than five

are affected disproportionately.4 Respiratory pathogens in postdisaster settings include viral (influenza, RSV, adenoviruses), bacterial (Strep  pneumoniae, pertussis, tuberculosis, Legionella, Mycoplasma pneumoniae), and diseases transmitted via the respiratory route (measles, varicella, nisseria meningitides). Among reported illnesses after Hurricane Katrina, the proportion of ARI was 12% four days after the levee overflowed and 20% during the next four weeks.9 Exposure to open-flame cooking, malnutrition, and lack of access to health care and antibiotics contribute to morbidity and mortality from ARI. ARI was responsible for most of the deaths among survivors of the tsunami in Aceh in 2004.11 The incidence of ARI quadrupled in Nicaragua in the month following Hurricane Mitch in 1998.13 Aspiration pneumonia is seen after flooding and tsunamis and is due to inhalation of soil-contaminated salt water. “Tsunami Lung” is a syndrome of cavitary lung disease and brain abscess seen among Southeast Asia tsunami survivors. It is initiated by the aspiration of soil, sand, and other particulate matter as a consequence of near-drowning. The syndrome is a polymicrobial pneumonia process that occurs up to six weeks later. Identified pathogens include water-borne organisms Aeromonas, Pseudomonas, Streptococcal species, Nocardia, Pseudallescheria boydi, and Burkholderia pseudomallei.9,14 Flooding constitutes approximately 40% of natural disasters, and it promotes both waterborne and vectorborne diseases.11 Upper respiratory infections and pneumonias were reported among multiple victims of hurricane Katrina, including a case of pertussis in a two-month-old infant who was rescued from a rooftop in New Orleans and evacuated to Tennessee. Appropriate antimicrobial prophylaxis was provided, and no additional cases were reported.7,15 Waterborne diseases include diarrheal pathogens, hepatitis, and leptospirosis. Several pathogens have been associated with diarrhea after disasters. Vibro cholerae and enterotoxigenic Escherichia coli have been isolated after flooding in West Africa. Diarrheal diseases have followed hurricanes and flooding in Bangladesh, Sudan, and Nepal and are the most lethal public health threat to refugees overall.2 Over 70% of deaths among Kurdish refugees in 1991 were due to diarrheal disease. The cholera epidemic that followed the 2010 Haiti earthquake sickened more than 170,000 people and killed more than 3,600.14 The US Centers for Disease Control and Prevention (CDC) confirmed that the form of cholera detected in Haiti is one that is typically found in South Asia and Africa.15 The Haitian outbreak originated from contaminated water near a facility that housed Nepalese troops, who are thought to have introduced the strain to an immunologically naïve local population. From Haiti, several new cases were identified in previously unaffected regions. The Dominican Republic detected its first case of cholera in a migrant worker who had returned home from Haiti after the outbreak there. Additional cases of cholera have since been

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reported in Bolivia, Brazil, Chile, Colombia, Nicaragua, Panama, Peru, and Venezuela. Subsequently, confirmed imported cases have been reported in Florida. The CDC has reported 13 suspected imported cases, with five confirmed as of December 2010. Researchers estimate that an additional 200,000 cases of cholera could arise in the Caribbean within the next 18 months.15 Paratyphoid fever, caused by E Salmonella enterica serotype Paratyphi A, resulted in diarrhea outbreaks in Indonesia in 1992–1993. Cryptosporidium parvum-related diarrhea followed flooding in Indonesia in 2001–2003.16 An outbreak of diarrheal diseases after flooding in Bangladesh in 2004 involved more than 17,000 cases of V.Cholerae and E.Coli infections.16 All survivors of the December 2004 tsunami in Aceh province in 2004 were forced to drink from unprotected wells, and 85% of these residents who were studied reported diarrhea.11 The risk of diarrheal disease outbreaks following natural disaster is higher in developing countries than in industrialized countries. The association of communicable diseases with malnutrition is well known. In many of these malnourished victims, diseases such as measles, malaria, ARI, and diarrheal diseases are the most common causes of death. After Hurricanes Allison and Katrina, initial reports were that Escherichia coli counts were 100 times higher than those normally found in river runoff. Among the 24,000 Katrina evacuees who were housed in the Reliant Park building in the Houston Astrodome complex,  18% developed acute gastroenteritis from September 2–12, 2005. Approximately 25% of adult and 40% of pediatric medical visits during this time were due to GI illness. Secondary spread to shelter and medical staff also occurred. While 50% of specimens were positive for norovirus, no other pathogen was identified.9,17 Clusters of diarrheal disease were reported among persons in evacuation centers in Louisiana, Mississippi, Tennessee, and Texas. In Louisiana, approximately 20 clusters of diarrheal illness in evacuation centers were reported to and investigated by the CDC. In Memphis, gastrointestinal illness was the most common acute disease complaint among evacuees. Approximately 1,000 cases of diarrhea and vomiting were reported among evacuees in Mississippi and Texas. Norovirus was detected in stool specimens from patients in Texas. Nontyphoidal Salmonella, nontoxigenic V. cholerae O1, and other infections were also identified. No confirmed cases of Shigella dysentery or typhoid fever were reported in evacuees, and by three weeks after the initial relocations following Katrina few additional cases of diarrheal disease were being reported.7,8 Following the 1976 Friuli, Italy, earthquake, there was a five- to sixfold increase in Salmonella secondary to food contamination, poor hygiene, and overcrowding.9 Following  Hurricane Katrina, an increase in mortality was reported by CDC from Vibrio (Vibrio vulnificus and parahaemolyticus) soft tissue infections. Sixty percent of cases were wound infections and 40% resulted  from eating raw shellfish. Necrotizing complicated some cases, and overall Vibrio

mortality was 40%, and it was 20% in the subset with Vibrio from wounds. Vibrio parahemolyticus cases after Katrina were mostly diarrhea, while V. vulnificus cases were mostly septicemia and wound infection, and very few were diarrhea. For those two species, secondary transmission is not seen. During the flooding following Katrina, Vibrio cases were also reported in Arkansas, Texas, and Louisiana. These were mostly in immuno-compromised, chronically ill people who were exposed seawater. Once contact with brackish seawater ceased, case reports ended and so did any apparent epidemic potential.8,16,17 In most refugee settings, the case fatality rates (CFR) for cholera are between 2-5%. In the 1994 Rwandan refugees in the Zairian town of Goma (now Republic of the Congo), the rate rose to almost 25%, with almost 90% of adult deaths due to diarrheal illness. This outbreak, which has come to be known as “The Great Lakes Disaster,” caused at least 48,000 cases and 23,000 deaths within one month in the refugee camps in Goma, Zaire. Shigella also erupted. Shigella dysenteria type 1, seen in displaced African populations, has a CFR of 10% in young children and in the elderly. Following Hurricane Mitch in 1998, cholera outbreaks occurred in Guatemala, Nicaragua, and Belize.4,5,6 The fecal-oral route (Tables 2 and 3) spreads Hepatitis A, B, and E. Usually infection results from drinking contaminated water, and there is current debate about the role of person-toperson spread. Hepatitis A and B are endemic in most developing countries, so children in these areas develop immunity to it early in life. In hepatitis E-endemic areas, generally mild disease outbreaks have followed flooding. Hepatitis E has only recently been introduced in most parts of Africa, so adults are unlikely to have immunity to it. Thus, any hepatitis-like illness in this region is assumed to be hepatitis E. Pregnant women are especially vulnerable, however, with mortality as high as 25%. Both hepatitis A and hepatitis E were noted in Aceh after the December 2004 tsunami and after the Pakistan earthquake in 2005. An increase in hepatitis A followed the 1983 Popaya, Columbia earthquake.9 Leptospirosis is a bacterial disease that is spread by contact with contaminated water. Rodents shed the organisms in their urine, and contact of the skin and mucous membranes with contaminated water, soil, or vegetation. Several floods in the last decade were followed by leptospirosis outbreaks, notably in Taiwan after Typhoon Nali in 2001, in Mumbai after flooding in 2000, in Portugal in 1967, and Brazil in 1975.4 Measles incidence and spread transmission after a disaster depends upon the baseline immunization rate of the affected population, especially those under15 years of age. More than 18,000 measles cases occurred after the eruption of Mount Pinatubo in the Philippines in 1991.18 Increased death rates from measles were reported in camps in Bangladesh (1978), Somalia (1980), Sudan (1985), Ethiopia (1987), Malawi (1988–1990), Mozambique (1988–89, 1991), Philippines (1991), Darfur, Somalia (1994), Haripur, Afghanistan, and Kakuma refugee


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camps, Kenya (2005). CFR of 2.3% up to 32% were reported.9 Crowded living conditions, as is common among people displaced by natural disasters, contributes to rapid transmission of the organism.12 Also contributing to measles outbreaks is a low baseline vaccination coverage rate among the affected population and, in particular, among children aged <15 years. These conditions that facilitate transmission are also ones that necessitate higher immunization coverage levels to prevent outbreaks. Neisseria meningitidis outbreaks have followed flooding and displacement in Pakistan and Aceh. Meningococcal meningitis outbreaks occurred also in refugees in Thailand in 1979, and among displaced Sudanese in1988, in Khartoum.9,16 Rapid response with antimicrobial prophylaxis interrupts transmission in disaster-affected populations. Important vectorborne diseases following disasters include malaria, dengue, Japanese encephalitis, and yellow fever, all of which are transmitted by mosquitoes. Disruption of water supplies promoting standing water, especially when associated with large numbers of displaced people sleeping outside, contributes to outbreaks. Months of severe flooding in Bolivia in 2007 triggered a dengue outbreak that killed 35 people. A dramatic rise in malaria cases followed the 1991 earthquake in Costa Rica, associated with changes in habitat that promoted mosquito breeding. Over 75,000 cases of Plasmodium falciparum malaria were associated with the 1966 Haitian hurricane Flora.17 Malaria-specific mortality is especially severe in situations in which refugees fleeing an area of low endemicity travel through or migrate to an area of high endemicity.2 Outbreaks of louse-borne relapsing fever were seen after refugee concentration in Somalia and Ethiopia. Other diseases that are seen after disasters are tetanus and coccidiomycosis. Spores of C. tetani reside in soil, entering the tissue in contaminated wounds, especially in populations where vaccination levels are low. Once in the wounds, the spores produce a metalloprotease, tetanospasmin, which travels by retrograde movement into the central nervous system. There, the toxin blocks neurotransmission and disinhibits the motor cortex, leading to extensive spasm. Contributing to the occurrence of tetanus after disasters are penetrating injury with spore delivery, co-infection with other bacteria, localized tissue ischemia, and devitalized tissue. An outbreak of tetanus peaked two and one-half weeks after the tsunami in Aceh. The 106 cases that were reported from December 30 – January 26, 2004, occurred in Banda Aceh 4–30 days post-tsunami. CFR for this outbreak was 18.9%.9 The infection is not transmitted person to person. Coccidioides immitis is a fungus that is found in soil in certain semiarid areas. Coccidiomycosis (valley fever) can be associated with exposure to increased levels of airborne dust after landslides and earthquakes. An outbreak occurred after the 1994 earthquake in Southern California. Large dust clouds generated by the earthquake dispersed the spores of Coccidioides. The disease incidence peaked two weeks after the earthquake, and there was a ninefold increase in coccidiodomycosis from January–March 1994. Two hundred and three cases were

reported in Ventura County, California, including three deaths. There were 30 cases per 100,000 population. Fifty-six percent of the cases and the highest attack rate (114 / 100,000) was in the town of Simi Valley, at the base of a mountain range that had numerous landslides associated with the earthquake. Risk was associated with being within, and amount of time spent in, the dust cloud. While tuberculosis (TB) is not a disease that is associated with natural disasters, it has emerged as a disease among displaced populations. Inadequate access to healthcare among refugees has resulted in an increased spread of TB among them.19 During the war in Bosnia and Herzegovina in 1991 and during the civil war and famine in Somalia in 1991-92, the incidence of TB increased four-fold.2 In 1985, 26% of deaths among refugees in Somalia were attributable to TB. Co-infection with HIV and malnutrition also contribute to the transmission, morbidity, and mortality of TB in displaced peoples. Control of TB among evacuees has consisted of both detecting new cases and providing treatment continuity for previously known cases. Immediately after hurricane Katrina, TB program staff sought out known TB patients to check their status and assure that therapy continued. As of September 23, 2004, all 27 currently known TB patients who resided in Alabama, all 21 in Mississippi, and 105 (71%) of 147 in Louisiana had been located. Of the 42 TB patients from Louisiana not yet located, 41 were considered noncontagious at the time the hurricane made landfall.19 A homeless person without a previous diagnosis of TB who was evacuated from New Orleans to Philadelphia was identified with symptoms consistent with pulmonary TB. The patient was isolated and begun on treatment for TB disease; a subsequent culture confirmed TB. At least eight other evacuees initially identified as potentially having TB were subsequently determined to have other conditions (e.g., lung cancer and infection with nontuberculous mycobacteria).7,17,19

Diagnosis of Communicable Diseases The diagnosis of waterborne, vectorborne, and direct contact diseases is summarized in Table 2. Diagnosis of cholera is made by the direct microscopic observation of the V. cholerae organisms in the stool of victims. Leptospira and hepatitis are detected by specific IgM serologic assays and by detecting anti-HAV or anti-HEV IgM antibodies, respectively. Typhoid is identified by culturing Salmonella typhi from blood, bone marrow, and bowel fluids, and by rapid antibody tests. The etiology of ARI is often suggested by the clinical presentation, and culture of respiratory secretions may identify a specific pathogen, such as Streptococcus pneumoniae or Haemophilus influenzae. Measles is generally diagnosed by its clinical features, while the etiology of meningitis is made by examination of the cerebrospinal fluid. In the case of vectorborne diseases, parasites are identified on blood smear and serum antibody testing with

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Table 3: Hepatitis A and E17

Features

Duration/Symptoms

Diagnosis/Treatment

Hepatitis A

Virus

Most reported vaccine-preventable disease. 33K acute cases. 61K new infections.70% children < 6yrs area symptomatic. Fecal-oral transmission via contaminated food, water,shellfish.

