Modern Resident - The newsletter of AAEM/RSA
October/November 2015
Volume 8: Issue 1 | Facebook  Twitter  LinkedIn

Inside This Issue

 

Abdominal Pain after Bariatric Surgery
Danielle Goodrich, MD
Stanford/Kaiser Emergency Medicine

With the current obesity epidemic, bariatric surgery rates have dramatically increased with an estimated 200,000 procedures performed each year in the United States.1 We are likely to be treating these bariatric surgery patients in the emergency department, since as many as 20 percent of patients are admitted for a postoperative complication within a year of the operation and up to 40 percent within three years.2 This article will review bariatric procedures and common abdominal complaints post-procedure.

Procedure Types
Roux-en-Y gastric bypass, the most common type of bariatric surgery in the United States, creates a gastric pouch from the proximal aspect of the lesser curvature of the stomach and connects it to the distal end of the small bowel.2 This procedure results in both restrictive and malabsorptive processes. The second most common bariatric procedure is adjustable gastric banding. Gastric banding involves an adjustable device that is secured, typically laparoscopically, around the upper portion of the stomach connecting to a port underneath the skin. This restrictive process is adjustable by injecting saline into a subcutaneous port. Though less common in the United States, biliopancreatic diversion and duodenal switch and sleeve gastrectomy are procedures that may be seen in the severely obese patient.

Presenting Symptoms and Complaints
Abdominal pain is the primary chief complaint in over half of patients who visit the emergency department within the first three years postoperatively, regardless of procedure type performed.1 Early postoperative complications vary by procedure but can include anastomotic leaks, obstruction, internal hernias, GI bleed, band slippage and wound infections. Esophageal reflux, biliary colic, ulcers, band erosion, strictures and stenosis are more likely to present later in the postoperative period.

Complications
Dumping syndrome is the most common complication, characterized by abdominal pain, cramping, flushing, palpitations, tachycardia and hypotension.2 It is caused by the rapid emptying of a hypertonic carbohydrate load into the small bowel. Early dumping syndrome occurs within the first hour after a meal. Late dumping occurs one to three hours after eating and may result in a rebound hypoglycemia from the rapid absorption of glucose triggering an exaggerated insulin release. The effects are self-limited and often improve with a change in diet.

Biliary colic is a well-documented cause of abdominal pain after bariatric surgery. Extreme weight loss after surgery is thought to contribute to bile lithogenicity and subsequently cholelithiasis. Since rapid weight loss occurs primarily in the first year, patients are more likely to present in the first year with symptoms of biliary colic.3

Internal hernias and obstructions may present similarly and are often difficult to diagnose as patients present with nonspecific symptoms including abdominal pain, cramping, nausea and vomiting. These patients often require CT or upper GI series for diagnosis. A nasogastric tube should not be placed without consultation from a bariatric surgeon, as it may perforate the gastric pouch, especially in the early postoperative period.2

Consider the broad differential in a bariatric surgery patient who presents with abdominal pain.

References:

  1. Greenstein AJ, and O'rourke RW. Abdominal pain after gastric bypass: Suspects and solutions. The American Journal of Surgery 201.6 (2011): 819-27. Web.
  2. Adams J. Complications of bariatric surgery. Emergency Medicine: Clinical Essentials. 2nd ed. Philadelphia, PA: Elsevier/Saunders, 2013. 390-97. Print.
  3. Abell TL, and Minocha A. Gastrointestinal complications of bariatric surgery: Diagnosis and therapy. The American Journal of the Medical Sciences 331.4 (2006): 214-18. Web.

A Novel Method of Active Intra-Thoracic Lavage during Cold Exposure Resuscitation in the Emergency Department
Gregory M. Apel, MD
Northwestern Memorial Hospital

Prolonged cold exposure, either through submersion/drowning or freezing ambient temperatures, results in significant pathophysiologic multi-system injury. From local tissue damage to significant dysrhythmias to cardiac arrest, the spectrum of cold injury is broad. As emergency physicians, we are at the forefront of resuscitation in cold related injuries. There are a multitude of techniques in active rewarming of a patient, obviously depending on the extent of tissue exposed and the associated core body temperature. When the injury supersedes simple frostnip/frostbite and results in profound hypothermia with resultant cardiopulmonary collapse, simple passive rewarming techniques including bear hugger devices, packing the axilla/groin (i.e. points of high vascular bundles) and warmed peripheral intravenous fluids fail to quickly and efficiently raise core body temperature. This is when active rewarming techniques come into play. Examples include bladder lavage, intra-thoracic fluid administration, dialysis/CVVH and even VA/VV ECMO. Depending on your institutional policies/practices along with the case scenario at hand, your emergency department approach to active rewarming will vary accordingly.

