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Volume 23 • Number 11 In This Issue Lesson 21 Lesson 22 Necrotizing Soft Tissue Infections . . . . . . . . . . . . . . . . . . . . . . . . Page 2 The Drug Box . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Page 8 The LLSA Literature Review . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Page 9 Hyperbaric Therapies . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Page 11 The Critical Image . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Page 21 CME Questions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Page 22 The Critical ECG . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Page 24 Contributors 2009 July H. Edward Seibert, MD, FACEP, and Alexander Fernandez, MD, wrote “Necrotizing Soft Tissue Infections.” Dr. Seibert is an assistant residency director at Thomas Jefferson University Hospital, Department of Emergency Medicine, Philadelphia, Pennsylvania. Dr. Fernandez is chief resident at Thomas Jefferson University Hospital, Department of Emergency Medicine. Amal Mattu, MD, FACEP, reviewed “Necrotizing Soft Tissue Infections.” Dr. Mattu is coordinator of the Emergency Medicine/Internal Medicine Combined Residency Training Program and director of academic development in the Emergency Medicine Residency Training Program at the University of Maryland School of Medicine in Baltimore. Colin G. Kaide, MD, FACEP, UHM, Sorabh Khandelwal, MD, UHM, and S. Erica Brown, MD, wrote “Hyperbaric Therapies.” Dr. Kaide is an associate professor of emergency medicine at Ohio State University Medical Center, Columbus, Ohio. Dr. Khandelwal is an associate professor of emergency medicine and director of hyperbaric medicine at Ohio State University Medical Center. Dr. Brown is a clinical instructor of emergency medicine at Ohio State University Medical Center. Sharon E. Mace, MD, FACEP, reviewed “Hyperbaric Therapies.” Dr. Mace is professor of medicine at the Cleveland Clinic Lerner College of Medicine, Case Western Reserve University, director of the Observation Unit and director of Pediatric Education and Quality Improvement at the Cleveland Clinic Foundation, and faculty for the MetroHealth Medical Center Emergency Medicine Residency Program in Cleveland, Ohio. Frank LoVecchio, DO, MPH, FACEP, reviewed the questions for these lessons. Dr. LoVecchio is research director at the Maricopa Medical Center Emergency Medicine Program and medical director of the Banner Poison Control Center, Phoenix, Arizona, and a professor at Midwestern University/Arizona College of Osteopathic Medicine in Glendale, Arizona. Louis G. Graff IV, MD, FACEP, is Editor-in-Chief of Critical Decisions. Dr. Graff is professor of traumatology and emergency medicine at the University of Connecticut School of Medicine in Farmington, Connecticut. Contributor Disclosures In accordance with ACCME Standards and ACEP policy, contributors to Critical Decisions in Emergency Medicine must disclose the existence of significant financial interests in or relationships with manufacturers of commercial products that might have a direct interest in the subject matter. Authors and editors of these Critical Decisions lessons reported no such interests or relationships. Method of Participation This educational activity consists of two lessons with a posttest and should take approximately 5 hours to complete. To complete this educational activity as designed, the participant should, in order, review the learning objectives, read the lessons, and complete the online posttest. Release date May 1, 2009. Expiration date April 30, 2012. Accreditation Statement The American College of Emergency Physicians (ACEP) is accredited by the Accreditation Council for Continuing Medical Education (ACCME) to provide continuing medical education for physicians. ACEP designates this educational activity for a maximum of 5 AMA PRA Category 1 Credits™. Physicians should only claim credit commensurate with the extent of their participation in the activity. Approved by ACEP for 5 Category I credits. Approved by the American Osteopathic Association for 5 hours of AOA Category 2-B credit (requires passing grade of 70% or better). Target Audience This educational activity has been developed for emergency physicians. Critical Decisions in Emergency Medicine Necrotizing Soft Tissue Infections Lesson 21 H. Edward Seibert, MD, FACEP, and Alexander Fernandez, MD n Objectives On completion of this lesson, you should be able to: 1. Describe the different types of necrotizing soft tissue infection (NSTI). 2. Identify the bacterial causes of NSTI. 3. Discuss the variable clinical presentations of NSTI. 4. Differentiate NSTI from other types of skin and soft tissue infections. 5. Discuss the importance of early surgical intervention in the treatment of NSTI. 6. Identify the appropriate antibiotics for the treatment of NSTI. n From the EM Model 4.0 Cutaneous Disorders 4.4 Infections Emergency department visits for skin and soft tissue infections are common and increasing in frequency. Emergency physicians encounter uncomplicated infections like cellulitis and abscess on a daily basis. Necrotizing soft tissue infections (NSTIs) are an uncommon but lethal subset of these infections. NSTIs are characterized by extensive inflammation, necrosis, and thrombosis involving the dermis, subcutaneous tissue, superficial fascia, deep fascia, or muscle. Necrotizing cellulitis, necrotizing fasciitis, and myonecrosis are more specific terms that denote the level of soft tissue involvement.1,2 Hippocrates described NSTI in the 5th century BC, “...the erysipelas would quickly spread widely in all directions. Flesh, sinews and bones fell away in large quantities... Fever was sometimes present and sometimes absent... There were many deaths. The course of the disease was the same to whatever part of the body it spread.”3 During the Civil War, NSTIs were called “hospital gangrene,” and the term “necrotizing fasciitis” was coined by Wilson in 1952. NSTIs share a common pathophysiology, clinical presentation, and prognosis and, consequently, a common diagnostic approach, treatment, and prognosis.4 Case Presentations n Case One A 50-year-old woman presents to the emergency department with 2 pain in her left groin. She had been recently discharged from the hospital following a cardiac catheterization. The pain began gradually but became progressively more severe over the course of 3 days. She reports a mild fever but denies any other symptoms. Her past medical history is significant for diabetes mellitus, coronary artery disease, and hypertension. Vital signs are blood pressure 110/86, pulse rate 68, respiratory rate 20, and temperature 35.9°C (96.6°F). Physical examination reveals an obese woman in moderate discomfort. She has tenderness to palpation of her right lower quadrant, and a large hematoma is present in her right groin with surrounding erythema. No purulent drainage is noted, but on deep palpation of the site soft tissue crepitus is appreciated. n Case Two A 41-year-old man who speaks no English presents to the emergency department with a chief complaint of redness to his right upper thigh and inability to urinate secondary to extreme pain. Through family members translating, he states that he does not feel like himself. He describes the pain as constant and severe and says that makes it very difficult to sit or lie in a comfortable position. He reports having an oral temperature of 38°C (100.4°F) about 2 days prior to arrival in the emergency department and occasional chills. He denies any past medical history or current medication use. Vital signs are July 2009 • Volume 23 • Number 11 Critical