Incubation 28 days average, (range 15-50 days).Viral shedding 2 weeks prior to onset jaundice. Jaundice in 70% of patients, abdominal pain, fatigue, loss of appetite, nausea, diarrhea, fever.15% with relapsing symptoms 6-9 months.

Serology positive for IgM antibody (antiIgM HAV) 5-10 days after onset jaundice up to 6 months. IgG antibody (anti-IgG HAV) positive early in course, confers lifetime immunity.Treatment supportive. Vaccine available for prevention.

Hepatitis E

Most common cause of non-A, non-B hepatitis worldwide. 2004 outbreak in Darfur, Sudan: 7791 cases and 99 deaths. Most common in young to middle-aged adults. Fecal-oral transmission via contaminated food, water,shellfish. Increased risk with flooding.

Incubation 40 days average, (range 15-60 days). Jaundice, abdominal pain, fatigue, dark urine, loss of appetite, nausea, vomiting. Secondary symptoms: arthralgias, diarrhea, pruritus, urticaria. Viral shedding for 2 weeks after infection.

Serology positive for IgM antibody (antiIgM HEV) 5-10 days after onset jaundice up to 6 months. However, not commercially available in US; research lab only. Also PCR, IFA research lab only. IgG treatment supportive. No vaccine available for prevention.

ELISA. A rapid dot-blot technique may be used in suspected dengue. Serologic assays are available for detecting IgM specific antibodies in Japanese encephalitis in CSF or blood. Similarly, serological assay is used for detection of yellow fever virus antibodies.

The Significance of Dead Bodies There is a widely held fear that the presence of dead bodies after a disaster contributes to disease transmission. This potential is vastly overstated.4 In reality, when death is directly due to the natural disaster, human remains pose no risk for outbreaks. There are a few specific circumstances in which dead bodies pose any risks, such as deaths from cholera21-24 or hemorrhagic fevers.22 It is recommended that workers who handle bodies employ universal precautions for blood and body fluids and that they use and correctly dispose of gloves. Hand washing with soap after handling bodies and before eating and use of body bags are also important. Except in cases of cholera, shigellosis, or hemorrhagic fever, bodies do not need disinfection before disposal, but disinfection of vehicles and equipment is suggested. In addition, burial, rather than cremation, is recommended, with the bottom of graves above the water table (Table 3).4,20-23

Disease Control after Disasters An accurate risk assessment for communicable diseases after a disaster is required in order to identify existing epidemic and endemic diseases that are common in the affected area. Similarly, the living conditions of the affected population are evaluated, with special attention to the availability of safe water and adequate sanitation facilities. Also assessed are the age distribution, nutritional status, and immunization coverage of those affected and their degree of access to healthcare. Prevention and control of disease begins with hand washing, with proper handling of water and food, and with sewage disposal. Oral rehydration therapy (ORT) is initiated for diarrheal illness. Where possible, victims and aid workers must avoid entering contaminated water. Preventive Health Measures against

the transmission of infectious agents related to natural disasters have been addressed by the WHO.11 WHO recommends: keep hands and vessels clean, avoid preparing food directly in areas surrounded by flood water, separate raw and cooked food, cook food thoroughly, keep food at safe temperatures, use safe water, wear appropriate protective clothing during rescue and cleanup operations, and immunization. Hepatitis and polyvalent Strep pneumonia vaccination may be appropriate. In the event of measles, rapid mass vaccination should be instituted within 72 hours of an initial case report, and vitamin A is administered in children six months to five years of age to prevent complications and to reduce mortality. Rapid mass vaccination is also instituted for meningitis. Malaria response includes mosquito control, provision of insecticide-treated nets, bedding, and clothing, and the emptying of standing water containers. In the case of dengue, Japanese encephalitis, and yellow fever, mosquito control, isolation of cases, and mass vaccination are implemented. Table 4: Recommended Handling of Dead Bodies11

Suggested Measures for Handling Dead Bodies Universal precautions for blood and body fluids. Disposal or disinfection of used gloves. Avoiding cross-contamination of personal items. Washing hands after handling bodies and before eating. Disinfection of vehicles and equipment. Use of body bags, especially for badly damaged bodies. Hepatitis B vaccination. No special arrangements, such as disinfection, with disposal of bodies. New burial areas sited at least 250 meters away from drinking water sources,and with at least 0.7 meters of distance above the saturated zone.


American Journal of Clinical Medicine® • Fall 2011 • Volume Eight, Number Three

Table 5: Disaster Myths and Realities13

MYTH

REALITY

Foreign medical volunteers with any kind of medical background are needed.

1. The local population almost always covers immediate lifesaving needs. 2. Only skills that are not available in the affected country may be needed. 3. Few survivors owe their lives to outside teams.

Any kind of assistance is needed, and it’s needed now!

1. A hasty response not based on impartial evaluation only contributes to chaos. 2. Unrequested goods are inappropriate, burdensome, divert scarce resources, and more often burned than separated and inventoried. 3. Not wanted, seldom needed – used clothing, OTC, prescription drugs, or blood products; medical teams or field hospitals.

Epidemics and plagues are inevitable after every disaster.

1. Epidemics rarely ever occur after a disaster. 2. Dead bodies will not lead to catastrophic outbreaks of exotic diseases. 3. Proper resumption of public health services will ensure the public’s safety (e.g., immunizations, sanitation, waste disposal, water quality, and food safety). Caveat: Criminal or terror-intent disasters require special considerations.

Disasters bring out the worst in human behavior.

1. While isolated cases of antisocial behavior exist, the majority of people respond spontaneously and generously.

The community is too shocked and helpless to respond.

1. Many find new strengths. 2. Cross-cultural dedication to common good is most common response to natural disasters. 3. Thousands volunteer to rescue strangers and sift through rubble after earthquakes from Mexico City, California, and Turkey. 4. Most rescue, first aid, and transport are from other casualties and bystanders.

Source: Noji E. Cutler lecture reference.

Conclusions Natural disasters have killed millions of people during the past two decades and have adversely affected the lives of over one billion others. These events include earthquakes, volcanic eruptions, landslides, tsunamis, floods, and drought. Because of their lack of resources, infrastructure, and emergency medical and disaster systems, developing countries are disproportionately affected by natural disasters. The potential for such disasters to be followed by epidemics of communicable diseases is often presumed to be very high, but this has been overstated (Table 5). In particular, the contribution of dead bodies in epidemic spread after disasters has been vastly exaggerated. In fact, dead bodies are not a significant contributor to disease. Rather, increases in the risk of communicable disease transmission has been demonstrated to be dependent upon: 1) the size, health status, and living conditions of the population displaced by the disaster; 2) crowding; 3) inadequate water and sanitation; and 4) poor access to health services. These factors are also characteristic of sudden population displacement in general.2

An understanding of epidemics after natural disasters has led to improved detection of, and response to, communicable diseases in these settings. By monitoring the incidence of such diseases and by documenting their impact, it is possible to better quantify the risk of outbreaks following natural disasters. Thus, by preparation for the inevitable, medical, epidemiological, and disaster response personnel will be more able to ameliorate the suffering that will occur after future natural disasters. David Lemonick, MD, is Attending Emergency Physician, Armstrong County Medical Center, Kittanning, PA, and PresidentElect of the American Academy of Emergency Physicians. Potential Financial Conflicts of Interest: By AJCM policy, all authors are required to disclose any and all commercial, financial, and other relationships in any way related to the subject of this article that might create any potential conflict of interest. The author has stated that no such relationships exist. ®

References 1.

Noji EK. The Nature of Disasters. In: Noji EK (ed.) The Public Health Consequences of Disaster. New York: Oxford University Press; 1997.

2.

Toole MJ. Communicable diseases and disease control. In: Noji EK,

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(ed.) The Public Health Consequences of Disaster. New York; Oxford University Press, 1997.

Medical News. Journal online. Available at: http://www.medscape.com/ viewcollection/31896. Accessed Feb. 12, 2011.

3.

Noji EK. Public Health Disaster Consequences of Disasters. Second Annual John C. Cutler Global Health Lecture and Award University of Pittsburgh; September 29, 2005.

15. CDC. Outbreak of Cholera - Haiti, 2010. Morbidity and Mortality Weekly Report (MMWR). December 10, 2010:59(48);1586-1590.

4.

Watson JT, Gayer M, Connolly MA. Epidemics after natural disasters. Emerg Infect Dis (serial on the Internet). 2007 Jan. Available from http:// www.cdc.gov/ncidod/EID/13/1/1.htm. Accessed February 3, 2011.

5.

Peters RE. Patterns of Disease after Natural Disasters.. San Diego County Medical Society. Article online. 2010, Nov 5. Available at: http://sdcms. org/article/patterns-disease-after-natural-disasters. Accessed Feb. 15, 2011.

6.

United Nations Cultural Scientific and Cultural Organization (homepage on the internet). Paris. About natural disasters. Available from: http://www. unesco.org/science/disaster/about_disaster.shtml. Accessed February 16, 2011.

7.

CDC. Infectious Disease and Dermatologic Conditions in Evacuees and Rescue Workers After Hurricane Katrina - Multiple States, AugustSeptember, 2005. Morbidity & Mortality Weekly Report. 2005;54(38):961964.

8.

CDC. Vibrio illnesses after Hurricane Katrina - multiple states, AugustSeptember 2005. MMWR. 2005;54(38):928-31.

9.

Sandrock C. Infectious Diseases After Natural Disasters. California Preparedness Education Network. A program of the California Area Health Education Centers. March 7, 2006. Funded by HRSA Grant T01HP01405. PowerPoint presentation online. Available at http://www. idready.org/ webcast/ spr06_cider. Accessed February 16, 2011.

10. Brady W. MPH, CDC, 1992, unpublished data. 11. World Health Organization. Communicable diseases following natural disasters: risk assessment and priority interventions. 2006. Geneva. Available at: Web site: http://www.who.int/diseasecontrol_emergencies/ en/. Accessed February 16, 2011. 12. Bissell RA. Delayed-impact infectious disease after a natural disaster. Journal of Emergency Medicine. (1):1.983:Pages 59-66. 13. Campanella N. Infectious diseases and natural disasters: the effects of Hurricane Mitch over Villanueva municipal area, Nicaragua. Public Health Reviews. 1999:27:311–319. 14. Hitt E. IMED 2011: International Meeting on Emerging Diseases and Surveillance. Vienna, Austria. February 4-7, 2011. Medscape

16. Ahern M, Kovats RS, Wilkinson P, et al. Global health impacts of floods: epidemiologic evidence. Epidemiol. Rev. 2005;27:36-46. 17. Linscott AJ. Natural Disasters- A microbe’s paradise. Clinical Microbiology News Letter. 29(8)April 2007. 18. Barclay L. Epidemiologic Consequences of Hurricane Katrina: A Newsmaker Interview With Raoult Ratard MD, Chief Epidemiologist for the Louisiana Department of Health and Hospitals. Medscape Medical News. Journal Online. Available at: http://www.medscape.com/ viewarticle/513376. Accessed Feb. 12, 2011. 19. Surmieda MR, Lopez JM, Abad-Viola G, Miranda ME, Abellanosa IP, Sadang RA, et al. Surveillance in evacuation camps after the eruption of Mt. Pinatubo, Philippines. MMWR. CDC Surveill Summ. 1992;41:963. 20. CDC. Treatment of tuberculosis: American Thoracic Society, CDC, and Infectious Diseases Society of America. MMWR. 2003;52(No. RR-11). 21. Sack RB, Siddique AK. Corpses and the spread of cholera. Lancet. 1998;352:1570. 22. Boumandouki P, Formenty P, Epelboin A, Campbell P, Atsangandoko C, Allarangar Y, et al. Clinical management of patients and deceased during the Ebola outbreak from October to December 2003 in Republic of Congo (article in French). Bull Soc Pathol Exot. 2005;98:218-23. 23. Morgan O. Infectious disease risks from dead bodies following natural disasters. Rev Panam Salud Publica. 2004;15:307-11. 24. Floret N, Viel JF, Hoen B, Piarroux R. Negligible risk for epidemics after geophysical disasters. Emerg Infect Dis. 2006;12:543-8. 25. UNESCO. About natural disasters. Paris, United Nations Cultural, Scientific and Cultural Organization 2004. Available at: http://www. unesco.org/science/disaster/about_disaster.shtml. Accessed February 18, 2011. 26. Waring S, Zakos-Feliberti A, Wood R, et al. The utility of geographic information systems (GIS) in rapid epidemiological assessments following weather-related disasters: Methodological issues based on the Tropical Storm Allison experience. International Journal of Hygiene and Environmental Health. Volume 208, Issues 1-2, 8 April 2005, pages 109-116.