Traditionally, the practice of intra-thoracic lavage with warmed IV fluids has necessitated placement of bilateral anterior and posterior chest thoracostomy tubes- one for rapid, continuous IV fluid administration and the other for passive drainage of the cavity. This universally results in a very messy, often leaky infusion, with the body becoming drenched in fluid that can in turn make continuous CPR and subsequent defibrillation quite difficult, if not outright dangerous.

During a recent cold water drowning and resuscitation, our ED team utilized a novel method of intra-thoracic lavage, which obviates the need for the anterior chest tube and its associated complications. Instead of the anteriorly placed chest tube, we utilized a central line cordis, placed anteriorly in the second or third intercostal space under catheter over wire technique. This is done similarly to a cordis placement in the internal jugular or subclavian vein, except without the anticipated bloody return. It is a procedure that can be done extremely rapidly compared to chest tube placement, has little to no risk of cardiac/lung parenchyma injury when used with the angiocath and has the distinct advantage of having an actual attachment to IV tubing to facilitate clean, rapid lavage.

This is obviously a novel technique and has no evidence-based improvement in outcomes. But, it is one with little downside and one that facilitates continuous cardiopulmonary resuscitation and controlled re-warming for the severely ill cold exposure patient.


Prehospital Naloxone Use: Does Route of Administration Matter?
Kaitlin Fries, DO
Doctors Hospital

Drug overdose is a major public health problem in the United States and has increased dramatically over the past decade. As of 2011, unintentional overdoses surpassed automobile accidents as the number one cause of accidental death in the United States.1 Prescription opioids are largely to blame for this epidemic as they were responsible for approximately half of the 40,000 drug overdose deaths reported by the Center for Disease Control in 2010.2 Public health policy has ramped up efforts to combat opioid misuse in the past few years by increasing health care personnels’ understanding of opioid prescribing guidelines. In addition, statewide prescription narcotic drug monitoring programs have allowed physicians to better identify those patients trying to abuse the system. However, despite increased efforts, the number of patients overdosing on opiates each year still continues to rise.

In response to the increase in opioid overdoses, the use of naloxone (Narcan©) has become more widespread. Naloxone works as a competitive antagonist at the mu-opioid receptor and is known for reversing the significant respiratory and mental status depression that is seen in those who have overdosed on opioids.3 This opioid antidote has been approved by the U.S. Food and Drug Administration since 1971 and has generally no effect unless opiates have been ingested.2 It can safely be administered via numerous different routes including intravenous, intramuscular, subcutaneous, endotracheal, sublingual, inhaled and intranasally.4 However, intravenous has been the preferred route due to its quicker onset of action.

It has become common practice for emergency medical services to administer Naloxone to patients prehospital in order to buy time and improve outcomes in those patients overdosing on opioids. Due to the increasing number of overdose deaths, many states allow first responders such as firefighters and police officers to administer the antidote as well. With an increasing number of prehospital personnel having access to naloxone, numerous studies have been done to look at routes of administration. While studies show that intravenous (IV) and intramuscular (IM) routes have a quicker onset of action, there are additional challenges faced with the IV route. IV administration requires placement of an IV catheter, which can be challenging in the prehospital setting, especially in IV drug abusers.2,3 Also, IV and IM administration increases the provider’s risk of needle sticks in a population of patients who have high rates of bloodborne pathogens.2,3 Studies have shown that IV administration of naloxone has a faster onset. However, when the amount of time it takes to obtain IV access is considered, time to medication onset is actually equal to those of needless forms of administration. From time of patient contact to naloxone response, there was no significant difference between IM and IV administration (20.3 min vs. 20.7 min, p=0.9).2

Studies have also compared IM and intranasal (IN) naloxone use, as IN provides responders a quick alternative not requiring the use of needles. IM response time was faster (6 min vs. 8 min) when comparing time until respirations were greater than ten per minute.2 However, when looking at time to Glascow Coma Scale of greater than eleven, there was no statistical difference between the two routes.2,3 The main difference between the IM and IN routes was the increased need for additional rescue doses in the IN patients (13% IM and 26% IN).2 Another benefit of the IN route is that it can be safely used by a layperson without training in an emergency situation.

In conclusion, IN naloxone provides prehospital personnel a safe route of administrating an opioid reversal agent without compromising its effectiveness.