Decisions • When should NSTI be suspected? • How can NSTI be differentiated from other, less life-threatening, soft tissue infections? • What role do radiologic studies have in the diagnosis of NSTI? • What is the treatment for NSTI? blood pressure 107/65, pulse rate 91, respiratory rate 20, and temperature 36.6°C (97.8°F). Physical examination reveals a slender man in obvious distress because of pain. A large area of erythema covers the anterior and medial aspects of his right thigh. Palpation of the affected area reveals warm, tender, erythematous skin, without any signs of crepitus. His genital examination is normal. n Case Three A 55-year-old man with a history of poorly controlled diabetes presents to the emergency department with scrotal swelling and pain that began 3 days ago while he was pushing a car. He rates his pain as a 7 on a scale of 10 and states that it has been constant. He has not taken any medicines for the pain. He denies fever, dysuria, and penile discharge. Vital signs are blood pressure 92/46, pulse rate 128, respiratory rate 16, and temperature 36.9°C (98.5°F). Physical examination reveals a man resting comfortably on his stretcher. His scrotum is swollen and mildly erythematous, with tenderness to palpation diffusely, but greater on the left. No crepitus or fluctuance is palpated. CRITICAL DECISION When should NSTI be suspected? Patient characteristics associated with NSTI include diabetes mellitus, peripheral vascular disease, alcohol abuse, end-stage renal disease, injection drug use, liver cirrhosis, adrenal insufficiency, and cancer. In approximately 15% of cases, however, the patient has no comorbidities.1,5,6 Group A streptococcus, in particular, • What antibiotics are appropriate for the treatment of NSTI, and how has this changed with the emergence of methicillin-resistant Staphylococcus aureus (MRSA)? • What role do adjunct therapies play in the treatment of NSTI? is a cause of NSTI in young, otherwise healthy patients.7 NSTI typically occurs following some sort of break in the skin that allows bacteria to enter the subcutaneous tissue. NSTI can arise at the site of surgical incisions and decubitus ulcers. Often this skin trauma is trivial, though, and NSTI has been described following minor abrasions, contusions, insect bites, subcutaneous insulin injections, and intravenous line placement. NSTI can also occur without any apparent skin defect or preceding event. In one case series, less than half of patients with NSTI had an identifiable portal of entry.5,8 The most common location for NSTI is the lower extremities, although it can affect the upper extremities, head and neck, trunk, and perineum (Fournier gangrene) as well.5,6 With necrotizing fasciitis, the progression of skin findings reflects the underlying pathology of the disease. Bacterial proliferation occurs within the superficial fascia (tissue between the skin and deep fascia overlying the muscles) causing local inflammation. Although not completely understood, it is thought that the bacteria produce enzymes like hyaluronidase, which degrade the fascia and allow infection to spread along fascial planes. This corresponds to the early clinical stage of necrotizing fasciitis, which is characterized by erythema, swelling, warmth, and tenderness. This stage is generally indistinguishable from severe cellulitis except that in necrotizing fasciitis, the tenderness can extend beyond the apparent area of skin involvement. Patients with necrotizing fasciitis can have severe pain that is disproportionate to cutaneous findings. Blood vessels in the superficial fascia become thrombosed resulting in ischemia of the overlying skin. Subsequently, blisters or bullae form in the intermediate clinical stage, where skin fluctuance and induration are also seen. In the late stages of necrotizing fasciitis, advanced liquefactive necrosis leads to the formation of hemorrhagic bullae and dusky discoloration of the skin that can progress to frank gangrene.7,9 In one case series, 100% of patients who presented to the emergency department with hemorrhagic bullae had necrotizing fasciitis.10 Destruction of subcutaneous nerves leads to skin anesthesia (which might precede signs of skin necrosis), and gasforming organisms can be present (in approximately 30% of NSTIs), resulting in crepitus.7,9 Fever is seen in roughly half of patients with NSTI, and hypotension in less than 20%.5 Table 1 summarizes clinical features that should prompt further evaluation or treatment for NSTI. Critical Decision How can NSTI be differentiated from other, less life-threatening soft tissue infections? Sometimes, clinical features alone can make the diagnosis of NSTI, particularly the finding of crepitus in the right clinical setting. More commonly, however, other diagnostic modalities are needed. Clinical features that differentiate NSTI from 3 Critical Decisions in Emergency Medicine more benign soft tissue infections like cellulitis are not always present, and the diagnosis is frequently missed, resulting in delays in treatment. Reported rates of correct diagnosis at the time of admission range from as low as 15% to as high as 60%.1,5,6 The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score is a tool derived from retrospective data to distinguish necrotizing fasciitis from other soft tissue infections (Table 2). In this system, results from the patient’s CBC, serum chemistry, and C-reactive protein (CRP) are given a score depending on a range that the value falls into. The scores are then added together. The score was 6 or higher in more than 90% of the study patients who had necrotizing fasciitis diagnosed retrospectively, and less than 6 in 97% of a group of randomly selected patients with cellulitis that was used as a cohort.11 The LRINEC score is described in multiple review articles but has never been prospectively validated. Because of this, a score less than 6 should not be used to rule out NSTI if it is clinically suspected. There does not seem to be any harm, however, in using a score of 6 or more to justify further evaluation for NSTI. Currently, there are no prospectively validated clinical decision rules for predicting NSTI. Other nonradiologic methods for diagnosing NSTI include frozen Table 1. Clinical features associated with NSTI8,9 Bullae – particularly hemorrhagic bullae Crepitus Rapid spread Severe pain disproportionate to cutaneous findings Skin anesthesia Systemic toxicity Tenderness extending beyond the region of apparent skin involvement 4 section biopsy and the “finger test.” To obtain a frozen section biopsy, a 1-cm3 piece of tissue is excised from the suspected area under local anesthesia and sent to a pathologist for immediate examination. The pathologist then determines whether or not NSTI is present. The “finger test” requires that a 2-cm incision be made down to the level of the deep fascia under local anesthesia, followed by digital probing. Positive test findings include lack of bleeding, murky dishwater pus and minimal tissue resistance to finger dissection.9 These methods of diagnosis would, in most cases, require a surgeon at the bedside to perform the test and, for frozen section biopsy, a willing pathologist. Tissue oxygen monitoring with near-infrared spectroscopy is a noninvasive method to identify NSTI that has shown promising results. Wang and Hung found that tissue oxygen saturation levels less than 70% over the suspected area of infection were 100% sensitive and 97% specific for NSTI. The study included only 19 patients with NSTI, however, and excluded patients with chronic venous stasis, peripheral vascular disease, shock, and systemic hypoxia.9,12 It is also unlikely