American Journal of Clinical Medicine® • Fall 2011 • Volume Eight, Number Three

United States Air Force Aeromedical Evacuation – A Critical Disaster Response Resource Bruce R. Guerdan, MD, MPH

Abstract

Definitions

The use of United States Air Force (USAF) aircraft and personnel to move wartime casualties is well established. This asset is also an integral part of the National Disaster Medical System (NDMS). The Aeromedical Evacuation (A/E) system, a part of Air Mobility Command, is a highly disciplined function capable of transporting thousands of civilian casualties at all levels of criticality. At the time of a large local or regional disaster, civilian medical treatment facilities, if still functional, would be overwhelmed. A core function of the NDMS would be the relocation of civilians currently hospitalized or in need of hospitalization to facilities outside the disaster area. This would be primarily accomplished by the USAF A/E system.

The below terms are routinely confused and, therefore, delineated below:

Introduction The United States Air Force (USAF) currently lists six unique core capabilities.1 One of these, Agile Combat Support, includes medical care. The United States Air Force, the United States Army, and the United States Navy provide medical care at all treatment levels. This includes medical evacuation (Medevac) to the initial medical treatment facility. Aeromedical Evacuation (A/E) is a mission solely assigned to the Air Force. In addition to its combat support role, the USAF A/E system is an integral part of the NDMS and is the main point where military and civilian assets interface in the time of regional or national disaster. A core tenet of the NDMS is the ability to move large numbers of casualties to medical facilities outside the affected area. Federal doctrine states that the Department of Defense (DOD) is the single manager for the movement of NDMS in-patients who require in-route care.2

Case-Evac

The evacuation of casualties outside the organized medical transport system.

Medevac Ground or rotary wing evacuation, typically pre-hospital. Medical care at some level is included.

Air-Evac The USAF A/E system of fixed wing aircraft and personnel functioning at a hospital level of medical care.

Aircraft Despite being involved in two separate conflicts thousands of miles from home, the Air Force has no dedicated Aeromedical aircraft.3 When the C-9 Nightingale was retired in 2005, the USAF made a conscious decision to abandon the concept of dedicated medical aircraft. Today, through the concept of dual-use aircraft, wounded are evacuated to a higher level of care on the same airframes that may have just delivered dozens of pallets of supplies or fresh warriors to the fight. Medical personnel convert the aircraft into a hospital-like environment using structural equipment specifically designed to hold litters securely while in flight.3,5,6,10 While a particular mission might be designated as an “aerovac,” the aircraft is not. Indeed, you

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Figure 1: Aircraft for A/E Evacuation

Aircraft

Availability

Range

Litters

Ambulatory

O2

Runway

C-130

Readily

Intra-continental

74

0

PTLOX

Un-improved

C-17

Readily

Inter-continental

36

54

Onboard

Un-improved

KC-135

Readily

Inter-continental

15

8

PTLOX

Improved

767

Requires refit

Inter-continental

87

40

Onboard

Improved

C-141

Retired

Inter-continental

103

14

Onboard

Improved

Notes: 1 - Additional ambulatory patients can be added when less than the maximum litter spaces are used. 2 - CCATT patients may need more space/electricity and decrease the maximum litter spaces available. 3 - C-141 is listed as a historical reference. 4 - The KC-135 and the 767 are unable to load patients from ground level and require additional equipment to complete this task.

will no longer see the red cross on the tail of any USAF aircraft. Essentially, any USAF non-fighter aircraft can be configured to carry patients. Some are much easier to configure as they were initially designed as a dual-use aircraft. Others provide a more inefficient configuration but nevertheless are sometimes the best option. Since the Vietnam War, the C-130 Hercules is the typical intratheater aero-vac airframe. The Hercules can be configured to carry a maximum of 74 litter patients and, due to its availability, would be the likely airframe used initially in a disaster response.5 The C-17 Globemaster is the typical aero-vac airframe for intertheater transportation. It can carry 36 litters and 54 ambulatory patients.6 Both the C-130 and the C-17 are capable of landing on unimproved runways. Typically the Hercules is used in tactical (combat) environments. The now-retired C-141 Starlifter was the workhorse of inter-theater aerovac. This aircraft was used from 1963 until 2006 and could carry 103 litter patients .4 Recently, KC-135 Strato-tankers have been modified to more easily accept A/E patients. Most of the A/E missions from Afghanistan to Germany are on these aircraft. These aircraft have a much longer range, are able to cruise at faster speeds, are more commonly available, and do not impact the highly tasked C-17 schedule. Some of the negatives with this aircraft are the low number of litter patients they can hold,13 the difficulty loading/ unloading litter patients, and an “either too hot or too cold” patient environment. Of these aircraft, only the C-17 has on-board patient oxygen. Portable liquid oxygen (PTLOX) is required on the C-130 and the KC-135. In addition to these military aircraft there is the Civilian Reserve Air Fleet (CRAF). These are commercial airliners which were built specifically as a backup to the USAF fleet. Much of the CRAF are cargo aircraft used to move supplies and equipment. The system also includes an A/E capability. These aircraft are Boeing 767s, which can be converted into Aeromedical airframes. They would be flown by civilian airline pilots and manned with flight attendants who would assist A/E crews. There are currently fifty 767s assigned to the CRAF flying com-

mercially.7,8 The Air Force maintains approximately forty Air Evacuation Shipsets (AESS). These include all the equipment (and an oxygen subsystem) to transform these aircraft into an A/E configuration. When they are configured, they can carry 87 litter patients and up to 40 ambulatory patients. The process takes approximately 24 hours per aircraft.7,8 To date CRAF aircraft have not been used in real world A/E missions.

Aircrew The personnel assigned to a standard aerovac mission are divided into medical and non-medical components. Typically, there are two pilots. There are one or more loadmasters and on some aircraft a flight engineer. These crew members fly the airplane and make all of the decisions related to flight.10 The pilot is in ultimate control. Medical personnel are in control of the care of the patients and make all decisions regarding medical care. The medical crew typically consists of two or more flight nurses as well as three or more aeromedical technicians. Mission requirements may require more nurses and technicians. One of the nurses is designated the Mission Commander. Approximately 90% of the aeromedical personnel in the USAF are assigned to the Air National Guard and the Air Force Reserve.9 School for Flight Nurses (RNs) is 5½ weeks long followed by months of follow-on training before being deemed fully trained. As well, there is constant refresher and upgrade training.10 Aeromedical technicians are certified Emergency Medical Technicians and require ongoing training as well. Many A/E crew have outside civilian occupations both in and out of the medical arena.

Critical Care Air Transport Prior to Desert Storm, aeromedical evacuation (A/E) patients were required to be designated as stable for flight. After Desert Storm there was a significant change in the aeromedical evacuation concept of operations. A/E did not transport critically ill or injured patients.13 On occasion a Medical Attendant, typically a physician non-crewmember, would accompany a


American Journal of Clinical Medicine® • Fall 2011 • Volume Eight, Number Three

unique patient and attend to that patient specifically. Critical care equipment was not specifically designed for flight, and A/E crews were not trained to this level. As well, A/E did not have physicians assigned as aircrew. Critical Care Transport Teams (CCATT) were developed to address this issue. CCAT Teams are composed of a critical care physician, a critical care nurse, and a cardiopulmonary technician (trained in both respiratory therapy and diagnostic cardiology). These teams allowed stabilized but not necessarily stable patients to be moved to a higher level of care. CCATT school is ten days long and is primarily mission-specific versus medically specific. These personnel are considered aircrew and control their patient medically.12 They are under the control of the A/E Medical Crew Director (Flight Nurse) for mission issues. This is despite rank or level of training. A/E doctrine defines stable patients as those that do not require advanced airway/ventilatory support, high flow oxygen, cardiac monitoring, pressors, or other cardiovascular agents, while stabilized patients require one or more of these agents or interventions with concurrent in-flight physician management.

Equipment/Supplies All medical equipment used by A/E must be cleared for flight on a basis of safety as well as efficacy. Much of the equipment is off-the-shelf civilian medical equipment that is specifically tested and approved for flight. Typically, each patient is transported with three days of medications, supplied by the sending facility, as delays and diversions are possible.

Support A/E assets typically have no organic support and require routine support functions such as security, food services, and housing to be provided by the Wing to which they are attached.10

Military Concept of Operations The organization which manages patient movement is the Global Patient Movement Requirements Center (GPMRC) located at Scott Air Force Base in Illinois.3 Theater Patient Movement Requirements Centers (TPMRC) are established in a theater of operations and control patient movement on a regional basis. Patients enter the A/E system when they are entered into the United States Transportation Command (TRANSCOM) Regulating and Command & Control Evacuation System (TRAC2ES).3 This is typically done at the originating medical treatment facility (MTF). Dedicated personnel, an Aeromedical Evacuation Liaison Team (AELT) are sometimes involved. They are cleared for flight by a flight surgeon and are readied for flight at the MTF or transported to a Mobile Aeromedical Staging Facility (MASF) or a Contingency Aeromedical Staging Facility (CASF). These facilities are capable of holding patents for up to seventy-two hours and are located on the flight

line.11 Intra-theater airlift may move a patient to a higher level of care regionally or to a regional base for transfer to Intertheater airlift.

Civilian-Military Interface In an NDMS response, Disaster Medical Assistance Teams (DMAT) would provide deployed acute (non-surgical) capabilities at or near the disaster. Those requiring in-patient care, if not locally available, would become the responsibility of USAF A/E. USAF A/E assets fill a void for which there is no civilian equivalent. A/E would be used to airlift these patients to accepting facilities outside the affected region. The civilian portion of this interface is the Disaster Aeromedical Staging Facility (DASF). This unit has a nearly identical function to the military’s CASF. This interface has been recognized as a potential weak link in the chain of response. Variance in-patient care protocols, use of non-flight approved equipment, lack of flight surgeon clearance for flight, and atypical medical conditions are all issues that could confound the efficiency of a disaster response. The care of the elderly, disabled, and small children are potential problems as A/E personnel are primarily involved in the care of otherwise healthy military members. These issues have been recognized and an emphasis has been placed on increasing the level of coordination for a response. To further integrate their capabilities with the DOD, the Department of Health and Human Services (DHHS), the entity which manages DMATs, has now developed Mobile Acute Care (MAC) Strike Teams. The purpose of the fourteen member MAC Strike Teams is to provide a critical care capability at the DASF. The MAC Strike Teams would provide continuity of care with USAF CCATT personnel. Fifteen MAC Strike Teams began receiving training from the USAF CCATT School beginning in 2010.

Conclusion Although primarily thought of as a wartime asset, the USAF A/E system is an integral part of the military’s Defense Support to Civilian Authorities (DSCA) mission. Disaster response, no matter what the cause, might require a significant volume of patient evacuations. The USAF A/E system is the only entity in the world capable of moving large numbers of complex patients over long distances. The seamless integration of the civilian and military disaster response resources is vital to a successful disaster response. Coordination between DHHS and the USAF is integral to a successful disaster response. Bruce R. Guerdan, MD, MPH, board certified in Emergency Medicine, Disaster Medicine, and Family Medicine, is an Emergency Medicine attending physician at UPMC-Northwest in Seneca, PA, and Lower Keys Medical Center in Key West, FL. He serves as the State Air Surgeon for the Florida Air National Guard and is an experienced Critical Care Air Transport (CCATT) physician.