References:

  1. Mack K. Drug-induced deaths - United States, 1999-2010. MMWR. 2013. 62 (03): 161-163.
  2. Wermeling D. Review of naloxone safety for opioid overdose: practical considerations for new technology and expanded public access. Ther Adv Drug Sar. 2015. 6: 20-31.
  3. Robertson T, Hendey G, Stroh G ,and Shalit M. Intranasal naloxone is a viable alternative to intravenous naloxone for prehospital narcotic overdose. Prehosp Emerg Care. 2009. 13:412-515.
  4. Weber J, Tataris K, Hoffman J, Aks S, and Mycyk M. Can nebulized naloxone be used safely and effectively by emergency medical services for suspected opioid overdose? Prehosp Emerg Care. 2012. 16:289-292.
  5. Robertson T, Hendey G, Stroh G and Shalit M. Intranasal naloxone is a viable alternative to intravenous naloxone for prehospital narcotic overdose. Prehosp Emerg Care. 2009. 13:412-515.
  6. Davis C, Southwell J, Niehaus V, Walley A, Dailey M. Emergency medical services naloxone access: a national systemic legal review. Acad Emerg Med. 2014. 21:1173-1177.

Board Review: Peritonsillar Abscess
Sophia Johnson, DO
Conemaugh Memorial Medical Center

A peritonsillar abscess (PTA) occurs when the weber glands, which are superior to the tonsils in the soft palate, become inflamed. Cellulitis develops, leading to further inflammation and abscess formation. Risk factors include smoking, poor dentition, chronic tonsillitis, previous PTA and multiple uses of oral antibiotics. Although it can occur at any age, PTA is most often seen in young adults.1 It can be difficult to differentiate from peritonsillar cellulitis.2

Patients with PTA are often toxic in appearance and complain of fever, chills, fatigue, severe sore throat, voice change, difficulty swallowing and painful swallowing. On physical exam, they may exhibit trismus, drooling, tender cervical lymphadenopathy, torticollis and a “hot potato” voice.1,2 Visual examination of the oropharynx reveals a bulging tonsil with deviation of the uvula away from the tonsil.2 Diagnosis can often be made by history and physical exam alone, but needle aspiration, CT or intraoral ultrasound can help when the diagnosis is unclear.1

Treatment is commonly needle aspiration, which treats over 90% of patients effectively. Extreme caution needs to be taken with aspiration, as the internal carotid artery is posterior and lateral to the posterior edge of the tonsil. To aid in avoiding the internal carotid artery, the needle should not penetrate more than 1cm.1 The aspirated material should be sent for gram stain and culture.2 Other less common treatment options are incision and drainage or immediate tonsillectomy.1

PTAs are usually polymicrobial. In patients who do not appear toxic, outpatient management is often attempted after aspiration or incision and drainage, in conjunction with oral antibiotics.2 A 10-day course of antibiotics, such as amoxicillin/clavulanic acid, penicillin VK or clindamycin, along with a single intravenous dose of a potent steroid is also recommended. All patients require follow up within 24 hours.1

References:

  1. Shah RN, Cannon TY, and Shores CG. Infections and disorders of the neck and upper airway. In: Tintinalli JE, Stapczynski J, Ma O, Cline DM, Cydulka RK, Meckler GD, et al.eds. Tintinalli's Emergency Medicine: A Comprehensive Study Guide. New York, NY: McGraw-Hill; 2011. http://accessemergencymedicine.mhmedical.com/content.aspx?bookid=693&Sectionid=45915592. Accessed September 21, 2015.
  2. Gunn JD, III. Stridor and drooling. In: Tintinalli JE, Stapczynski J, Ma O, Cline DM, Cydulka RK, Meckler GD, et al.eds. Tintinalli's Emergency Medicine: A Comprehensive Study Guide. New York, NY: McGraw-Hill; 2011. http://accessemergencymedicine.mhmedical.com/content.aspx?bookid=693&Sectionid=45915457. Accessed September 21, 2015.

Case Presentation: A Vomiting Infant
Phillip Fry, OMSIV
Midwestern University-Arizona College of Osteopathic Medicine

A mother brings her five-week-old male infant to the emergency department for increased fussiness and vomiting for the past two weeks. The patient was seen a week earlier in the emergency department for the same symptoms and was discharged on ranitidine with a diagnosis of colic. Since then, the infant has had increased fussiness and gagging events followed by forceful vomiting after feedings. The mother also noted decreased wet diapers, but denies any fevers, cough, decreased appetite or lethargy of the infant. The patient was born at term via vaginal delivery without complication and is being breastfed.

Vitals include a blood pressure of 88/62, a temperature of 98.6° F, a heart rate of 134 and respiration rate of 34. The child weighs 4.6kg, up from 4.3kg at his previous visit. The general appearance of the infant is non-toxic, although he is lying on the bed gagging infrequently. His mucus membranes are moist and the fontanelles are open and flat. Heart has regular rate and rhythm without murmur and lungs are clear to auscultation in all fields without crackles, wheezing or rhonchi. Abdominal exam reveals no masses and bowel sounds are present.