that many emergency departments have this technology readily available. CRITICAL DECISION What role do radiologic studies have in the diagnosis of NSTI? Radiologic studies should not delay definitive treatment for obvious NSTI. When there is suspicion for NSTI but a paucity of physical examination findings, radiologic studies can actually expedite the diagnosis and subsequent treatment by detecting NSTI in its early stages. Plain radiographs can be performed rapidly, and if they show subcutaneous air in the right clinical setting, no further diagnostic studies are needed. The absence of subcutaneous air does not rule out NSTI, however. In one case series, gas on plain radiographs was only present in 17% of patients with NSTI.5 The “flesh-eating bacteria,” group A -hemolytic streptococci, do not produce subcutaneous air when they are the sole pathogen causing NSTI.7 Plain radiographs and ultrasonography are more sensitive than clinical examination for detecting subcutaneous air, and computed tomography (CT) is more sensitive than plain radiographs.13 Table 2. Laboratory risk indicator for necrotizing fasciitis (LRINEC) score. From: Anaya D, Dellinger EP. Necrotizing soft-tissue infection: diagnosis and management. Clin Infect Dis. 2007;44:706. With permission from The University of Chicago Press. Variable C-reactive protein (mg/L) WBC (per mm3) Hemoglobin (g/dL) Sodium (mmol/L) Creatinine (mg/dL) Glucose (mg/dL) Value >150 < or = 150 <15 15 to 25 >25 >13.5 11 to 13.5 <11 > or = 135 <135 < or = 1.6 >1.6 < or = 180 >180 Score 0 4 0 1 2 0 1 2 0 2 0 2 0 1 July 2009 • Volume 23 • Number 11 Bedside ultrasonography has been used by emergency physicians to diagnose Fournier gangrene (typically a polymicrobial infection). Ultrasonography will demonstrate focal regions of high-amplitude echoes with posterior acoustic shadowing in the presence of subcutaneous gas.14 It has also been used to diagnose NSTI in the upper and lower extremities using the findings of “diffuse thickening of the subcutaneous tissue accompanied by a layer of fluid accumulation more than 4 mm in depth along the deep fascial layer, when compared with the contralateral position on the corresponding normal limb.”15 Even for Fournier gangrene, though, CT probably has greater specificity than ultrasonography and is better for demonstrating the extent of disease involvement.16 In general, the role of ultrasonography in diagnosing NSTI is limited. However, emergency physicians commonly use bedside ultrasonography to evaluate soft tissue infections for drainable fluid collections; the presence of ultrasound findings consistent with subcutaneous gas in this setting should prompt immediate treatment for NSTI. The sensitivity and specificity of CT for NSTI are unclear. As mentioned, CT can detect subcutaneous air better than plain radiographs; it can also demonstrate fascial thickening (a particularly useful finding if the thickening is at least twice that of the contralateral side), fat infiltration or stranding (linear soft tissue attenuation within the fat), and focal fluid collections. For NSTI of the trunk, CT can reveal if the source of infection is intraabdominal. Wysoki et al studied CT characteristics of necrotizing fasciitis in 20 patients with pathologically proven necrotizing fasciitis. Two of these patients had no CT findings to suggest NSTI.13 Magnetic resonance imaging (MRI) is not always an available option to evaluate for NSTI and can be more time consuming than CT, but it is probably the most sensitive study. Schmid et al evaluated the diagnostic value of MRI in differentiating necrotizing fasciitis from cellulitis. MRI examinations performed over 4 years on 17 patients with clinically suspected necrotizing fasciitis were retrospectively reviewed. Final diagnoses were necrotizing fasciitis in 11 patients (proven surgically or at autopsy) and cellulitis in 6 patients. Thickening of the subcutaneous tissue and an increase of signal intensity on T2-weighted images and contrast enhanced T1-weighted images were seen on all 17 patients and, therefore, do not differentiate cellulitis from necrotizing fasciitis. They considered the MRI to be positive for necrotizing fasciitis only if deep fascial involvement could be identified on T2-weighted and contrast-enhanced T1-weighted images. Using these criteria, they identified all 11 cases of necrotizing fasciitis and had one false-positive; conferring a sensitivity of 100% and specificity of 86%.17 Loh et al demonstrated that the specificity of MRI for NSTI is even lower than this. They found that only 1 out of 22 patients with abnormally high signal intensity on T2-weighted images within deep fascial planes and 1 out of 13 patients with gadolinium enhancement of the deep fascial planes had necrotizing fasciitis. Most of the patients had nonnecrotizing cellulitis or abscess.18 Therefore, MRI may be the best test for ruling out NSTI due to its high sensitivity, but can’t be used alone to make the diagnosis. It must be interpreted in the context of the clinical scenario and physical examination. Of note, MRI also tends to overestimate the extent of infection compared to surgical findings.17 The small numbers of patients in even the largest studies evaluating the use of radiologic imaging in suspected NSTI make it difficult to draw definitive conclusions regarding which is best. The decision to use one over another is, therefore, case dependent, with many variables to consider. It is important to remember that the diagnosis of NSTI should be made clinically, when possible, and that radiologic studies should only be ordered if they can be expected to expedite the diagnosis and decrease the time to definitive treatment. Surgical consultation should not be delayed when there is a strong suspicion for NSTI. CRITICAL DECISION What is the treatment for NSTI? The treatments for NSTI are aggressive surgical débridement of all necrotic tissue and intravenous antibiotics. Treatment with antibiotics alone, however, results in a mortality rate approaching 100%, because thrombosed blood vessels prevent antibiotic delivery to the affected area. Delays in surgery and incomplete débridement are associated with increased mortality. Necrotic tissue should be debrided back until healthy, bleeding tissue is seen at the wound margins. In most cases, the patient is brought back to the operating room in 24 to 48 hours for reexploration of the wound and further débridement, if necessary. This process might need to be repeated multiple times. Frequently, large areas of skin must be excised, and patients typically require future skin grafting. Tissue cultures should be obtained to guide antibiotic therapy.4,5,8 CRITICAL DECISION What antibiotics are appropriate for the treatment of NSTI, and how has this changed with the emergence of MRSA? Necrotizing fasciitis has traditionally been divided into two categories based on the bacteria causing the infection. Type 1 necrotizing fasciitis is caused by mixed aerobic and anaerobic bacteria. It tends to begin at the site of surgical incisions, mucosal tears, or where skin breakdown is present in patients with diabetes and peripheral vascular disease. Type 1 necrotizing infections are generally associated with subcutaneous gas. Type 2 necrotizing 5 Critical Decisions in Emergency Medicine fasciitis is caused by group A streptococci, and can occur in young patients without any comorbidities. It has been described following blunt trauma, muscle strain, and chickenpox, as well as after surgery or penetrating skin injury.19 More recent case series have revealed the emergence of MRSA as a cause of NSTI. MRSA was the most common bacteria cultured