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Potential Financial Conflicts of Interest: By AJCM policy, all authors are required to disclose any and all commercial, financial, and other relationships in any way related to the subject of this article that might create any potential conflict of interest. The author has stated that no such relationships exist.

6.

Boeing: C-17 Globemaster III-Technical Specifications. www.boeing. com/defense-space/military/c17/c17spec.htm.

7.

Bolkcom C. Civil Reserve Air Fleet (CRAF) Congressional Research Service, October 18, 2006.

8.

Civil Reserve Air Fleet (CRAF) Aeromedical Evacuation Shipset (AESS) Contractor Logistics. www.fbo.gov/index.

References

9.

Aeromedical evacuation ‘brings them back.’ www.scott.af.mil//news/ story.asp?id=123269274.

®

1.

About the Air Force: Our Mission. www.airforce.com/learn-about/ourmission/.

10. Air Force Tactics, Techniques, and Procedures 3-42.5. Aeromedical Evacuation. November 1, 2003, pp 1-41.

2.

National Disaster Medical System. http://fhpr.osd.mil.

3.

Gooch D. Aeromedical Evacuation: Validating Civil Reserve Air Fleet. 2009, pp 1-40.

11. Air Force Instruction 44-165. Administering Aeromedical Staging Facilities. November 6, 2007, pp 1-28.

4.

Joint Health Services Flight%Provider.

5.

Factsheets: C-130 Hercules. www.af.mil/information/factsheets/factsheet. asp?fsID=9.

Operations.

www.usasam.amedd.army/d/

12. Air Force Tactics, Techniques, and Procedures 3-42.51. Critical Care Air Transport Teams (CCATT). September 7, 2006, pp 1-49. 13. CCATT Concept of Operations. Airforcemedicine.AFMS.mil/idc/groups/ public/documents…ctb_151108.pdf.


American Journal of Clinical Medicine® • Fall 2011 • Volume Eight, Number Three

Y’S RNS YOUR FAMIL TU ER ST A IS D A READY. BEFORE P TO YOU TO BE U ’S IT , N W O D E WORLD UPSID GET A KIT. MAKE

A PL AN. BE IN FO

RM ED.

Call 311 or visit READYNYC.ORG

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M e d i c a l E t h i c s Without the Rhetoric Cases presented here involve real physicians and patients. Unlike the cases in medical ethics textbooks, these cases seldom involve human cloning, bizarre treatments, or stem cell research. We emphasize cases more common to the practice of medicine. Most cases are circumstantially unique and require the viewpoints of the practitioners and patients involved. For this reason, I solicit your input on the cases discussed here at councile@aol.com. Reader perspectives along with my own viewpoint are published in the issue following each case presentation. We are also interested in cases that readers submit. The following case involves a potential conflict between the role of the physician as medical gatekeeper and the physician’s medical judgment.

Mark Pastin, PhD Mark Pastin, PhD, is president and CEO of the Council of Ethical Organizations, Alexandria, VA. The Council, a non-profit, non-partisan organization, is dedicated to promoting ethical and legal conduct in business, government, and the professions.

cas e TE N

TI M M Y THE TO R CH

The parents of a teenager, Timmy, with behavior problems request an in-patient psychiatric admission for their son. Timmy has taken to lighting living things on fire, starting with centipedes and spiders and progressing to his pet hamster. The parents are frightened that he will light the house on fire or torch someone’s pet dog or cat, as he has threatened. Their family physician concludes that Timmy’s behavior, though problematic, may not warrant in-patient treatment. It is a behavior associated with teens trying to get the attention of their parents and usually doesn’t escalate. When he informs the family of this, the mother breaks down sobbing, saying she can’t take it anymore. The father says that if they don’t get a break from Timmy, it will jeopardize their marriage. The physician wonders if admitting the son to the psych unit for a few days might be justified based on the total set of circumstances. Would you admit Timmy the Torch? This is an actual case. Of course, there are any number of complicating circumstances and additional details; but please address the case on the basis of the information provided. There will be an analysis of this case and a new case in the next issue.

Your input is requested. Email your responses to: councile@aol.com. © 2011 Council of Ethical Organizations

Medical Ethics Without the Rhetoric


American Journal of Clinical Medicine® • Fall 2011 • Volume Eight, Number Three

M e d i c a l E t h i c s Without the Rhetoric CASE N INE AN ALYSIS

W h o ’ s o n F i r s t

In our case from the last issue, you are called to the emergency room to assist with the consequences of a massive highway accident involving a school bus full of parents that was struck head on by an 18-wheeler. You are the first physician on the scene and are forced to choose between treating a physician colleague who was on the school bus and the still drunk driver of the 18-wheeler. The drunk driver is more likely to benefit from treatment, and either patient may suffer critically if not chosen first for treatment. Many readers felt that the right decision is to treat the drunk driver as the individual most likely to benefit from your treatment. A minority would treat the physician-parent on the grounds that he or she might benefit many more individuals if saved than the drunk driver, who has already caused immeasurable harm. I side with the latter view. While deciding purely on the basis of medical considerations prevents various kinds of decision-making bias, you are a scarce medical resource in this case. And such resources should, other things being equal, be used to maximum benefit.

Medical Ethics Without the Rhetoric

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A Systematic Approach for the Assessment and Diagnosis of Abdominal Pain in the Premenopausal Female Cornell Calinescu, MD Ilissa Jackson, PA-C Mark Mauriello, MD Ilya Chern, MD E. Robert Schwarz, MD

Abstract The complaint of abdominal pain in a premenopausal female is a challenging task for any medical provider faced with making an accurate diagnosis. The pathophysiology of women has to be considered when a female patient is presenting with a complaint of abdominal pain. Sometimes the diagnosis is easy to make, other times it can be elusive. The variance of a patient’s initial clinical presentation providers should trust their medical knowledge, their medical work up, and their instincts when making the final diagnosis. As always, the most life-threatening causes of the patient’s pain should be ruled out. Our article will provide medical providers a systematic approach for the assessment and diagnosis of abdominal pain in the premenopausal female. Each year approximately 3.4 million patients present to the emergency department with the chief complaint of abdominal pain. Their symptoms range broadly from the colicky pain of acute cholecystitis to the sharp, migrating pain of the right lower quadrant in acute appendicitis.1 Abdominal pain is one of the most challenging complaints to diagnose accurately, as 34% of abdominal pain is categorized as nonspecific.2 Given what is known about the extent of abdominal pathology and the broad range of diagnostic testing available, there still remains a level of uncertainty when discharging the patient whose workup has been negative. An algorithmic approach, which is directed by

the location of the pain including a comprehensive history and physical as well as appropriate laboratory and radiographic tests, will allow for more accurate disposition and treatment. This paper addresses abdominal pain in women of childbearing age (Table 1). Acute abdominal pain is defined as pain of one week’s duration or less. Abdominal pain can be divided into three categories: visceral, parietal, and referred. Visceral pain, caused by stretching of the fibers which innervate the walls of hollow or solid organs, can be described as a steady ache or discomfort to excruciating or colicky, again, often making the diagnosis a challenge.4 Pain can, however, be localized to the organ(s) involved, since the visceral afferents follow a segmental distribution. For example, foregut organs, including the stomach, duodenum, and biliary tract, produce pain in the epigastric area. Parietal pain is caused by irritation of the fibers that innervate the parietal peritoneum. This type of pain can be localized to the dermatome area superficial to the site of the painful stimulus. This differs from visceral pain in that visceral pain is usually felt in the midline due to the bilateral innervation of intraperitoneal organs. Visceral and parietal pains are not necessarily discrete. They can sometimes blend together, and as a disease process evolves, parietal signs, such as tenderness, guarding, rebound, and rigidity, usually overpower visceral signs.4, 6

A Systematic Approach for the Assessment and Diagnosis . . .


American Journal of Clinical Medicine® • Fall 2011 • Volume Eight, Number Three

Table 1: Abdominal Pain in Women of Child-Bearing Age

Diagnosis Appendicitis

History

Exam

Additional Testing

Treatment

Periumbilical pain, non- specific pain, fever, nausea, vomiting, diarrhea, anorexia

Tenderness (diffuse) McBurney’s point, Rovsing’s sign, rebounds, guarding, psoas sign

Pregnancy test, CBC, chemistry, LFTs, UA, CT abd/pelvis, ultrasound (if pregnant)

Fluid resuscitation, analgesics, antibiotics, surgery

Ovarian cysts (torsed, ruptured, or infected)5

Sudden onset of pelvic pain, usually unilateral

Tenderness, peritoneal signs

Pregnancy test, CBC, UA, ultrasound

Expectant management, hormone replacement, biopsy, removal, laparoscopy

Hydatidiform molar pregnancy10

Lower abdominal pain (atypical), irregular vaginal bleeding, hyperemesis

Tender lower abdominal mass, uterus larger than expected

Pregnancy test, CBC,UA, ultrasound

Uterine suction or surgical curettage, F/U serum hCG, may need chemotherapy

Ovarian torsion11

Sudden onset of pelvic pain, usually unilateral, history of cyst or tumor

Tenderness, peritoneal signs may indicate rupture

Pregnancy test, CBC,UA, ultrasound with color Doppler flow

Surgery/laparoscopy

Pelvic Inflammatory Disease1,5

Lower abdominal pain, pelvic pain, unilateral or bilateral, fever, urinary sx, vaginal bleeding/ discharge

Fever, tenderness, cervical motion tenderness (CMT), mucopurulent discharge

Pregnancy test, CBC, cervical cultures, ESR, CRP, ultrasound

Analgesia, removal of IUD, if present, antibiotics, possibly surgery if abscess is present/ laparoscopy

Tuboovarian abscess5

Fever, unilateral lower abdominal or pelvic pain, vaginal bleeding or discharge

Fever, lower abdominal/adnexal tenderness, CMT

Pregnancy test, CBC, cervical cultures, ultrasound

Analgesia, antibiotics, surgery/ laparoscopy

Endometriosis12,13

Dysmenorrhea, chronic pelvic pain, usually in 30s/40s

Pelvic or ovarian tenderness or enlargement

Pregnancy test, CBC, urinalysis, ultrasound

Hormonal therapy, analgesia, laparoscopy, pregnancy may lead to remission/cure

Ectopic pregnancy5

Abdominal pain, sudden and sharp if ruptured, vaginal bleeding, amenorrhea,

Shock, syncope, hypovolemia peritoneal signs, adnexal mass/ tenderness, CMT, vaginal bleeding, Chadwick sign

Pregnancy test, ultrasound, progesterone level

Laparoscopy, salpingectomy, salpingostomy, Methotrexate

Leiomyomas (fibroids)6

Pelvic pain or mass

Tenderness, pelvic or abdominal mass

Pregnancy test, ultrasound

Analgesia, hormonal therapy, myomectomy, hysterectomy

Adenomyosis5

Dysmenorrhea, menorrhagia

Symmetrically enlarged uterus or fibroid-like mass

Pregnancy test, CBC, Ultrasound

Analgesia, hormonal therapy, laparoscopy/hysterectomy

Diverticulitis (uncommon but should be considered)8

Steroid use, LLQ pain, constipation, nausea/vomiting, fever, diarrhea, urinary symptoms,

Tenderness at LLQ, rebound, guarding, peritonitis, sepsis

Pregnancy test, CT abdomen/ pelvis, acute abdominal series

Inpatient: NPO, fluids, antibiotics, bowel rest, NGT suction, surgery

Incarcerated hernia4

Abdominal, pelvic, inguinal pain, mass, distention, vomiting

Distention, non-reducible mass

Acute abdominal series, ultrasound, CT abdomen/pelvis

Attempt reduction ONLY IF RECENT ONSET; otherwise, surgery, analgesia, antibiotics

Cholecystitis/cholelithiasis/cholangitis 4,14

Abdominal pain (colicky early... parietal later), fever, nausea, vomiting, anorexia, tachycardia

RUQ pain (colicky early...parietal later), Murphy’s sign, jaundice, AMS and shock (with cholangitis)

CBC, chemistry, LFTs, lipase, pregnancy test, U/A, ultrasound, CT, HIDA scan

Ulcerative colitis4

Typical: bloody diarrhea, constipation, rectal bleeding, severe: frequent BMs, fever, tachycardia,anemia, weight loss, hypoalbuminemia

CBC, chemistry, LFTs, stool cultures, sigmoid/colonoscopy

IV steroids, fluids, replete electrolytes, broad-spectrum ABT, hyperalimentation, topical steroids, sulfasalazine, 5-aminosalicylics, topical steroids

Crohn’s disease4

Acute or chronic abdominal pain, fever, diarrhea, perianal fistulas, abscesses, rectal prolapse, vomiting, palpable mass, arthritis, uveitis, liver disease

CBC, chemistry, abdominal series, barium enema, upper GI series colonoscopy, CT

IV fluids, replete electrolytes, NGT suction for obstruction, broad-spectrum ABT, IV steroids, sulfasalazine, 5-aminosalicylates, topical steroids, others, symptomatic treatment, surgery

Irritable Bowel Syndrome (IBS)3,16

Chronic or recurrent abdominal pain or discomfort with altered bowel habits.