What imaging modality should one obtain in the emergency department to help make the diagnosis?
A. Abdominal X-ray
B. CT Abdomen and Pelvis
C. Upper gastrointestinal contrast study
D. Abdominal ultrasound
E. A diagnosis can be made without imaging

Answer: D

This infant is presenting to the emergency department with infantile hypertrophic pyloric stenosis, or IHPS. The increasingly forceful nature of vomiting along with the infant’s age and sex suggest imaging and lab work should be obtained. While this infant does not have the classic “olive” and peristaltic waves on physical exam, the lack of findings do not rule out pyloric stenosis. Due to the mean age at diagnosis of IHPS becoming younger and younger (diagnosed at 3.4 weeks as of 1995), the classic physical findings are not as pronounced.1 One study even suggested that a hypertrophied pylorus was only palpable in 50 percent of infants with IHPS, thus limiting the sensitivity of abnormal exam findings.2

The imaging modality of choice is an abdominal ultrasound. In experienced hands, the sensitivity and specificity of ultrasonography for IHPS are above 95 percent.3 An abdominal X-ray will not reveal the diagnosis and involves radiation. A CT scan also exposes the infant to a great deal of radiation and should thus be avoided. An upper gastrointestinal study with barium contrast may be used if physical exam and ultrasound fail to confirm IHPS and the clinician has a strong suspicion for the disease process.4 However, this study involves radiation as well, and is less likely to be available in the emergency department. A diagnosis of IHPS without any obvious physical findings in this setting would be inappropriate.

References:

  1. Breaux CW Jr, Georgeson KE, Royal SA, and Curnow AJ. The changing patterns in the diagnosis of hypertrophic pyloric stenosis. Pediatrics. 1988; 81(2):213.
  2. Godbole P, Sprigg A, Dickson JA, and Lin PC. Ultrasound compared with clinical examination in infantile hypertrophic pyloric stenosis. Arch Dis Child. 1996; 75(4):335.
  3. White MC, Langer JC, Don S, and DeBaun MR. Sensitivity and cost minimization analysis of radiology versus olive palpation for the diagnosis of hypertrophic pyloric stenosis. J Pediatric Surg. 1998; 33(6):913.
  4. Mandell GA, Wolfson PJ, Adkins ES, et al. Pediatrics. 1999; 103:1198.


Cocaine Associated Chest Pain
Erica Schramm, MSIV
Cooper Medical School of Rowan University

Cocaine is a drug notorious for causing severe and potentially fatal cardiovascular events. Cocaine is the second most popular illegal drug in the United States, with approximately 14.7 percent of the population 12 years and older admitting to trying cocaine at least once in their lifetime.1 Demographic studies of cocaine use in America have shown that males 18-25 years comprise the majority of cocaine users.2 Due to widespread use and high complication potential, it is not surprising that cocaine is also the most common illegal drug to precipitate an emergency department visit in the United States.1 Chest pain is the number one cocaine associated presenting complaint, comprising approximately 40 percent of cocaine associated ED visits. Of those patients presenting with cocaine associated chest pain, an estimated 0.7-6 percent are found to have a cocaine related acute myocardial infarction.2

Cocaine has multiple cardiovascular effects that contribute to the potential for myocardial ischemia or infarction. The sympathomimetic effects of cocaine increase heart rate, blood pressure and contractility — all leading to increased myocardial oxygen demand and shear stress. Cocaine directly causes coronary artery vasoconstriction via alpha agonist effects, leading to decreased myocardial oxygenation. Vasoconstriction is even more pronounced in patients with concurrent underlying atherosclerotic disease. Cocaine also leads to increased platelet aggregation. Chronic use has been linked to premature coronary artery atherosclerosis and thrombosis.2 Peak blood levels of the drug are reached faster when smoked as compared to inhaled. Within the first hour after cocaine use, relative risk of MI increases 24 times and most cocaine associated MI’s occur within one to two hours of last use.1

Patients with cocaine associated chest pain may admit to recent cocaine use. Patients often will state that the pain is “pressure-like” and associated with dyspnea, diaphoresis, anxiety, palpitations and nausea. Vital signs will likely show both tachycardia and hypertension. Cocaine metabolites are detectable in urine 24-48 hours after last use.2 EKG findings are nonspecific and may be difficult to interpret. If the patient is young with early repolarization at baseline, the EKG can be easily misinterpreted as an ST elevation MI.1 CK, CK-MB and myoglobin are of little diagnostic value, and should not be relied upon due to high false positive rates.3 Cardiac troponins are the most sensitive and specific serum markers for cocaine associated ACS, thus a patient with a positive troponin should be evaluated for possible MI.2 It is also important to keep in mind that cocaine associated chest pain has multiple potential etiologies other than ACS — including musculoskeletal pain, acute pulmonary syndrome (“crack lung”), myocarditis, aortic dissection, arrhythmia and vasculitis.3