from patients with NSTI between 2001 and 2006 at a large urban hospital in Texas. In most cases, MRSA was the sole pathogen and thought to be community acquired.20 Case series from hospitals in California and Taiwan have reported similarly high incidences of MRSA in patients with NSTI.6,21 Infectious Diseases Society of America (IDSA) guidelines (from 2005) recommend antibiotic therapy tailored to the specific infection-causing pathogens. For mixed infections (type 1), the IDSA recommends ampicillinsulbactam plus clindamycin and ciprofloxacin. A carbapenem as a single agent is another option. For patients with severe penicillin hypersensitivity, they recommend clindamycin or metronidazole with an aminoglycoside or fluoroquinolone with additional coverage for staphylococcus if that organism is present or suspected. For streptococcus infection (type 2), the IDSA recommends penicillin plus clindamycin.19 Emergency physicians treating NSTI do not typically know the causative organism and must chose antibiotics empirically. These recommendations also do not take into account the high incidence of MRSA in NSTI that has been reported since these guidelines came out. More current recommendations for empiric therapy are to use vancomycin plus clindamycin and piperacillin/tazobactam, or linezolid plus piperacillin/tazobactam. A carbapenem can be used in place of piperacillin/tazobactam. Daptomycin can be used in place of vancomycin. Clindamycin and linezolid are particularly efficacious because of their ability to inhibit bacterial toxin production.2 The use of clindamycin is associated with decreased mortality compared to other antibiotics in the treatment of necrotizing fasciitis caused by group A streptococcus.22 CRITICAL DECISION What role do adjunct therapies play in the treatment of NSTI? Hyperbaric oxygen (HBO2) therapy and intravenous immunoglobulin (IVIG) have also been used as adjunct therapies for treatment of NSTI. There is no convincing evidence that either treatment has any efficacy. HBO2 therapy involves the delivery of oxygen at increased pressure, which can increase the oxygen saturation in infected wounds by a thousand fold, leading to a bactericidal effect and enhanced wound healing. Several retrospective studies have shown no reduction in mortality or in the number of débridements needed with the use of HBO2 therapy.23,24 HBO2 therapy should never be a consideration for the emergency physician involved in the initial care of patients with NSTI. Its only role, if any, is as an adjunct therapy following aggressive débridement. IVIG may be beneficial to patients who have developed streptococcal toxic shock syndrome from group A streptococcal infection.4,7 Figure 1. Transverse (A) and longitudinal (B) magnetic resonance images of the right leg of a 41-year-old man with NSTI caused by group A streptococci (the patient described in Case Two). The arrows point to areas of edema in the muscle, fascia, and subcutaneous tissues. A 6 B July 2009 • Volume 23 • Number 11 Case Resolutions n Case One A surgeon was consulted emergently, and empiric antibiotics were initiated for suspected NSTI. The patient’s WBC count was markedly elevated, and radiographs of the pelvis revealed a large amount of air within the soft tissues extending from the groin into the labia. She was taken to the operating room for excision of a large area of necrotic skin over her abdomen and a vulvectomy performed with the assistance of a gynecologist. The patient continued to receive intravenous antibiotics and returned to the operating room several times for autologous skin grafting. She recovered and was released from the hospital with home wound care after 3 weeks. n Case Two Intravenous antibiotics were initiated for suspected cellulitis. A radiograph of the patient’s thigh and pelvis was normal, with no evidence of subcutaneous air. However, initial laboratory results revealed a WBC count of 25 and a lactate level of 31. Because of the patient’s severe discomfort, which seemed disproportionate to his skin findings on physical examination, an MRI of his lower extremities was obtained to evaluate for NSTI (Figure 1). The MRI with contrast demonstrated severe inflammation affecting the musculature of the medial compartment of the thigh, with severe muscle swelling and muscle edema. Interfascial and marked subcutaneous edema were also seen. The radiologist concluded that these findings were most suggestive of severe infectious myositis, and that necrotizing fasciitis remained possible despite the absence of visible gas on MRI or radiographs performed previously. The patient was taken to the operating room emergently for excision and débridement. The fascia was observed to be grossly swollen and necrotic with pockets of purulence running superiorly and inferiorly on the muscle bellies of the thigh. The fascia was stripped from the involved muscles and debrided back to clean healthy tissue. The patient remained hospitalized for intravenous antibiotics and required multiple reexplorations and débridements for continued spread of the infection. -Hemolytic group A streptococcus was cultured from tissue obtained intraoperatively. He was eventually discharged from the hospital with a wound vacuum device, to return for future skin grafting. n Case Three A urologist was consulted immediately but was in the operating room and unable to evaluate the patient until finished with his case. He questioned the presumptive diagnosis of Fournier gangrene given the lack of physical examination findings and normal temperature and insisted that a testicular ultrasound be ordered to evaluate for testicular torsion, epididymo-orchitis, or scrotal abscess. Ultrasonography revealed marked scrotal skin thickening and gas bubbles within the scrotal wall. The left testis was difficult to visualize because of shadows from the overlying gas. The urologist was notified, and the patient transferred to the operating room where he underwent emergent débridement. He was discharged from the hospital after 10 days with plastic surgery followup for skin grafting. Summary NSTIs are a rare but frequently fatal form of soft tissue infection. The indolent nature of early NSTI and its nonspecific clinical signs in the early stages of infection can considerably delay the diagnosis. Emergency physicians should be aware of this disease and always consider it in the differential diagnosis of an acute cellulitis. When differentiating cellulitis from NSTI, clinical suspicion alone could warrant early surgical evaluation. There are no prospectively validated clinical decision rules for NSTI. The diagnosis of NSTI should be made clinically whenever possible, but in early cases, in which the patient might have severe pain but minimal physical examination findings and normal vital signs, Pearls • Severe pain out of proportion to physical examination findings should raise suspicion for NSTI. • Hemorrhagic bullae, crepitus, and skin anesthesia are very specific but insensitive physical examination findings for NSTI. • NSTI in a young, otherwise healthy patient without significant skin trauma is typically caused by group A streptococcus. • NSTI should be considered in patients with a LRINEC of 6 or greater. • Aggressive surgical débridement is the mainstay of therapy for NSTI. • Clindamycin inhibits bacterial toxin production and is associated with decreased mortality compared to other antibiotics in patients with NSTI caused by group A streptococcus. Pitfalls • Assuming that the absence of subcutaneous gas on plain radiographs rules out NSTI. • Delaying surgical consultation to order radiologic studies when signs of NSTI are obvious on physical examination. • Assuming that absence of fever rules out NSTI. • Not accounting for MRSA when choosing empiric antibiotic therapy for NSTI. 7 Critical Decisions in Emergency Medicine for example, radiologic studies can expedite care. Plain radiographs can be performed quickly but are often negative in patients with NSTI and should never be used to rule out the disease. MRI is the most sensitive radiologic test for NSTI but may not be available, is often time consuming, and is nonspecific. Early and aggressive surgical débridement decreases mortality in NSTI. Intravenous antibiotics have an important role as well, but are ineffective without débridement. Any antibiotic regimen should include clindamycin, which is associated with decreased mortality in patients with NSTI due to group A streptococci. MRSA is now a common pathogen in NSTI, and empiric antibiotic coverage should account for this. References 1. Frazee BW, Fee C, Lynn J, et al. Community-acquired necrotizing soft tissue infections: a review of 122 cases presenting to a single emergency department over 12 years. J Emerg Med. 2008;34:139-146. 