Psychosocial interview with positive stress related symptoms

Rome III criteria using bowel habit predominance for diagnosis, symptom-based diagnosis.

Good provider-patient relationship, diet alterations, antidiarrheal agents/ laxatives, SSRIs

Pancreatitis 4,14

Acute or chronic-most often caused by alcohol use or gallstones-epigastric pain, mid-back pain, diffuse abdominal pain

Epigastric tenderness or generalized tenderness, nausea, vomiting, jaundice, fever

CBC, chemistry including LFTs, amylase/lipase, ultrasound, CT radionuclide scanning, MRCP

Supportive, IV fluids, analgesics, possible surgery for abscess drainage, parenteral feeding if severe, antibiotics

Urinary retention4

Distended bladder and lower abdominal pain

Solid mass palpable, midline lower abdominal tenderness to palpation

Urinary catheterization, urinalysis, additional labs if indicated

Urinary catheter will diagnose and provide relief; follow up urology

Nephrolithiasis6,15

Abrupt onset of unilateral flank pain with possible radiation to groin/labia, hematuria, lower quadrant pain, dysuria, urgency

Unilateral CVA tenderness, nausea, vomiting

Urinalysis, KUB, ultrasound, CT, IVP, 24-hour urine

Analgesia, fluids, treatment of underlying conditions (hyperparathyroid, hypercalciuria, hyperuricosuria), ESWL, nephrolithotomy ureteroscopic stone removal, calculi urine strainer, antibiotics if necessary

1,6,8,9

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Referred pain is pain that is felt at a location distant from the diseased organ. It is based on patterns of developmental embryology, similar to visceral pain, and it is usually ipsilateral and produces symptoms as opposed to signs.4 Abdominal pain can be intraabdominal or extraabdominal. Intraabdominal causes include gastrointestinal, genitourinary, and gynecologic. Extraabdominal pain causes include cardiopulmonary, toxic, metabolic, neurogenic, or have abdominal wall etiology. Another classification, vascular, is less common and generally not considered in the childbearing-aged female, but should be considered in the differential .4, 5 As previously stated, nonspecific abdominal pain is the most common cause in the emergency department (ED).2, 3

History A full history includes pain attributes, symptoms, and a past medical and surgical history. Past medical history should include current and recently added medications, especially antibiotics and NSAIDs, past hospitalizations, surgeries, diabetes, trauma, or other chronic conditions. A social history should also be obtained, including tobacco, alcohol, and recreational drug use. One also needs to consider occupation and living conditions as well as assess the psych-social mental status of a given patient. During the history, the pain’s onset, duration, severity, location, quality and aggravating and relieving factors are principle characteristics to be noted.7 Gastrointestinal (GI) symptoms, including anorexia, nausea, vomiting, diarrhea, and constipation are helpful.15 The most common symptom pointing to a genitourinary (GU) cause of abdominal pain is an alteration in micturition, including frequency, urgency, dysuria, hematuria, incomplete emptying, or incontinence. A gynecologic (GYN) etiology is difficult to distinguish from a GI cause of pain and so a thorough GYN history should be obtained, including regularity of menses, sexual activity, STD history, including PID, vaginal bleeding or discharge, pregnancies, miscarriages, abortions, ectopic pregnancies, fibroids or cysts, and pelvic surgeries or laparoscopies.5,6

Physical Exam General Appearance can give the clinician some sense of the severity of pain. A pale, diaphoretic, grimacing patient would be of concern; however, the pain of early appendicitis may be vague and mild, so any abdominal pain should be taken seriously. Patients who are unable to sit still are most likely experiencing visceral pain, whereas those who prefer to remain immobile most likely have peritoneal pathology.4 Vital signs should be monitored continuously as subtle changes in temperature, blood pressure, respiratory rate, and pulse can indicate various pathophysiologic changes. In evaluating vital signs, consider factors such as age, medications, and concomitant medical conditions, which may alter normal processes. For example, if taking orthostatic vitals, a patient on a beta-blocker

may not show a suspected increase in the pulse if hypovolemia is suspected. The abdominal exam includes inspection, auscultation, and palpation. Any distention, scars, or obvious masses should be noted. Hyperactive bowel sounds can be helpful in evaluating a small bowel obstruction, and, although they help with this diagnosis, they are of limited value.1, 4 Normal or absent bowel sounds, in addition, are not entirely valuable. Palpation reveals the most information and should be performed gently and beginning farthest away from the area of the most pain.4 Patients can assist with the exam by palpating with the clinician. The knees may also be flexed to aid in patient comfort and can also decrease involuntary guarding. Tenderness is a sign elicited by palpation and can be specific or diffuse. Rigidity, rebound, and referred pain can be indicative of peritoneal irritation.1, 4, 6 Enlargement of the liver, spleen, bladder, and palpable masses should be noted. The pelvic exam is essential in this population and may provide additional information not otherwise obtainable by simple palpation. Cultures should be taken and tested for gonorrhea, Chlamydia, and other infections. A rectal exam is useful with suspected GI bleeding, and rectal pain on exam can indicate appendicitis, PID, and ectopic pregnancy.5, 6, 7

Laboratory and Radiographic Tests Although limited, the complete blood count (CBC) and acute abdominal series are the most commonly used studies in the evaluation of abdominal pain. One should be suspicious of a very high white blood cell count; however, one should not be reassured by a normal white count or a nonspecific bowel gas pattern.7 If obstruction or perforation is suspected, abdominal films or ultrasound may be helpful. Computed tomography (CT) can detect almost any abnormality.1 In the childbearingaged female, a pregnancy test should be obtained quickly, and its result received as rapidly as possible.6, 7 If the pregnancy test is positive, then radiation exposure should be avoided, and ultrasonography (US) will be the radiographic test of choice in evaluating lower quadrant abdominal pain.6

Specific Diagnoses The majority of final diagnoses in acute abdominal pain include nonspecific abdominal pain, appendicitis, and biliary tract disease. Specifically for females of childbearing age, the differential diagnosis of nontraumatic abdominal and pelvic pain and their presentations and treatments are shown in Table 1. Despite the multitude of distinct causes of abdominal pain and the various studies available to diagnose a patient, the clinician may find himself discharging a patient home with a nonspecific diagnosis. Before doing so, however, one must consider other factors when making a disposition determination for the female patient. A patient who appears ill or who is immunocompromised should be seriously considered for admission. One with

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intractable abdominal pain, uncontrolled vomiting, or altered mental status should stay for further work up. At times a patient may have to be admitted for social reasons, either homelessness, alcohol abuse, or drug abuse. Clinicians should trust their instincts and may even admit a patient with non-specific abdominal pain, which could possibly be diagnosed later as appendicitis. Regardless of one’s decision to admit or discharge a patient, the most life-threatening causes of the patient’s pain should always be ruled out. The pathophysiology of women has to be taken under consideration when a female patient is presenting with a complaint of abdominal pain.5

References 1.

Paulson EK, Kalady MF, Pappas TN. Suspected Appendicitis. N Engl J Med. 2003;348:236-42.

2.

Sandhu GS, Redmond AD, Prescott MV. Non Specific Abdominal pain: A Safe Diagnosis? J R Coll Surg Edinb. 1995 Apr; 40(2) 109-11.

3.

Heaton KW. Diagnosis of Acute Non-Specific Abdominal Pain. Lancet. 2000 May 6;355(9215):1644.

4.

Flasar MH, Cross R, Goldberg E. Acute Abdominal Pain. Prim Care Clin Office Pract. 33(2006) 659-684.

5.

Forcier M. Emergency Department Evaluation of Acute Pelvic Pain in the Adolescent Female. Clin Ped Emerg Med. 10(2009) 20-30.

6.

Kilpatrick CC, Monga M. Approach to the Acute Abdomen in Pregnancy. Ostet Gynecol Clin N Am. 34(2007) 389-402.

7.

Cartwright SL, Knudson MP. Evaluation of Acute Abdominal Pain in Adults. Am Fam Physician. 2008;77(7): 971-978.

Ilissa Jackson, PA-C, is Physician Assistant, Department of Emergency Medicine, Plantation General Hospital, Plantation, FL, and Graduate Professor, Physician Assistant Program, Keiser University.

8.

Dominguez EP, Sweeney JF, Choi YU. Diagnosis and Management of Diverticulitis and Appendicitis. Gastroenterol Clin N Am. 35(2006) 367391.

9.

Mark Mauriello, MD, is Medical Director and Assistant to Research and Case Management at St. Michael’s Medical Center, Norwick, NJ.

Flum DR, Morris A, Koepsell T, et al. Has Misdiagnosis of Appendicitis Decreased Over Time? JAMA. Oct 10, 2001-Vol 286(14)1748-1753.

10. Tabas JA, Strehlow M, Isaacs E. A False Negative Pregnancy Test in a Patient with a Hydatidiform Molar Pregnancy. N Engl J Med. 2003;349:2172-73.

Cornell Calinescu, MD, is Assistant Medical Director, Department of Emergency Medicine, Plantation General Hospital, Plantation, FL.

Ilya Chern, MD, is Medical Director, Department of Emergency Medicine, Plantation General Hospital, Plantation Florida. E. Robert Schwarz, MD, is Professor and Chair, Department of Family Medicine and Community Health, Miller School of Medicine, University of Miami, FL. Potential Financial Conflicts of Interest: By AJCM policy, all authors are required to disclose any and all commercial, financial, and other relationships in any way related to the subject of this article that might create any potential conflict of interest. The author has stated that no such relationships exist. ®

11. Griffin D, Shiver SA. Case Report-Unusual Presentation of Acute Ovarian Torsion in an Adolescent. AJEM. (2008)26,520.e1-520.e3. 12. Scully RE, Mark EJ, McNeely WF, et al. Case 13-2000: A 26-year old women was admitted… bouts of abdominal pain with vomiting, diarrhea and hematochezia. N Engl J Med. 2000;342:1272-78. 13. Muto MG, O’Neill MJ, Oliva E. Case 18-2005: A 45-Year- Old Women with a Painful Mass in the Abdomen. N Engl J Med. 2005;352:2535-42. 14. Attasaranya S, Fogel EL, Lehman GA. Choledocholithiasis, Ascending Cholangitis and Gallstone Pancreatitis. Med Clin N Am. 92(2008)925-960. 15. Jindal G, Ramchandani P. Acute Flank Pain Secondary to Urolithiasis: Radiologic Evaluation and Alternate Diagnoses. Radiol Clin N Am. 45(2007)395-410. 16. Videlock EJ, Chang L. Irritable Bowel Syndrome: Current Approach to Symptoms, Evaluation, and Treatment. Gastroenterol Clin N Am. 36(2007)665-685.

IT ’ S N O T T O O L ATE ! The Distinguished Degree of Fellow Applications are due

December 31, 2011. You can download the application from the AAPS web site (www.aapsus.org) or request an application by contacting the Executive Office at 813-433-2277. Check for current criteria at http://www.aapsus.org/academies/fellow.html

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Manuscript Criteria and Information The American Journal of Clinical Medicine® (AJCM®), the official journal of the American Association of Physician Specialists, Inc. (AAPS), is a peer-reviewed journal dedicated to improving the clinical practice of medicine by publishing educational and informational articles. AJCM® is the official journal of the American Association of Physician Specialists, Inc. Send all manuscripts via email to editor@aapsus.org in Microsoft Word format. No other file formats will be accepted. Manuscripts submitted by fax or mail to the Journal WILL NOT BE ACCEPTED AND WILL NOT BE RETURNED. Manuscripts received are not to be under simultaneous consideration by another publication. Accepted manuscripts become the permanent property of the American Journal of Clinical Medicine® and may not be published elsewhere without permission from the publisher. Authorship Responsibility, Financial Disclosure, Assignment of Copyright, and Acknowledgment Forms: Authorship responsibility forms must be completed and signed by each author and accompany submitted manuscripts. Each author must submit a statement that specifies whether he or she has financial or proprietary interest in the subject matter or materials discussed in the manuscript. These forms may be downloaded from the AAPS website www.aapsus.org or may be obtained by request to the AAPS office at 813-433-2277 ext 18 or 30. Authorship Responsibility: All accepted manuscripts are copyedited; an edited typescript is sent for the author’s approval. The author is responsible for all statements in the work, including the copy editor’s changes. Data Access and Responsibility: For reports containing original data, at least one author (e.g., the principal investigator) should indicate that he or she “had full access to all the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis” (DeAngelis CD, Fontanarosa PB, Flanagin A. Reporting financial conflicts of interest and relationships between investigators and research sponsors. JAMA. 2001;286:89-91). Units of Measure: Conventional units of measure are preferred, with Système International (SI) units expressed secondarily (in parentheses). In tables and figures, a conversion factor to SI may be presented in the footnote or legend to economize space. Exceptions to this policy include calories, hematocrit, glycosylated hemoglobin, blood cell counts, and ejection fraction, for which conventional units alone should be expressed. The metric system is preferred for length, area, mass, and volume. Manuscript Preparation: Manuscript preparation should generally follow the guidelines outlined in The International Committee of Medical Journal Editors: “Uniform requirements

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American Journal of Clinical Medicine® • Fall 2011 • Volume Eight, Number Three

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Binocular Double Vision – A Review Nancy Lutwak, MD

Abstract A 62-year-old male with history of hypertension presented to our emergency department with new onset diplopia. He denied recent trauma. The patient had binocular double vision with abducens nerve palsy. There were no other complaints. We review the relevant anatomy, multiple etiologies, necessary diagnostic testing, and treatment of diplopia. Careful physical examination and detail to the patient’s past history is essential for making an accurate diagnosis. Since sudden onset of this entity may represent a serious condition requiring urgent attention, emergency physicians should be familiar with this dysfunction. Most importantly, visual disturbances may be the initial manifestation of occult disease - tumors, multiple sclerosis, vascular disease, myasthenia gravis, or Miller-Fisher syndrome.