According to 2008 ACC/AHA guidelines for management of cocaine associated chest pain, patients with unequivocal ST elevation MI should undergo immediate reperfusion therapy via primary percutaneous coronary intervention.2,3 Recommended initial management of cocaine chest pain not attributable to ST elevation MI is similar to management of ACS, with two very important exceptions, namely use of benzodiazepines and avoidance of beta blockers. Unlike ACS management, cocaine chest pain patients should be given benzodiazepines IV as an early management strategy. Benzodiazepines may be enough to lower blood pressure and heart rate in cocaine intoxicated patients by simply decreasing anxiety.

As in ACS management, nitrates can be given to manage hypertension as well as counteract coronary artery vasoconstriction caused by cocaine. Aspirin should also be given early, as in ACS management. Unlike ACS management, beta blockers are avoided in cocaine chest pain, as unopposed alpha adrenergic effects may exacerbate coronary artery vasoconstriction caused by cocaine, worsening ischemia. Stable patients with nonspecific EKG changes, elevated troponins or high index of suspicion for cardiac complications should be admitted to a monitored bed for observation.1

References:

  1. Finkel JB and Marhefka GD. Rethinking cocaine-associated chest pain and acute coronary syndromes. Mayo Clin Proc. 2011. Dec; 86(12):1198-207.
  2. McCord J, Jneid H, Hollander J, et al. Management of cocaine-associated chest pain and myocardial infarction: A scientific statement from the American Heart Association Acute Cardiac Care Committee of the Council on Clinical Cardiology. Circulation. 2008. Apr 8;117(14):1897-907.
  3. Houchens N, Czarnik S, and Mack M. How should a patient with cocaine-associated chest pain be treated? The Hospitalist. Apr 2013.

Diascopy
Alexandra Murray, DO
Mercy St. Vincent Medical Center Emergency Medicine Residency

Rashes and skin lesions are oftentimes a challenge to diagnose and treat in the emergency department. Many dermatological diseases have similar presentations and biopsies can take days to yield any type of useful information. Fortunately, diascopy is a simple technique that can be used in any medical setting to help narrow down the differential diagnosis. Diascopy is the practice of placing a glass slide or clear material over a skin lesion to determine if the lesion will blanch under pressure. The purpose of this procedure is to empty blood from the superficial vessels to determine if skin redness is due to blood within the vessels or blood that has extravasated into the skin. This technique can help determine whether erythematous lesions are vascular (vasculitis), nonvascular (nevus) or a result of vasodilation.1 Vascular lesions will not blanch under pressure whereas nonvascular and vasodilated lesions will blanch.1-2 Diascopy can also be performed on the tongue, gums or lips to aid in differentiating simple trauma from vasculitic disease.3-4

Vasculitis encompasses a wide range of diseases that all result from inflammation and damage to blood vessels. Some examples of primary vasculitis syndromes that may be encountered in the emergency department include IgA Vasculitis, Polyarteritis Nodosa, Kawasaki Disease and Giant Cell Arteritis.2 Each of these syndromes can present with dermatological manifestations that will not blanch on diascopy.1-2 Furthermore, diascopy can be used to differentiate between urticarial vasculitis versus ordinary urticaria. Most lesions caused by vasculitis have a component of inflammation which can sometimes mask the underlying vessel damage. If diascopy is applied over an area of urticaria for a few seconds, the inflammation can dissipate and reveal an underlying petechia.4

Diascopy can also be used to detect granulomatous disease such as Sarcoidosis, Lupus Vulgaris, Cutaneous Tuberculosis and Granuloma Annulare. Even though these diseases can have nonspecific dermatological manifestations, on diascopy these lesions can have a characteristic opaque to transparent, yellow-brown appearance known as the “apple jelly sign.”6-7

Identifying and determining how to treat erythematous lesions in the emergency department can feel overwhelming. Fortunately, diascopy is a simple and cost effective tool that can help differentiate vasculitis from other dermatologic conditions. This technique is well tolerated by patients and there are virtually no contraindications to performing this test.