2. Abrahamian FM, Talan DA, Moran GJ. Management of skin and soft-tissue infections in the emergency department. Infect Dis Clin North Am. 2008;22:89-116. 3. Descamps V, Aitken J, Lee MG. Hippocrates on necrotising fasciitis. Lancet. 1994;344:556. 4. Anaya D, Dellinger EP. Necrotizing soft-tissue infection: diagnosis and management. Clin Infect Dis. 2007;44:705–710. 5. Wong CH, Chang HC, Pasupathy S, et al. Necrotizing fasciitis: clinical presentation, microbiology, and determinants of mortality. J Bone Joint Surg Am. 2003;85:1454-1460. 6. Hsiao CT, Weng HH, Yuan YD, et al. Predictors of mortality in patients with necrotizing fasciitis. Am J Emerg Med. 2008;26:170-175. 7. Levine EG, Manders SM. Life-threatening necrotizing fasciitis. Clin Dermatol. 2005;23:144-147. 8. Stevens DL, Bisno AL, Chambers HF, et al. Practice guidelines for diagnosis and management of skin and soft-tissue infections. Clin Infect Dis. 2005;41:13731406. 9. Wong CH, Wang YS. The diagnosis of necrotizing fasciitis. Curr Opin Infect Dis. 2005;18:101-106. 10. Hsiao CT, Lin LJ, Shiao CJ, et al. Hemorrhagic bullae are not only skin deep. Am J Emerg Med. 2008;26:316-319. 11. Wong CH, Khin LW, Heng KS, et al. The LRINEC (Laboratory Risk Indicator for Necrotizing Fasciitis) score: a tool for distinguishing necrotizing fasciitis from other soft tissue infections. Crit Care Med. 2004;32:1535-1541. 12. Wang TL, Hung CL. Role of tissue oxygen saturation monitoring in diagnosing necrotizing fasciitis of the lower limbs. Ann Emerg Med. 2004;44:222-228. 13. Wysoki MG, Santora TA, Shah RM, et al. Necrotizing fasciitis: CT characteristics. Radiology. 1997;203:859-863. 14. Morrison D, Blaivas M, Lyon M. Emergency diagnosis of Fournier’s gangrene with bedside ultrasound. Am J Emerg Med. 2005:23;544-547. 15. Yen ZS, Wang HP, Ma HM, et al. Ultrasonographic screening of clinically-suspected necrotizing fasciitis. Acad Emerg Med. 2002;9:1448-1551. 16. Levenson R, Singh AK, Novelline RA. Fournier gangrene: role of imaging. Radiographics. 2008;28:519-528. 8 17. Schmid MR, Kossmann T, Duewell S. Differentiation of necrotizing fasciitis and cellulitis using MR imaging. AJR Am J Roentgenol. 1998;170:615-620. 18. Loh NN, Ch’en IY, Cheung LP, et al. Deep fascial hyperintensity in soft-tissue abnormalities as revealed by T2-weighted MR imaging. AJR Am J Roentgenol. 1997;168:1301-1304. 19. Stevens DL. Necrotizing fasciitis, gas gangrene, myositis and myonecrosis. In: Cohen J, Powderly WG, eds. Infectious Diseases. 2nd ed. St Louis, MO: Elsevier; 2004. 20. Lee TC, Carrick MM, Scott BG, et al. Incidence and clinical characteristics of methicillin-resistant Staphylococcus aureus necrotizing fasciitis in a large urban hospital. Am J Surg. 2007;194:809-813. 21. Miller LG, Perdreau-Remington F, Rieg G, et al. Necrotizing fasciitis caused by community-associated methicillin-resistant Staphylococcus aureus in Los Angeles. N Engl J Med. 2005;352:1445–1453. 22. Kaul R, McGeer A, Low ED, et al. Population-based surveillance for group A streptococcal necrotizing fasciitis: clinical features, prognostic indicators, and microbiologic analysis of seventy-seven cases. Am J Med. 1997;103:18-24. 23. George ME, Rueth NM, Skarda DE, et al. Hyperbaric oxygen does not improve outcome in patients with necrotizing soft tissue infection. Surg Infect (Larchmt). 2008 Nov 8 [Epub ahead of print]. 24. Brown DR, Davis NL, Lepawsky M, et al. A multicenter review of the treatment of major truncal necrotizing infections with and without hyperbaric oxygen therapy. Am J Surg. 1995;169:187-188. The Drug Box Vancomycin By Michelle D Walters, MD; Summa Health System Emergency Medicine Residency The use of the antibiotic vancomycin has become more common as the prevalence of methicillin-resistant Staphylococcus aureus (MRSA) has increased. Vancomycin must be administered slowly to decrease the risk of histamine release (“red man” syndrome), and the dose must be adjusted for patients with renal dysfunction. Use of vancomycin should be avoided in patients with inflammatory bowel disease because it can cause pseudomembranous colitis. Co-administration of aminoglycosides should also be avoided because it increases the risk of ototoxicity. Vancomycin Mechanism of Action Indications Dosing Side Effects Estimated Cost to Hospital and Patienta Contraindication/ Precautions a Binds precursor units of bacterial cell walls inhibiting cell wall synthesis. Inhibits RNA synthesis in gram-positive bacteria Skin infections, pneumonia, bone/joint infections, endocarditis, bacteremia, septicemia, urinary tract infection, and peritonitis Oral treatment of colitis due to Clostridium difficile or Staphylococcus aureus Intravenous: 15 mg/kg every 12 hrs; blood levels must be checked to maintain appropriate intravenous dosing; administer no faster than 10 mg/min to avoid infusion-related reactions Oral: 125-500 mg every 6 hrs for 7-10 days Anaphylaxis; histamine release (flushing, hypotension, tachycardia, wheezing, dyspnea, urticaria, pruritus, muscle spasms, paresthesias); neutropenia; thrombocytopenia; eosinophilia; leukopenia; vasculitis; exfoliative dermatitis; Stevens-Johnson syndrome $4.50 per 1,000 mg PO Contraindicated in patients with known hypersensitivity to vancomycin or corn products; must be renally dosed to decrease ototoxicity and nephrotoxicity; administer slowly, less than 10 mg/min, to avoid histamine release; avoid in patients with irritable bowel disease as this could predispose to pseudomembranous colitis; risk of ototoxicity when administered with aminoglycosides Oral preparation is pregnancy category B; intravenous preparation is pregnancy category C Cost data provided by Summa Health System Pharmacy Feature Editor: Michael S. Beeson, MD, FACEP July 2009 • Volume 23 • Number 11 The LLSA Literature Review “The LLSA Literature Review” summarizes articles from ABEM’s “2010 Lifelong Learning and Self-Assessment Reading List.” Many of these articles are available online in the ACEP LLSA Resource Center (www.acep.org/llsa) and on the ABEM web site. bacterial peritonitis is suggested if the polymorphonuclear cell count is greater than 250 cells/mm3. Article 5 Highlights Paracentesis • Perform paracentesis in patients with new-onset ascites or suspected spontaneous bacterial peritonitis or to alleviate the discomfort of tense ascites. Reviewed by Alisha Perkins Garth, MD, and J. Stephen Bohan, MD, MS, FACEP; Harvard Affiliated Emergency Medicine Residency; Brigham and Women’s Hospital • The incidence of clinically significant bleeding complications is low. Thomsen