Discussion Anatomy

and past medical histories. The ocular exam should include visual acuity, extraocular motility, pupillary response, and ophthalmoscopy to rule out papilledema of the optic disc.

Etiology, Differential Diagnoses, and Treatment of Diplopia Etiologies include vasculopathic, trauma, tumors, multiple sclerosis, diabetes, stroke, meningeal inflammation/infection, and giant cell arteritis. Differential diagnoses include thyroid eye disease, myasthenia gravis, orbital inflammatory disease, orbital trauma (medial wall fracture resulting in entrapment of the ipsilateral medial rectus muscle), post-procedural complications (after strabismus surgery), migraine, and Duane Syndrome (congenital innervation disorder causing limited ability to move the eye inward). Medications may also be associated with diplopia. These causes will be discussed, in addition to the appropriate treatments and prognoses.

The abducens nerve innervates the lateral rectus muscle. After the nerve exits the brainstem, it enters the cavernous sinus where it is lateral to the internal carotid artery. It then proceeds to the orbit. The sixth cranial nerve also traverses the pons.1

Trauma

Dysfunction

Vascular Pathology

Injury to the nerve results in deviation inward of the affected eye from unopposed pull from the medial rectus muscle. Compression or stretching of the nerve may result in injury.1 Dysfunction of the nerve may lead to double vision with ocular misalignment.2-4 Ruling out cranial nerve palsies, including III, IV, V, in addition to VI, should be kept in mind. Patients with sudden onset of monocular diplopia require complete ophthalmological examinations as well as detailed review of current

Cranial nerve VI palsy may be the result of trauma causing avulsion and brainstem displacement.1

Cases of diplopia have been reported secondary to vascular pathology.5-7 Palsies of the ocular muscles secondary to ischemia from carotid artery occlusion has been reported.5 Dissection of the internal carotid artery with pseudoaneurysm and cavernous sinus fistula has led to binocular diplopia; this was diagnosed with computer tomographic angiogram.6 Orbital varices, which was treated with gamma knife radiosurgery, has caused diplopia.7 Abducens nerve palsy secondary to infarct of the lateral

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and paramedian areas at the base of the pons has been reported. This was diagnosed with magnetic resonance imaging.8

Tumors Multiple cases of diplopia have been described as a result of tumor growth.9-12 Orbit metastasis is an uncommon cause.9 Soft tissue neoplasm, such as primitive neuroectodermal tumor involving the parasellar area and optic chiasm, has also been reported; this was diagnosed with magnetic resonance imaging and treated with gamma knife surgery, chemotherapy, and radiotherapy.10 Schwannomas of the abducent nerve, although rare, have led to diplopia. These were treated with gamma knife surgery.11 Double vision has been reported as a result of spheno-orbital meningioma.12

Endocrinopathies

Endocrinopathies may lead to visual disturbances including diplopia.13-15 Diabetic patients may have ophthalmological emergencies and need close monitoring.13 They may develop neuropathy leading to dysfunction of the abducens nerve.1 Diabetics develop ocular motor neuropathy secondary to ischemia.14 Pituitary disorders and thyroid disease may lead to ophthalmological problems.15 Graves eye disease may result in severe diplopia.15 The patients may develop massively enlarged extraocular muscles, congestion of the orbit, and strabismus.15 Patients with Graves eye disease require medical care for this autoimmune disorder as well as surgical care.15 Orbital decompression and strabismus surgery may be required.15

Metabolic and Nutritional Etiologies

Metabolic and nutritional disease may also lead to visual problems.16,17 Nutritional disorders and vitamin deficiencies, which result from gastrointestinal surgery and malabsorption, can lead to eye manifestations.16 Alcohol abuse and WernickeKorsakoff’s Syndrome with severe thiamine deficiency lead to peripheral neuropathies with abnormal oculomotor function.17

Inflammatory Disorders

Inflammatory diseases may also cause ophthalmological manifestations.18,19 Temporal arteritis may result in diplopia and headache.19 Any patient over 50 suspected of having giant cell arteritis needs immediate sedimentation rate, C-reactive protein, and platelet count performed. Biopsy of the temporal artery is needed for definitive diagnosis.19 If positive, treatment with steroids is required.19

Infectious Etiologies

Cranial nerve palsies with abducens involvement resulting in diplopia may be a complication of herpes zoster ophthalmicus.20 Treatment includes oral acyclovir, acyclovir ointment, and oral steroids.20 Oculomotor palsies may occur with other infectious disorders.21 Miller-Fisher Syndrome , a variant of Guillain-Barre Syndrome, may result in ophthalmoplegia.21 It is an immune-mediated post-infectious disease, which is diagnosed with lumbar puncture. Immunotherapy with intravenous immunoglobulin and plasma exchange may be required in severe cases.21 Multiple infections, e.g., campylobacter jejuni,

cytomegalovirus, and Epstein-Barr virus, may cause antibodies to ganglioside with resultant demyelinating polyradiculoneuropathy and ophthalmoplegias.22

Neuromuscular Junction Transmission Failure Myasthenia gravis is an auto-immune disorder leading to muscle weakness, which is painless.23 Chemical transmission at the neuromuscular junction fails because of antibody formation.23 The patient may exhibit diplopia and ptosis, which waxes and wanes.23 There may be precipitating factors such as emotional stress and intercurrent illness.23 Diagnostic testing includes edrophonium chloride test, electromyography, and the presence of antiacetylcholine antibiodies.23,24 Treatment is with acetylcholinesterase-blocking agents, such as pyridostigmine.23 Immunomodulatory therapy and steroids may be needed for substantial improvement, but respiratory support during a myasthenia crisis can occur at some point.23,24 Patients may present with ocular manifestations initially, but 80% of them go on to have generalized weakness.23 Respiratory weakness may be fatal.22 Two-thirds of patients with ocular myasthenia gravis develop generalized weakness within two years.25 These patients require the care of ophthalmologists and neurologists and recognition by physicians that the disease is life-threatening.25

Central Nervous System Demyelinization Multiple sclerosis, a disorder of the spinal cord, optic nerve, and brain, frequently presents initially with eye complaints.26 It is reported as high as 70%.26 The disorder is inflammatory and degenerative. Diagnosis is based on lumbar puncture, revealing oligoclonal bands in the spinal fluid, and magnetic resonance imaging, demonstrating white matter lesions.26 Visual dysfunction may present with eye abduction paresis.27 Neuro-ophthalmic abnormalities in patients with multiple sclerosis result from central nervous system demyelination.27 If the diagnosis is made early, immunomodulary treatment will optimize the patient’s care.28

Post-Procedural Complications There have been reports of patients developing intracranial subdural hematoma after spinal anesthesia resulting in prolonged headache and sixth cranial nerve paresis.29 Patients have also developed double vision as a complication of strabismus surgery.30 Diplopia rarely occurs following cataract extraction.31

Medication-Related Associations between diplopia and medication have been reported.32,33 Patients taking lacosamide, a new antiepileptic medication, have developed diplopia with neurotoxicity.32 A relationship between diplopia and use of fluroquinolones is possible.33

Fracture as an Etiology Diplopia has also been described in association with malarzygomatic fractures.34

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Migraine-Related

5.

Sander T, Gottschalk S, Hertel S, Neppert B, Helmchen. MRI of the eye muscles in a case of ophthalmoplegia caused by common carotid artery occlusion suggests ischemic myopathy. J Neurol Sci. 2011;300(1):176-8.

6.

Vaphiades MS, Roberts BW. Abducens nerve palsy from an occult high flow carotid cavernous fistula. Am Orthopt. 2004;139-45.

7.

Xu D, Liu D, Zhang Z, Zhang Y, Song G. Gamma knife radiosurgery for primary orbital varices: a preliminary report. Br J Ophthalmol. 2010;Oct 22.doi;10.1136/bjo.2009.17001.

8.

Ogawa K, Suzuki Y, Kamei S. Two patients with abducens nerve palsy and crossed hemiplegia (Raymond syndrome). Acta Neurol Belg. 2010;Sep;110(3):270-1.

9.

Ng E, Ilsen PF. Orbital metastases. Optometry. 2010;Dec;81(12):647-57.

In addition, migraines have been reported as a cause of diplopia.35

Prognosis Isolated abducens nerve palsy is a common cause of binocular diplopia.35 If caused by microvascular disease as a result of diabetes and/or hypertension, the prognosis is good. One study reported 87% spontaneous recovery at five months and 95% at twelve months. Patients with cranial nerve palsies resulting from non-microvascular disease, the etiologies of which included multiple sclerosis, myasthenia gravis, trauma, and space-occupying lesions, had a reported complete recovery at one year of 62%. Patients with abducens nerve palsy not caused by microvascular disease had a 44% rate of no recovery at the end of one year.35

Conclusion Patients may present to emergency departments with binocular diplopia. This eye misalignment may be the result of cranial nerve palsies, a problem with neuromuscular transmission, or mechanical dysfunction of the ocular muscles. It may be related to vascular disease, procedures performed, trauma, medication, nutritional deficits, endocrinopathies, infection, or occult disease.1-34 The possible etiologies are diverse and range significantly in seriousness, some of which are life-threatening. Fortunately, many patients have spontaneous recovery at twelve months.35 Magnetic resonance imaging and angiography identify vascular problems, tumors, and infarcts leading to diplopia.5-12 Emergency physicians should be aware of the etiologies of this entity as well the appropriate diagnostic tests and management. Most importantly, diplopia may be the initial presentation of occult illness. Particular focus should be on investigating the possibility of previously undiagnosed tumors, vascular disease, multiple sclerosis, Miller-Fisher syndrome, or myasthenia gravis.5-12,22-28 Nancy Lutwak, MD, is Attending Physician, Department of Emergency Services, Veterans Administration New York Harbor Healthcare Center, NYC. Potential Financial Conflicts of Interest: By AJCM policy, all authors are required to disclose any and all commercial, financial, and other relationships in any way related to the subject of this article that might create any potential conflict of interest. The author has stated that no such relationships exist. ®

References 1.

Milanes-Rodríguez G, Ibañez-Valdés L, Foyaca-Sibat H, Perez-Fernandez M. The Abducens Nerve in Neurology. The Internet Journal of Neurology. 2009;10,2. Last modified on Fri, 13 Feb 09 13:46:55-0600.

2.

Rucker JC, Tomsak RL. Binocular diplopia. A practical approach. Neurologist. 2005;11(2):98-110.

3.

Rucker JC. Oculomotor disorders. Semin Neurol. 2007:Jul;27(3):244-56.

4.

Friedman DI. Pearls: diplopia. Semin Neurol. 2010;Feb;30(1):54-65.