References:

  1. McKay M. Office techniques for dermatologic diagnosis. In: Walker HK, Hall WD, Hurst JW, editors. Clinical methods: The history, physical, and laboratory examinations, 3e. Boston: Butterworths; 1990. Chapter 109. Available from: http://www.ncbi.nlm.nih.gov/books/NBK212/
  2. Lawley TJ and Yancey KB. Approach to the patient with a skin disorder. In: Kasper D, Fauci A, Hauser S, Longo D, Jameson J, Loscalzo J. eds. Harrison's Principles of Internal Medicine, 19e. New York, NY: McGraw-Hill; 2015. http://accessmedicine.mhmedical.com.proxy.library.ohiou.edu/content.aspx?bookid=1130&Sectionid=79727116. Accessed September 05, 2015.
  3. Nadeau C and Stoopler E. The clinical value of diascopy. J Can Dent Assoc. 2013; 79:d11
  4. Ganesh C, et al. Lymphangioma circumscriptum in an adult: An unusual oral presentation. J Clin Imaging Sci. 2013 Oct 29; 3:44.
  5. Dahl MV. Clinical pearl: Diascopy helps diagnose urticarial vasculitis. J Am Acad Dermatol. 1994 Mar;30 (3):481-2.
  6. Wolff K, Johnson R, and Saavedra AP. Section 14. The skin in immune, autoimmune, and rheumatic disorders. In: Wolff K, Johnson R, Saavedra AP. eds. Fitzpatrick's Color Atlas and Synopsis of Clinical Dermatology, 7e. New York, NY: McGraw-Hill; 2013. http://accessmedicine.mhmedical.com.proxy.library.ohiou.edu/content.aspx?bookid=682&Sectionid=45130146. Accessed September 05, 2015.
  7. Ömer Ç, et al. A case of generalized lupus vulgaris leading to joint manipulation. J Turk Acad Dermatol. 2013; 7 (4): 1374c2.

Wilderness Medicine: Dermatologic Conditions
Josh Symes, MSIV
Loyola University Chicago Stritch School of Medicine

Some dermatologic conditions or skin manifestations of underlying disease processes encountered in the wilderness are well known. For example, the most common sign of Lyme disease is erythema migrans.1 However, the differential for skin conditions encountered in the wilderness expands beyond erythema migrans, sunburns and mosquito bites. Thankfully the primary strategy for handling skin conditions in the wilderness is simple: avoidance. This is accomplished via sunscreen, protective footwear and clothing, insect repellant and avoidance of causative plants and insects. However, this is not always possible, so when affected, identifying and removing the offending agent is an important step. This can involve washing the affected skin, vacating the area, washing bedding and tick removal.2

Knowing general principles of managing such conditions coupled with medical training can allow one to prepare by including items in a Wilderness Medical Kit. Symptomatic management and wound care of common dermatologic conditions may include corticosteroids, systemic antihistamines, soothing ointments (calamine lotion, Caladryl Clear®, aloe vera, etc.), cool compresses, pain control and wound care. Monitor for and manage complications such as anaphylaxis, airway compromise, ophthalmologic involvement, burn complications, infection and tetanus.2 A few specific dermatologic manifestations pertinent to wilderness medicine will be discussed below.

Spider Bites
True spider bites are much less common than often perceived. In the U.S., spiders with medical implications include black widow spiders, recluse spiders, hobo spiders and tarantulas. Skin manifestations are varied (erythematous macules, papules, wheals, vesicles, cellulitis, pyoderma gangrenosum and cutaneous necrosis).3,4 Treatment includes local wound care and supportive therapy.3 Monitor for systemic symptoms and tissue necrosis and seek appropriate definitive medical care.

Heat Miliaria
Miliaria rubra (also known as “prickly heat”) is a benign pruritic skin eruption that can manifest as papulovesicules, erythematous vesicles and papules frequently beneath tight clothing.5,7 It can often be mistaken as an allergic reaction or insect bites, and is typically seen in infants, but can occur in adults.4 The pathogenesis is related to occlusion of sweat glands during periods of increased perspiration, typically secondary to environmental heat and humidity.5 Treatment involves cooling and drying affected skin, and it may take 7-10 days to resolve.7

Flea Bites
Flea bites manifest as clusters of multiple pruritic erythematous macules and papules, classically “breakfast, lunch and dinner” lesions when clustered in threes.4,6 Bites are generally located on the lower legs, however sleeping outdoors in flea-infested areas can result in bites elsewhere.4 Treatment consists of symptomatic treatment, removal of fleas and vacating the area.2,8