TW, Shaffer RW, White B, Setnik GS. Paracentesis. New Engl J Med. 2006;355(19):e21. Abdominal paracentesis is indicated for patients with newonset ascites of unclear etiology, for those with suspected spontaneous bacterial peritonitis, and to alleviate discomfort or respiratory compromise in patients with tense ascites. This procedure is contraindicated in patients with disseminated intravascular coagulation. It should be used with caution in patients who are pregnant or who have organomegaly, bowel obstruction, adhesions, or a distended bladder. It should not be done through the site of a skin or soft tissue infection, engorged vessel, surgical scars, or hematoma. Patients can have underlying coagulopathy or thrombocytopenia, but the incidence of significant bleeding complications from paracentesis is low. Routine use of fresh-frozen plasma or platelets is not recommended. To perform the procedure, begin by placing the patient in the supine position with the head of the bed slightly elevated. The recommended sites for needle insertion are 2 cm below the umbilicus in the midline or in the right or left lower quadrant 2 to 4 cm medial and cephalad to the anterior superior iliac spine. Use ultrasonography, if it is available, to mark the appropriate site. Use sterile technique. Anesthetize the area using a 22- or 25-gauge, 1.5-inch needle and 1% to 2% lidocaine. Place a wheal of anesthetic in the epidermis, and then continue along the anticipated trajectory of the catheter injecting anesthetic. Remove the needle and make a small incision at the insertion site to facilitate advancement of the catheter. Insert the catheter device at a 45-degree angle to the skin, and advance it until ascitic fluid returns. Immediately stop advancing the needle and guide the catheter over the needle. Remove the needle, and collect fluid as desired. Place the fluid in specimen tubes and send for analysis. The serum-albumin gradient can be calculated; if it is greater than 1.1 g/dL portal hypertension is indicated. Spontaneous • Use caution when performing paracentesis in patients who have organomegaly, bowel obstruction, adhesions, or distended urinary bladder or who are pregnant. • Recommended needle-insertion sites are 2 cm below the umbilicus or in the right or left lower quadrant 2 to 4 cm medial and cephalad to the anterior superior iliac spine. 9 Critical Decisions in Emergency Medicine The LLSA Literature Review “The LLSA Literature Review” summarizes articles from ABEM’s “2010 Lifelong Learning and Self-Assessment Reading List.” Many of these articles are available online in the ACEP LLSA Resource Center (www.acep.org/llsa) and on the ABEM web site. Article 6 Transient Ischemic Attack: Risk Stratification and Treatment Reviewed by Alisha Perkins Garth, MD, and J. Stephen Bohan, MD, MS, FACEP; Harvard Affiliated Emergency Medicine Residency; Brigham and Women’s Hospital Cucchiara B, Ross M. Transient ischemic attack: risk stratification and treatment. Ann Emerg Med. 52(2):2008;52(2):S27-S39. Evaluation and management of patients with transient ischemic attacks (TIAs) in the emergency department is difficult. Currently, three clinical risk scores have been developed and validated: the ABCD, the California, and the ABCD². All three scores aim to identify patients at high risk for stroke up to 90 days after a TIA. Points are assigned for clinical features, and the sum of the points determines whether the patient fits in a higher-risk group. Clinical factors shown to have predictive value include age older than 60 years, diabetes, symptoms lasting longer than 10 minutes, symptoms of unilateral weakness or speech impairment, and an elevated blood pressure. Validation of these scores has shown them to be helpful to clinicians but not a replacement for clinical judgment. In addition to risk scores, diffusion-weighted magnetic resonance imaging may also be important for risk stratification. Patients who have lesions consistent with cerebral ischemia on imaging are at high-risk. Similarly, patients who have large vessel disease confirmed on vascular imaging are at a higher short-term risk of stroke. Disposition of these patients in the emergency department is challenging, and this review found limited clinical data on the benefit of hospitalization. The best guidelines cited are the 2006 National Stroke Association guidelines, which recommend hospitalization for patients with crescendo symptoms, duration of symptoms for more than 1 hour, symptomatic carotid stenosis greater than 50%, known cardiac embolic source, hypercoagulable state, or an appropriate score from the California or ABCD scores. Treatment options for TIAs include basic supportive care to optimize cerebral blood flow with positioning the head of 10 the bed flat, permissive hypertension, and isotonic fluid administration to maintain intravascular volume. Additionally, once hemorrhage has been excluded antithrombotic therapy with aspirin should be given. Currently there are no data supporting the use of clopidogrel, ticlopidine, heparin, or low-molecular-weight heparin alone or in combination with aspirin in the acute management of TIAs. Long-term prevention and management must, however, be based on the underlying etiology of the cerebrovascular event. Highlights • Patients with high short-term risk of stroke after TIA include older patients and those with hypertension, diabetes, symptom duration more than 10 minutes, and symptoms of weakness or speech impairment. • Magnetic resonance imaging and vascular imaging may be tools to help risk stratify patients with TIA. • Immediate treatment should include positioning the patient with the head of the bed flat, isotonic fluids, permissive hypertension, and aspirin (once hemorrhage has been ruled out by imaging). • Long-term treatment and prevention must be tailored to the individual patient. Critical Decisions in Emergency Medicine Hyperbaric Therapies Lesson 22 Colin G. Kaide, MD, FACEP, UHM; Sorabh Khandelwal, MD, UHM; and Erica Brown, MD n Objectives On completion of this lesson, you should be able to: 1. Illustrate the mechanisms by which hyperbaric oxygen exerts its effect. 2. List the emergency conditions for which hyperbaric oxygen has a role in the treatment process. 3. Identify patients who may benefit from hyperbaric oxygen therapy. 4. Identify conditions that may warrant emergent transfer to a hyperbaric facility. 5. List the contraindications to hyperbaric oxygen therapy. n From the EM Model 6.0 Environmental Disorders 6.2 Dysbarism In 1976, an evidence-guided list of indications for hyperbaric therapy was developed by a multispecialty subcommittee of the Undersea and Hyperbaric Medicine Society (UHMS).1,2 As of the most recent revision of the hyperbaric guidelines (2003), there are 13 conditions for which hyperbaric oxygen therapy has been shown to be an effective treatment modality (Table 1).2 Hyperbaric oxygen (HBO2) therapy involves the exposure of the entire body to 100% oxygen at a pressure greater than one atmosphere absolute (ATA), in either a single-patient hyperbaric chamber (monoplace) or in a larger chamber capable of providing treatment to many patients simultaneously (multiplace chamber). Under normobaric conditions, humans live under the downward pressure exerted by the weight of the atmosphere above. This pressure is usually measured in millimeters of mercury (mm Hg). At sea level, one atmosphere is 760 mm Hg (14.7 lbs/ in2, 760 Torr). In dive medicine, a branch of hyperbaric medicine that deals with scuba diving and other situations involving the breathing of compressed gasses, it is customary to refer to pressure in terms of feet of seawater. One atmosphere