10. Hormozi AK, Ghazisaidi MR, Hosseini SN. Unusual presentation of peripheral neuroectodermal tumor of the maxilla. J Craniofac Surg. 2010;Nov;21(6):1761-3. 11. Hayashi M, Chernov M, Tamura N, Yomo S, et al. Gamma knife surgery for abducens nerve schwannoma. J Neurosurg. 2010;Dec.:136-43. 12. Saeed P, van Furth WR, Tanck M, Kooremans F, et al. Natural history of spheno-orbital meningiomas. Acta Neurochir. (Wien) 2010;Dec. DOI 10.1007/s00701-010-0878-0. 13. Wipf JE, Paauw DS. Ophthalmologic emergencies in the patient with diabetes. Endocrinol Metab Clin North Am. 2000;Dec;29(4):813-29. 14. Wu GF, Balcer LJ. Ophthalmol Clin North Am. 2004;Sep,17(3):427-34. 15. Del Monte MA. 2001 an ocular odyssey: lessons learned from 25 years of surgical treatment for graves eye disease. Am Orthopt J. 2002;40-57. 16. Berman EL. Clues in the eye: ocular signs of metabolic and nutritional disorders. Geriatrics. 1995;Jul;50(7):34-6,43-4. 17. Kenyon RV, Becker JT, Butters N, Hermann H. Oculomotor Function in Wernicke-Korsakoff’s Syndrome: I. Saccadic Eye Movements. Intern J Neurosci. 1984;25:53-65. 18. Borruat FX. Neuro-ophthalmologic manifestations of rheumatologic and associated disorders. Curr Opin Ophthalmol. 1996;Dec;7(6):10-8. 19. Harder N. Temporal arteritis: an approach to suspected vasculitides. Prim Care. 2010;Dec;37(4):757-66. 20. Sanjay S, Huang P, Lavanya R. Herpes Zoster Ophthalmicus. Curr Treat Options. Neurol. 2010;Oct12.doi:10.1007/S 11940-010-0098-1. 21. Schabet M. Miller-Fisher Syndrome and the Spectrum of Oculomotor Palsies with anti-GQ1b Antibodies. Klin Monbi Augenheilkd. 2010;Nov;227(11):857-859. 22. Hughes RAC, Hadden RDM, Gregson NA, Smith KJ. Pathogenesis of Guillain-Barre syndrome. J of Neuroimm. 1999;100(1):74-97. 23. Spillane J, Kullman D. History central to diagnosing myasthenia gravis. Practicioner. 2010;Sep;254(1732):15-18. 24. Stojkovic T, Behin A. Ocular myasthenia: Diagnosis and treatment. Rev Neurol. (Paris) 2010;Dec;166(12):987-997. 25. Boumendil J, Clermont-Vignal C, Gout O, Fechner C, et al. Clinical polymorphism of myasthenia gravis beginning with isolated ocular symptoms; a five years retrospective analysis. J Fr Ophthalmol. 2010;Dec;33(10):728-738. 26. Jenkins PF. The multiple facets of multiple sclerosis. Am Orthopt J. 2007;69-78. 27. Jasse L, Vighetto A, Vukusic S, Pelisson D, Tilikete C. Unusual Monocular Pendular Nystagmus in Multiple Sclerosis. J Neuroophthalmol. 2010;Nov 30. doi:10.1097/WNO.0b013e3181f8dc23. 28. Maxner CE. Neuro-ophthalmology and multiple sclerosis. Am Orthopt J. 2006;72-85. 29. Amorim JA, Remigio DS, Damazio FO, Barros MA, et al. Intracranial Subdural Hematoma Post-Spinal Anesthesia: Report of Two Cases and Review of 33 cases in the Literature. Rev Bras Anesthesiol. 2010;NovDec;60(6):620-9.

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30. Wallace DK. Preoperative issues in adult strabismus. Am Orthopt J. 2001;116-20.

33. Fraunfelder FW, Fraunfelder FT. Diplopia and fluoroquinolones. Ophthalmol. 2009;116(9):1814-7.

31. Strominger MB. Diplopia following cataract extraction. Am Orthopt J. 2004;120-4.

34. Barclay TL. Diplopia in association with fractures involving the zygomatic bone. JPRAS. 1958;11:147-57.

32. Novy J, Patsalos PN, Sander JW, Sisodiya SM. Lacosamide neurotoxicity associated with use of sodium channel-blocking antiepileptic drugs: A pharmacodynamic interaction? Epilepsy Behav. 2010;Nov5.doi:10.1016/j. yebeh.2010.10.002.

35. Comer RM, Dawson E, Plant G, Acheson JF, Lee JP. Causes and outcomes for patients presenting with diplopia to an eye casualty department. Eye. 2007;21:413-8.

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Re-Radiation and Casodex in Locally Advanced, Radiation Recurrent, Locally Progressing Prostate Cancer Gary Shultz, DO, FAAR

Abstract This report is to present the results of re-radiation and Casodex 150mg/day in patients with locally advanced, previously radiated prostate cancer. These 45 patients with locally advanced progressing prostate cancer were treated with further radiation to total prescription dose of 3120 cGy and Casodex 50mg T.I.D. These patients have shown alternative therapeutic treatment resulting in significant improvement in quality of life. Further clinical studies are warranted.1

Introduction There are at present limited effective treatment options in patients with locally advanced, previously radiated and progressing prostate cancer.1,2 The purpose of this study is to present the results of re-radiation and Casodex.

Materials and Methods In 2005, a program for re-radiation and Casodex for patients with locally advanced and previously radiated prostate cancer was started at Christie Clinic Cancer Center. The 45 patients were 60% formally prostatectomy; 40% had definitive radiation treatments. The range of radiation dose in these patients was 5300 cGy to 6480 cGy. The re-radiation consisted of planning with CT-scan later with MRI plus the CT-scan with the GTV

outlining the prostate fossa or prostate. The CTV was set at .5 cm and the PTV was at .5 cm. The patients received treatment with the Varian without and with CT cone beam with adaptive radiation using IMRT. The Casodex 150mg/day was started approximately one week prior to the radiation. The radiation was 3120 cGy in 26 fractions twice a day and four to six hours apart. Forty-five were enrolled from 2005 to 2011. All 45 have been locally progression free.

Discussion Prostate cancer is the most common malignancy and the second leading cause of cancer death among men in the USA. In the year 2000, it was estimated that 180,400 new cases of prostate cancer would be diagnosed and that 31,900 patients would die of the disease.1,16 The overall incidence of biochemical progression following treatment with radical prostatectomy, radiation, and radiation plus hormones is 15% to 40%.1,14,15 A significant number of patients will, therefore, develop recurrent prostate cancer after radiation.1 Patients with recurrent prostate after radiation are commonly retreated with anti-androgens or orchiectomy.1,2 The antitumor effects of such hormonal treatment last for approximately one to two years, after which time the tumors become hormone refractory.1,17 Prostate cancer has a long natural history, and patients with early biochemical failure following radiation, with-

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out other clinical evidence of local or systemic progression, are expected to have an average survival of five to ten years.1,2,3 As a consequence of the long survival and limited treatment options for progressive disease, some of these develop symptoms due to disease. These can be due to progression in the pelvis with tumor invasion into the urethra and bladder. The result is urinary outlet obstruction, hematuria, and hydronephrosis. The tumor invasion can go into the rectum, resulting in bleeding, fistula formation, and rectal obstruction. The tumor invasion into the pelvic nerves and pelvic bones may result in intractable pelvic and perineal pain as well as pathological fracture.4 The treatment options presently available for locally advanced, previously radiated progressing prostate cancer include palliative surgical procedures such as TURP, ureteric stenting, cystoscopic tumor fulguration to limit urinary bleeding, and colostomy/urinary diversion to overcome rectal/bladder obstruction or fistula. The medical measures utilized in these patients included hormone manipulation, chemotherapy, narcotic or nonnarcotic analgesics, anti-depressants, and blood transfusions.1,4 Re-radiation has been used for treatment of previously radiated tumors in several areas including head and neck, breast, lung, and brain. The local control rates achieved with re-radiation range from 40% to 75%.1,7-9 Re-radiation has generally been used in combination with radiosensitizing agents, such as hormones, chemotherapy, and hyperthermia.1,7,8 In a report from Thomas Jefferson University, patients with recurrent rectal cancer were re-treated to a median dose of 3060 cGy plus 5-flurouracil. Bleeding, pain, and mass effect were palliated in 100%, 65% and 24%. The RTOG grade 3 and 4 late toxicity was 23% and 10%. Small bowel obstruction occurred in 17%, with only 3% requiring re-operation.1,10 Re-radiation of locally advanced pelvic tumors may, therefore, result in significant palliation with tolerable side effects.1 In this study we have used similar doses to those used in the Jefferson and Robert Lurie Comprehensive Cancer Center Northwestern Memorial Hospital studies.1 So far one patient has had significant late RTOG 3 toxicity; follow up with hyperbaric oxygen showed remarkable improvement. No urinary incontinence was present. The symptoms of diarrhea occur in 24% and constipation in 19%. The rectal bleeding was 6% and improved greatly with hyperbaric oxygen. Penile discomfort was 1%. We may successfully control the local disease with the prostate or prostate fossa in some patients, despite the fact that the cancer failed to respond to the initial radiation or surgery/radiation. Gary Shultz, DO, FAAR, is Chairman of Christie Clinic Cancer Center, Department of Radiation Oncology, and Assistant Professor, University of Illinois, Urbana/Champaign, IL. Potential Financial Conflicts of Interest: By AJCM policy, all authors are required to disclose any and all commercial, financial, and other relationships in any way related to the subject of this article that might create any potential conflict of interest. The author has stated that no such relationships exist. ®

References 1.

Kalapurakal JA, Mittal BB, Sathiaseelan V. Re-irradiation and external hyperthermia in locally advanced, radiation recurrent, hormone refractory prostate cancer: a preliminary report. British Journal of Radiology. 2001;74:745-751.

2.

Parker CC, Dearnaley DP. The management of PSA failure after radical radiotherapy for localized prostate cancer. Radiother Oncol. 1998;49:103-10.

3.

Sandler HM, Dunn RL, McLaughlin PW, Hayman JA, Sullivan MA, Taylor JMG. Overall survival after prostate-specific-antigen-detected recurrence following conformal radiation therapy. Int Radiat Oncol Biol Phys. 2000;48:629-33.

4.

Holaman M, Carlton CEjr, Scardubi PT. The frequency and morbidity of local tumor recurrence after definitive radiotherapy for stage C prostate cancer. J Urol. 1991;146:1578-82.

5.

Oh Wk, Kantoff PW. Management of hormone refractory prostate cancer: current standards and future prospects. J Urol. 1998;160:1220-9.

6.

Pienta KJ, Redman B, Hussain M, Cummings G, Esper PS, Appel C, et al. Phase II evaluation of oralestrmustine and oral etoposide in hormone –refractory adenocarcinoma of prostate. J Clin Oncol. 1994;12:2005-12.

7.

DeCrevoisier R, Bourhis J, Domenge C, Wibault P, Koscieiny S, Lusinchi A, et al. Full-dose reradiation for unresectable head and neck carcinoma: experience at the Gustave-Roussy Institute in a series of 169 patients. J Clin Oncol. 1998;16:3556-62.

8.

Kapp DS, Barnett TA, Cox RS, Lee ER, Lohrbach A, Fessenden P. Hyperthermia and radiation therapy of local-regional recurrent breast cancer: prognostic factors for response and local control of diffuse or nodular tumors. Int J Radiat Oncol Biol Phys. 1991;20:1147-64.

9.

Kim hk, Thornton AF, Greenberg HS, Page MAJunck L, Sandler HM. Results of reirradiation of primary intracranial neoplasms with threedimensional conformal therapy. Am J Clin Oncol. 1997;20:358-63.

10. Lingareddy V, Ahmad NR, MohiuddinM. Palliative reirradiation for recurrent rectal carcinoma. Int J Radiat Oncol Biol Phys. 1997;38:785-90. 11. Vernon CC, Hand JW, Field SB, Machin D, Whaley JB, Van Der Zee J, et al. Radiotherapy with or without hyperthermia in the treatment of superficial localized breast cancer. Results from five randomized controlled trials. International Collaborative Group. Int J Radiat Oncol Biol Phys. 1996;35:731-44. 12. Overgaard J, Gonzalez GD, Hushof MC, Arcangeli G, Dahl O, Mella O, et al. Hyperthermia as an adjuvant to radiation therapy of recurrent or metastatic malignant melanoma. A Multicentre randomized trial by the European Society for Hyperthermic Oncology. Int J Hyperthermia. 1996;12:3-20. 13. Van Der Zee J, Gonzalez DG, Van Rhoon GC, Van Dijk JDP, Van Putten WIJ, Hart AAM, et al. Comparison of radiotherapy alone with radiotherapy plus hyperthermia in locally pelvic tumors: a prospective, randomized, multicentre trial. Lancet. 2000;355:1119-25. 14. Bolla M, Gonzalez D, Warde P, Dubois JB, Mirimanoff RO, Storme G, et al. Improved survival in patients with locally advanced prostate cancer treated with radiotherapy and goserelin. N Engl J Med. 1997;337:295-300. 15. Leopold KA, Dewhirst M, Samulski T, Harrelson J, Tucker JA, George SL, et al. Relationships among tumor temperature, treatment time and histopathological outcome using preoperative hyperthermia with radiation in soft tissue sarcomas. Int J Radiat Oncol Bio Phys. 1992;22:989-98. 16. Greenlee RT, Murray T, Bolen S, Wingo PA. Cancer statistics, 2000. CA Cancer J Clin. 2000;50:7-33. 17. Prostate Cancer Trialists’ Collaborative Group. Maximum androgen blockade in advanced prostate cancer: an overview of randomized trials. Lancet. 2000;355:1491-8. 18. Shipley WU, Thames H, Sandler HM, Hanks GE, Zietman AL, Perez C, et al. Radiation therapy for clinically localized prostate cancer: a multiinstitutional pooled analysis. JAMA. 1999;281:1598-604.