Plant-Induced Dermatitis
Plant-induced dermatitis can occur through Type I Immediate Hypersensitivity or Type IV Delayed Hypersensitivity reactions. The most commonly seen Type IV Delayed Hypersensitivity in the wilderness setting is due to urushiol oil in poison ivy, poison oak and poison sumac. Type IV reactions tend to persist longer than Type I in the absence of treatment. Type I reactions occur anywhere from a few minutes to a few hours after exposure and typically the eruption (linear wheal and flare) is transient, lasting minutes to hours.2 Treatment consists of steroids and/or antihistamines. The patient should be monitored for signs of anaphylaxis, and if the plant was ingested or burned, airway compromise or ophthalmologic involvement.2,6

References:

  1. Shapiro ED. Lyme disease. New England Journal of Medicine. 2014; 370:1724-1731.
  2. Miller DM, Brodell RT, and Herr R. Wilderness dermatology: Prevention, diagnosis, and treatment of skin disease related to the great outdoors. Wilderness & Environmental Medicine. 1996; 7(2):146-169.
  3. Kang JK, Bhate C, and Schwartz RA. Spiders in dermatology. Seminars in cutaneous medicine and surgery. 2014 Sep; 33(3):123-127.
  4. Fleischer Jr AB, et al. Emergency dermatology: A rapid treatment guide. McGraw Hill; 2002. 10:32-35, 80:286-287.
  5. Maj MS, et al. Pruritus, papules, and perspiration. Annals of allergy, asthma & immunology. 2007 Mar; 98:299-302.
  6. Auerbach PS. Wilderness medicine. Mosby; 2001. 32-37:754-895,47:1088-1091.
  7. Craig KS, Way D, and O’Connor N. Environmental illness in athletes. Clinical Sports Medicine. 2005; 24:695-718.
  8. Demain, JG. Papular urticaria and things that bite in the night. Current Allergy and Asthma Reports. 2003 Jul; 3(4):291-303.

Wilderness Medicine Update: Water Disinfection Methods
Linda Sanders, MD
Temple University Hospital

International and wilderness travelers are at a substantial risk of waterborne illness from bacteria, viruses, protozoa and parasites. This risk depends on the number of organisms consumed and the infectious dose of that particular organism.1 The purpose of disinfection is to remove and destroy enough harmful organisms so as to create an acceptably small risk of illness.1,2

Clarification
Clarification is the process of reducing the turbidity of the water, thereby enhancing the efficacy of disinfection. Clarification can be done by sedimentation or coagulation-flocculation and should be followed by a disinfection method.

Sedimentation is accomplished by allowing water to sit for one to three hours, and decanting the top layer. Coagulation-flocculation is a technique in which a chemical substance such as alum is added to water, causing smaller particles to stick together, which are then removed by filtration. In a wilderness setting, baking soda or even fine white ash from a campfire can be substituted for alum, stirred and then agitated for five minutes, allowed to settle and then filtered. There are also commercial tablets which combine coagulation-flocculation with chlorination.1,2

One Step Disinfection Methods
Heating kills all enteric waterborne pathogens. Clarification is unnecessary because it is not compromised by contaminants. Although a temperature as low as 60°C is sufficient, boiling for a minute at any altitude is the standard because it is the most easily recognizable end point without a thermometer.2 Unfortunately, heating requires a fire or portable propane, which are often unavailable.

Portable UV units require battery power, but are effective against all waterborne pathogens. If the water is turbid, this method should be preceded by clarification because particulate matter acts as a shield.3,4

Two Step Disinfection Methods
A multi-barrier approach is recommended if using filtration or halogenation. Hand pump filters remove protozoa and bacteria effectively, though a second method is needed for viruses. The disadvantage with hand pumps is the weight of the filter itself. Furthermore, filters frequently clog, requiring increased pumping pressures, which force microorganisms through the filter.1,2

Halogenation using chlorine or iodine acts by oxidizing cellular structures. It should be preceded by clarification since halogens interact with contaminants, decreasing their effective concentration. The reaction time is slower in cold water, and thus either an increased contact time or a double dose of halogen is recommended. Halogens are not effective against Cryptosporidium or Giardia and should be combined with heat or filtration.1,2,5

References:

  1. Backer, H. Water disinfection for international and wilderness travelers. Travel Medicine. 2002; 34: 355-364.
  2. Backer, HD. Field water disinfection. Auerbach P.S., ed. Wilderness Medicine. 6th Ed. Phialdelphia, PA: Mosby; 2012. 1324-1359.
  3. Abd-Elmaksoud S, Naranjo JE, and Gerba CP. Assessment of a portable handheld UV light device for the disinfection of viruses and bacteria in water. Food Environ Virol. 2013; 5(2): 87-90.
  4. Vilhunen, S., Sarkka, H., and Sillanpaa, M. Ultraviolet light-emitting diodes in water disinfection. Environmental Science and Pollution Research International, 2009; 16 (4): 439-442.
  5. Gerba, CP, Johnson, DC, and Hasan MN. Efficacy of iodine water purification tablets against Cryptosporidium oocysts and Giardia cysts. Wilderness Environ Med. 1997; 8(2): 96-100.