is equal to the pressure exerted at a depth of 33 feet (10 meters) of seawater. Under hyperbaric treatment conditions, the body is exposed to pressures that are typically in the range of 2 to 3 ATA—one atmosphere from the earth’s atmosphere plus an additional one to two atmospheres exerted by pressurizing the hyperbaric chamber. All of the physiologic effects of HBO2 are based on the ideal gas laws. The Dalton law states that the total pressure of a mixture of gases is equal to the sum of the partial pressures of each of the individual gases.3,4 The air we breathe is 21% oxygen, 78% of nitrogen and 1% trace gases. The Henry law states that the amount of gas that dissolves in a liquid is proportional to the pressure exerted on the surface of the liquid.3,5 Therefore, as the partial pressure of the gas above a liquid increases, the amount of the gas that dissolves in the liquid also increases. Conversely, when the partial pressure of the gas decreases, dissolved gases will come out of solution and return to the gaseous state. HBO2 therapy capitalizes on the Henry law by significantly increasing the ambient pressure of oxygen, causing a dramatic increase in the amount of dissolved oxygen carried by the blood. As the partial pressure of oxygen reaches 100 mm Hg, hemoglobin becomes fully saturated. Under normobaric conditions, the dissolved oxygen is negligible, representing only 0.3 mL of oxygen per 100 mL of blood (called volumes percent—vol%), compared to 20 vol% carried by hemoglobin. Under hyperbaric conditions the Pao2 at 3 ATA is above 2,200 mm Hg. This is high enough to generate 5.4 vol% of dissolved oxygen, which can sustain basal metabolic functions in the 11 Critical Decisions in Emergency Medicine Critical Decisions • When is HBO2 therapy indicated for acute carbon monoxide (CO) poisoning? • What clinical presentations and signs and symptoms should raise suspicion for air embolism? • What treatments should be undertaken as soon as the diagnosis of air gas embolism is suspected? complete absence of any hemoglobin (Table 2). Hyperoxygenated plasma can transport oxygen to areas that are inaccessible to red cells, delivering oxygen to relatively hypoxic tissues in proportion to the oxygen tension of the plasma. This is especially important in areas of the body that are deprived of blood flow when arteries are blocked by gas bubbles and in tissue that has experienced a hypoxic insult (Table 3). The only absolute contraindications to HBO2 therapy are untreated pneumothorax and concurrent or recent (within 7 days) use of doxorubicin. Relative Table 1. Approved indications for HBO2 therapy2 1. Air embolism 2. Decompression sickness 3. CO poisoning 4. Crush injury, compartment syndrome, and other acute ischemias 5. Exceptional blood loss, anemia 6. Delayed radiation injury (osteo and soft-tissue) 7. Skin grafts and flaps 8. Thermal burns 9. Enhancement of healing in selected problem wounds 10. Necrotizing soft tissue infections 11. Clostridial myositis and myonecrosis (gas gangrene) 12. Osteomyelitis (refractory), includes malignant otitis externa 13. Intracranial abscesses 12 • What signs and symptoms should prompt an emergency physician to consider decompression sickness? • How does the physician distinguish between type I and type II decompression sickness? • What therapies should be initiated in patients with decompression sickness? contraindications are listed in Table 4. They should not preclude the use of HBO2 therapy in emergency situations in which it is considered the primary and possibly only effective treatment modality. Case Presentations n Case One A 28-year-old woman was found with a depressed level of consciousness by her husband upon his return home from work. He called 911, and the woman was transported to the emergency department on highflow oxygen via nonrebreathing face mask. The house was being heated by a wood-burning stove. The patient’s husband states that his wife is 32 weeks pregnant and has no medical problems. Her carboxyhemoglobin (HbCO) level in the emergency department is 30%. n Case Two A 35-year-old woman with a history of Crohn disease presents with complaints of abdominal pain that is typical of a Crohn exacerbation. After multiple attempts at intravenous access, a triple- lumen central venous catheter is placed into the internal jugular vein under ultrasound guidance without complication. Frustrated at the wait for assistance when she calls for help going to the bathroom, she disconnects the catheter from the IV drip, leaving the distal port open to air. Seated on the commode, she breathes deeply to strain for a bowel movement and collapses, falling off the commode. A nearby patient hears the fall and calls for help. The patient is discovered on the floor, cyanotic and with agonal respirations. She is immediately transferred to a resuscitation room. Physical examination findings after the event reveal an unconscious, cyanotic patient in severe distress. Vital signs are blood pressure 60/palpable, heart rate 130, respiratory rate 6, and temperature 36.8°C (98.2°F). The patient’s pupils are mid-position and sluggishly reactive. The lungs are clear bilaterally to auscultation (post-intubation), and heart sounds are obscured by a “churning” sound of the precordium. The abdomen is soft. The extremities show cyanosis with absent pedal Table 2. Oxygen content equation Normobaric Conditions Oxygen content = oxygen carried by hemoglobin + oxygen dissolved in plasma Arterial oxygen content = 1.34 (Hgb)(%Sat) + .003 (Pao2) = 1.34 (15)(100%) + .003 (100) = 20.1 + 0.3 = 20.4 Vol% Hyperbaric conditions—3 ATA Arterial oxygen content = 1.34 (15)(100%) + .003 (2,200) = 20.1 + 6.6 Vol% July 2009 • Volume 23 • Number 11 pulses. A formal neurologic examination is not possible; however the un-paralyzed patient does not make any attempt at movement. The patient is immediately intubated and placed on a ventilator and turned on her left side with her head down in Trendelenburg position. She is given a bolus of normal saline and an arterial line is placed. The presumptive diagnosis of venous air embolism is made, and the emergency physician on call for hyperbaric medicine is immediately contacted. A chest radiograph is unremarkable, and an ECG shows sinus tachycardia with right bundle-branch block. On preliminary evaluation, a computed tomography (CT) scan of the head appears normal (Figure 1). n Case Three A 32-year-old woman presents to the emergency department complaining of progressive lower extremity pain and weakness. She had been in the surgical waiting area of the hospital where her son was having an urgent appendectomy. She states she and her husband had been on a scuba diving trip off the coast of Oregon when she received word that her son was going to have surgery. She and her husband had returned home that same day. The couple had spent most of the past week doing two dives per day, and her last dive was early this morning. She went to a depth of 38 m (125 feet), and owing to what she believed to be a dive computer malfunction, her bottom time could only be estimated at 25 minutes, with a total dive lasting 40 minutes (this exceeds the maximum allowable bottom time). She had a slow ascent and made all the appropriate safety stops. The couple received word about their son’s illness, and they flew home 7 hours after surfacing. She had fainted on the return flight and seemed to be out for 5 minutes. The couple attributed this to stress and declined transport by EMS after landing. She states that during the flight she did have some mild leg pain in addition to her fainting spell. Since landing, she continued to have persistent leg pain. While