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Orthopedic Issues in Family & Emergency Medicine

Clavicle Fractures 101 Ben Jones, MS2 Roberto R. Gonzalez, MD

Introduction

Case 1 (Figures 1 and 2)

Physicians need skills in the diagnosis and management of commonly occurring injuries. In many places, subspecialist help is not available or affordable.1 These basic skills reflect the reality of community medical practice for a variety of specialties staffing rural emergency rooms, primary care offices, and mission hospitals. For younger physicians, most academic medical centers teach a curriculum of “Refer to Ortho.” Hatch et al have described the epidemiology of common fractures in the community.2

A 22-year-old female tripped and fell last night. Recent open access policies at the clinic allowed her to “walk-in” without an appointment. Her past medical history is noncontributory, but she reports pain in her right shoulder. This is aggravated by moving her right arm. Her vital signs are normal, and neurovascular exam of the right arm is normal. She has difficulty localizing the pain and wants a shot for pain relief.

Many training programs have no incentive to install and maintain basic imaging equipment. Patients with possible fractures are triaged to the hospital before they receive any evaluation at the point of initial service. This is a lost opportunity for the development of these skills. Most injuries require screening with imaging. When detected, most fractures can be managed conservatively while maintaining quality in the community. The trick is to find the fracture. Then physicians can start to develop the knowledge of selecting those cases that require surgery and conservatively manage the others.3-6 This series is dedicated to those physicians serving in areas where resources are scarce and the hours are long.

1. Based on the radiographic image below (Figure 1), the most likely diagnosis is: a. A severe sprain of the right shoulder rotator cuff b. Non-displaced, non-angulated fracture c. Non-displaced, angulated fracture d. A fracture that is angulated and displaced e. A fracture that is displaced but not angulated 2. The most appropriate management would be: a. Refer to the emergency room b. Refer to surgery for open reduction and internal fixation c. Place into figure of eight splint for now d. Place right arm in sling for comfort

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Figure 1: Case 1 - Right shoulder x-ray

4. This injury and the subsequent result will likely result in: a. Gradually worsening arthritis of the R shoulder. b. A subtle but discernible loss of strength for the right arm. c. A cosmetic deformity leading to avoidance of evening gowns. d. Full return to work and with no restrictions. e. Full return to work with no restrictions but an annoying cosmetic deformity.

Case 2 A 57-year-old Latino construction worker fell one week ago and reports continuing pain despite daily massage therapy by “huesero” who provides services for orthopedic injuries. He has not been getting better and wishes to return to work as soon as possible. His past medical history is unremarkable, and his neurovascular examination is normal. He has limited range of motion of his right shoulder. 3. Below is an image (Figure 2) of the same patient taken nine months later. She reports no symptoms relating to the right arm and shoulder. Based on this image, the best choice below would be:

Figure 3: Right shoulder x-ray

a. An operation was performed and the result is satisfactory b. An operation was performed but the result was not satisfactory c. No operation was performed and the result is satisfactory d. No operation was performed and the result is not satisfactory Figure 2: Case 1 - Follow-up x-ray

1. Upon obtaining this radiograph, what is your diagnosis? a. Type II (lateral third) displaced, angulated, comminuted fracture. b. Type I (mid-shaft) displaced, angulated, comminuted fracture. c. Type III (medial third) non-displaced, non-angulated, comminuted fracture. d. Type I non-displaced, angulated, comminuted fracture. 2. After diagnosis, what would be most appropriate? a. Panic, send patient to emergency room and refer to orthopedics. b. Have him schedule another appointment with a different huesero. c. Give patient pain medication and a work excuse for Orthopedic Issues in Family & Emergency Medicine

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three weeks and have him follow up in the office. d. Put the patient in a figure-8 brace and advise no lifting for six weeks. 3. With conservative management, what is the likelihood of a good result for this patient? (Good meaning bone union, resolution of pain, without gross deficit in function or cosmetic abnormality) a. 73%

1. Upon obtaining this radiograph (Figure 4), is there anything wrong with this picture? a. No, this is a normal infant X-ray. b. Yes, non-displaced, non-angulated fracture. c. Yes, displaced, angulated fracture. d. Yes, displaced, non-angulated fracture. Figure 5: Baby will not move arm – second view

b. 27% c. 0% d. 50% 4. Which case of clavicular fracture must be considered for surgical consult? a. Simple fracture with severe pain and deformity b. Patient has neurovascular compromise c. Angulated fracture d. Comminuted fracture 5. When can wearing the figure-8 brace be discontinued? a. When the patient gets tired of wearing it. b. When the patient no longer experiences pain, and there is no palpable fracture motion when scapula is retracted or elevated.

2. After obtaining your diagnosis, what would be appropriate?

c. Only after six weeks and a satisfactory follow-up film is obtained.

a. Panic and call the orthopedic resident.

d. After one year.

c. Apologize to the family for causing this very rare and dangerous event during delivery.

Case 3: (Figures 4 and 5) This four-day-old baby will not move his arm. He was a term delivery with Apgars of 8 and 9. His birth weight was reported to be 9 pounds 7 ounces. He is feeding normally. His vital signs are normal, and the only physical finding is a limited use of the right arm. Figure 4: Baby will not move arm - first view

b. Put the child in an infant-sized figure-8 brace.

d. Reassure the family that this is a common complication of vaginal delivery and that the child will do fine. 3. Which treatment is appropriate for this child? a. Attempt closed reduction of the fracture. b. Obtain written consent from family for open reduction internal fixation (ORIF) surgical procedure. c. Do nothing. d. Put the patient in a body cast. 4. If the patient seems to be in significant discomfort, what can be done? a. Give the infant pain medicine and a referral to Ortho. b. Place child in figure-8 splint for one week and lay the child on his back. c. Immobilize the ipsilateral arm by safety-pinning the long shirtsleeve to the shirt (for 7-10 days) and counsel parents to avoid unnecessary movement of extremity. d. Nothing.

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5. What is a key element in the treatment of this patient?

b. Massage therapy c. Therapeutic ultrasound

a. Reprimanding the physician who broke the patient’s clavicle during delivery. b. Apologizing to family for this rare complication that should have never happened. c. Tell the parents that their child will require a longer hospital stay to monitor his progress.

d. Forward elevation, and external rotation stretches of affected extremity while supine. Figure 7: Nine months later, the 17-year-old returns for evaluation of a groin abscess

d. Reassure the parents that their child will be fine and that they will notice a bump over the broken bone that will heal and go away in about six months.

Case 4: (Figures 6 and 7) A 17-year-old boy falls and experiences immediate pain in his left shoulder. Normally, a pediatrician sees him, but they do not have radiology services. He has been sent to the ER but comes to Medicos instead. His past medical history is unremarkable, and his vital signs are normal. His physical examination is normal except for pain in the area of the left shoulder and limited range of motions secondary to pain.

4. Based on the information available in Figure 7, the physician would conclude which one of the following.

Figure 6: Left shoulder

a. Unsatisfactory result with loss of function. b. Satisfactory healing with normal function and strength. c. Painful malunion in need of surgical correction. d. Malunion requiring figure-8 brace. 5. Which immobilization technique for clavicle fracture is best? a. Figure-8 brace b. Sling c. Sling and swathe

1. Based on the information available in Figure 6, the physician concludes: a. Non-displaced, angulated oblique fracture. b. Displaced, angulated, spiral fracture. c. Displaced, angulated, transverse fracture. d. Displaced, angulated torus fracture. 2. For this young man, which conservative measure would be appropriate? a. Send patient on to emergency room.

d. All are adequate; there is no evidence supporting one form as superior. Benjamin A. Jones is a medical student, Year Two, University of Tennessee College of Medicine, Memphis. Roberto R.Gonzalez, MD, is a Fellow, Surgical Family Medicine Obstetrics, and Medicos para la Familia, Memphis. Potential Financial Conflicts of Interest: By AJCM policy, all authors are required to disclose any and all commercial, financial, and other relationships in any way related to the subject of this article that might create any potential conflict of interest. The author has stated that no such relationships exist. ®

b. Set up referral for orthopedics. c. Put patient in an arm sling and have him follow up in two weeks. d. Put the patient on bed rest for three weeks. 3. As part of recovery, which therapy is recommended for this fracture? a. Lightweight shoulder raise while standing.

Bibliography 1.

Rodney WM. Forward in Pfenningere JL, Fowler GC. Procedures for Primary Care Physicians. Mosby, St. Louis, 1994. New edition 2002.

2.

Hatch RL, Rosenbaum CI. Fracture care by family physicians: A review of 295 cases. J Fam Pract. 1994;38:238-244.

3.

Warren JS, Lara K, Hahn RG. Correlation of emergency department radiographs: results of a quality assurance review in an urban community hospital. J Am Board Fam Pract. 1993;6:255-9.

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Answer Key

4.

Halvorsen JG, Kunian A, Gjerdingen D, et al. The interpretation of office radiographs by family physicians. J Fam Pract. 1989;28:426-432.

5.

Simon HK, Khan NS, Nordenberg DF, Wright JA. Pediatric emergency physician interpretation of plain radiographs: Is routine review by a radiologist necessary and cost-effective? Ann Emerg Med. 1996;27:295298.

Case 1:

6.

Smith P, Temte J, Beasley J, Mundt M. Radiographs in the Office: is a second reading always needed? J Am Board Fam Prac. 2004;17:256-263.

3-c

7.

Nordqvist A, Petersson CJ, Redlund-Johnell I. Mid-clavicle Fractures in Adults: End Result Study After Conservative Treatment. Journal of Orthopaedic Trauma. 1998;12(8),572-576.

8.

Pujalte GGA, Housner JA. Management of Clavicle Fractures. Current Sports Medicine Reports. 2008(September/October);7(5),275-280.

9.

Stefanos Lazarides, MD, and George Zafiropoulos MD, MPhil. Conservative treatment of fractures at the middle third of the clavicle: The relevance of shortening and clinical outcome. Journal of Shoulder and Elbow Surgery. Mar-Apr 2006;15(2),191-194.

Recommended Reading 1.

Beaty JH, Kasser Jr (eds.). Rockwood and Wilkins’ Fractures in Children. 5th Edition. Philadelphia: Lippincott Williams & Wilkins. 2001. ISBN 0781725097. Pages 757-765.

2.

Rockwood CA Jr., Green DP, Bucholz RW (eds.). Fractures in adults. 3rd edition. Philadelphia: Lippincott. 2001. ISBN 0397512309 (v.1). pp 10411074.

3.

Resnick D. Bone and Joint Imaging. 2nd edition. Philadelphia: W.B. Saunders. 1996. ISBN 0721660436. pp 761-762.

4.

Muller NL, Silva CIS (eds.). Imaging of the Chest. 1st edition. Saunders Elsevier. 2008. ISBN 978-1-4160-4048-4.

5.

Connolly JR. Fractures and Dislocations – Closed Management. WB Saunders. 1984. Two volumes. ISBN 0-7216-2601-7.

6.

Greens WB (ed.). Essentials of Musculoskeletal Care. 2nd edition. American Academy of Orthopedic Surgeons. 2001. ISBN 0-89203-217-0.

Recommended Websites Procedural Skills and Office Technology. Senior Editor Wm. Rodney. www.psot.com www.learningradiology.com.

1-e 2-c 4-d Case 2: 1-b 2-d 3-a Explanation: Nordqvist and colleagues found that 62/85 cases of comminuted Type I fractures had a good outcome with conservative measures.7 4-b 5-b Case 3: 1-d 2-d Explanation: Type I fractures account for 90% of all obstetrical fractures and occur in 1-13% of all vaginal deliveries. 3-c 4-c 5-d Case 4: 1-c 2-c 3-d Explanation: Rockwood and Green give these exercises as helpful rehab activities. 4-b 5-d Explanation: Pujalte and colleagues state that there is not enough evidence to deem one method best for immobilization.8

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