 

Journal Club - Mechanical Versus Manual Chest Compression for Out-of-Hospital Cardiac Arrest (PaRAMeDIC): A Pragmatic, Cluster Randomized Controlled Trial
Jimmy Tam Huy Pham, DO MA MHS and Jemius Lee, DO
Garden City Hospital, Michigan State University

Historically, chest compressions have been delivered manually, but there are many challenges to achieving continuous high quality CPR: adequate compression depth, sufficient training and fatigue, to name a few. Given the challenges in performing human-powered CPR, biotechnology has been working on mechanical devices that would tirelessly deliver accurate chest compressions in virtually any situation. Physio Control’s LUCAS™ Chest Compression System is a mechanical chest compression device that has been designed with the purpose to help improve outcomes of sudden cardiac arrest victims and to improve operations for medical responders.

In March 2015, the Lancet published the results of the prehospital randomized assessment of a mechanical compression device in cardiac arrest (PaRAMeDICS) trial, by Gavin D. Perkins, from University of Warwick, Coventry, UK, and colleagues.1 The PaRAMeDIC study assessed the survival improvement in prehospital LUCAS-2 mechanical CPR from out-of-hospital cardiac arrest as compared to manual compressions.

In this study, a total of 4,471 patients from 418 emergency vehicles were enrolled. Of the 1,652 patients in the LUCAS-2 group, 985 received mechanical chest compressions. The control group included 2,819 patients, with only 11 receiving mechanical chest compressions. All were followed up at three months and 12 months. The primary outcome was 30-day survival.

Results from this study indicated that survival to 30 days (primary outcome) was no different in the LUCAS-2 (6%) vs. control (7%) groups. Utilization of LUCAS-2 demonstrated no significant difference in return of spontaneous circulation (ROSC), survival of event, survival to three months or survival to 12 months as compared to control. A trend towards decreased favorable neurologic outcomes were seen in the LUCAS-2 group as compared to control group

The study concludes that the use of LUCAS-2 in non-traumatic, out-of-hospital cardiac arrests did not show improvement over manual CPR in patient survival to 30 days. Researchers thus neither recommend nor discount the routine use of mechanical CPR devices in cardiac arrest; and suggest that more research is needed to further delineate advantages and disadvantages of mechanical devices such as the LUCAS-2.

References:

  1. Perkins GD. et al. Prehospital randomised assessment of a mechanical compression device in cardiac arrest (PaRAMeDIC) trial protocol. Scandinavian Journal of Trauma, Resuscitation and Emergency Medicine. 2010; 18:58
  2. Perkins GD. et al. Mechanical versus manual chest compression for out-of-hospital cardiac arrest (PARAMEDIC): a pragmatic, cluster randomised controlled trial. Lancet. 2015; 385(9972):947-55.

Your 2015-2016 Leaders:

President
Victoria Weston, MD

Vice President
Michael Gottlieb, MD

Secretary-Treasurer
Nicole Battaglioli, MD

Immediate Past President
Meaghan Mercer, DO

At-Large Board Members
Phillip Dixon, MD
Mary Haas, MD
Nathan Haas, MD
Amy Ho, MD
Megan McKay, MD
Gregory Wanner, DO

Medical Student Council President
Michael Wilk, MSIV

Copy Editor:
Nathan Haas, MD

Managing Editor:
Madeleine Montony, MSM
AAEM/RSA Staff

Modern Resident Contributors

Special thanks to this issue's contributors:
Gregory M. Apel, MD; Kaitlin Fries, DO; Phillip Fry, OMSIV; Danielle Goodrich, MD; Sophia Johnson, DO; Jemius Lee, DO; Alexandra Murray, DO; Jimmy Tam Huy Pham, DO MA MHS; Linda Sanders, MD; Erica Schramm, MSIV; Josh Symes, MSIV

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Articles appearing in Modern Resident are intended for the individual use of AAEM members. Opinions expressed are those of the authors and do not necessarily represent the official views of AAEM/RSA. Articles may not be duplicated or distributed without the explicit permission of AAEM/RSA. Permission is granted in some instances in the interest of public education. Requests for reprints should be directed to AAEM/RSA, 555 East Wells Street, Suite 1100, Milwaukee, WI 53202, Tel (800) 884-2236; Fax: (414) 276-3349, Email: info@aaemrsa.org.

 

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