awaiting the completion of her son’s Table 3. Effects of HBO2 therapy Mechanical Effects of Increased Pressure Reduction in the size and shape of gas bubbles in proportion to the increase in pressure Effects of Increased Partial Pressure of Dissolved Oxygen Delivery of increased amounts of oxygen to tissues Vasoconstriction/edema reduction Increased healing of hypoxic wounds Antimicrobial effects Antibiotic synergism Anti-anaerobic organism effects Enhanced efficacy of leukocyte-mediated killing Reduced production of clostridial alpha toxin Suppression of bacterial growth in hyperoxygenated tissues Toxic oxygen radical modulation Blunting of ischemic-reperfusion injury Antagonizing lipid peroxidation of cellular membranes Generation of reactive oxygen scavengers Bubble size reduction Diffusion of oxygen into mixed gas bubbles procedure, she tried to stand up and said she “almost collapsed because her legs were so weak.” At that time, her husband insisted she come to the emergency department. She is otherwise healthy, and her only medication is a birth control pill. Her physical examination reveals an age-appropriate, anxious woman. Her vital signs are blood pressure 126/74, pulse rate 97, respiratory rate 14, and oral temperature 36.8°C (98.2°F). She has clear, bilateral breath sounds. Heart has a regular rate and rhythm without murmurs, gallops, or rubs. Her skin is without rash, and there is no evidence of subcutaneous emphysema. Her neurologic examination reveals normal cranial nerves and normal Table 4. Relative contraindications to HBO2 therapy* Surgical Procedures A history of recent thoracic surgery Recent retinal repair Reconstructive ear surgery Untreated Conditions Congestive heart failure Severe claustrophobia Uncontrolled high fever Untreated acidosis Severe obstructive lung disease Past Medical Problems History of optic neuritis History of spontaneous pneumothorax Current Medical Conditions Pulmonary lesions on CT scan or chest radiograph Seizure disorder Acute viral infections Congenital spherocytosis Other Presence of hydrocarbon-based ointments and gels on the skin (spontaneous ignition hazard). They can be cleaned off of the skin and this removes the risk *None of these conditions should preclude hyperbaric treatment in an emergency situation, especially if it is the primary or only effective treatment modality 13 Critical Decisions in Emergency Medicine strength in the upper extremities. She has 3/5 strength in her lower extremities bilaterally and is unable to stand. She has decreased sensation in her feet, and 3+ patellar reflexes. Her chest radiograph, laboratory studies, and ECG are essentially normal. Carbon Monoxide Poisoning Carbon monoxide (CO) is the leading cause of poisoning in the United States and the most common cause of injury and death from poisoning in the world.6,7 CO toxicity develops from CO-induced tissue hypoxia and direct CO-mediated cellular damage. Tissue Hypoxia The tissue hypoxia from CO results from its competitive binding of hemoglobin, with an affinity 230 to 270 times stronger than that of oxygen. Additionally, binding of CO to hemoglobin shifts the oxyhemoglobin dissociation curve to the left (Haldane effect) resulting in decreased tissue oxygen delivery and, ultimately, cellular hypoxia. Tissue hypoxia prompts an increase in minute ventilation, which in turn causes a respiratory alkalosis. This further exaggerates the leftward shift Figure 1. Cerebral air on CT. Image courtesy of Colin Kaide, MD. 14 of the oxyhemoglobin dissociation curve, perpetuating a vicious cycle of worsening hypoxia. The deleterious effects of CO are potentiated when CO binds to skeletal and cardiac myoglobin, the affinity of which is three times stronger than that for hemoglobin.8 This increased affinity results in a slow dissociation and delayed release of CO from those tissues. The reintroduction of the dissociated CO into the circulation can cause a deleterious rebound effect when CO again binds to hemoglobin.9 CO poisoning in the fetus involves additional complexities; CO is bound more tightly to fetal hemoglobin than to hemoglobin A. This, in conjunction with the naturally leftward-shifted fetal oxyhemoglobin dissociation curve, intensifies tissue hypoxia in the fetus. The consequence of this physiology is that a CO level that could be nonfatal in an adult can be deadly in a fetus.10,11 Cellular Damage Although tissue hypoxia can explain most of the cardiac and neurologic symptoms commonly seen with acute CO poisoning, additional effects develop as the result of direct CO-mediated cellular damage. Peripheral oxygen utilization and oxidative phosphorylation are hindered because of CO’s interaction with a variety of cellular proteins including myoglobin, cytochromes, and triphosphopyridine nucleotide reductase.12 Tissue perfusion is decreased through several CO-mediated mechanisms including myocardial depression, ventricular arrhythmias, and peripheral vasodilation.13 As tissue perfusion is reestablished, postischemic reperfusion injury, brain lipid peroxidation, and subsequent demyelization of central nervous symptom lipids can develop.14 These CNS effects are mediated mainly by leukocytes.15 Finally, CO-induced oxidative stress on cells can lead to generation of oxygen free radicals that can exacerbate cellular damage.16,17 Clinical Manifestations Acutely, CO leads to injury of the brain, heart, and other organs as manifested by myocardial ischemia, syncope, and metabolic acidosis. A well-recognized syndrome that develops in survivors of severe CO poisoning, delayed neurologic sequelae (DNS), manifests after a latent period of 2 to 21 days and has an incidence that ranges from 12% to 68%. Symptoms include, but are not limited to, memory loss, impairments of concentration and language, parkinsonism, and affective changes such as depression.18 The rationale for the use of HBO2 therapy for CO poisoning has two main principles. First, HBO2 therapy provides a more rapid detoxification than normobaric oxygen (HbCO halflife is 300 minutes at atmospheric conditions, 100 minutes with 100% Fio2, and less than 30 minutes at 3 ATA). Second, it decreases the incidence of DNS. There is good scientific literature available that discusses how hyperbaric oxygen mitigates the mechanisms of CO toxicity.9,10 However, the debate over HBO2 therapy for CO poisoning has been ongoing in the literature for many years, with arguments both in support of and against its use.8,12 The American College of Emergency Physicians’ “Clinical Policy on Critical Issues in the Management of Adult Patients Presenting to the Emergency Department with Carbon Monoxide Poisoning”18 includes two Level C recommendations (Table 5). The authors judge the best study to date is the randomized, controlled trial by Weaver et al, published in 2002.13 This is the only randomized, controlled trial that addresses long-term neurologic sequelae after CO poisoning. It demonstrated a statistically significant reduction in the incidence of DNS measured at 6 weeks, 6 months, and 1 year after treatment. July 2009 • Volume 23 • Number 11 CRITICAL DECISION When is HBO2 therapy indicated for acute CO poisoning? The exact criteria for the use of HBO2 therapy in CO poisoning is still a matter of controversy. It clearly should not be used in everyone with CO poisoning. It makes sense to look at the specific patient population that derived benefit from this therapy in the study by Weaver et al. The UHMS published its current recommendations for the treatment of CO poisoning in 2008 (Table 6). HBO2 therapy should be initiated in those with a loss of consciousness, metabolic acidosis (as defined by a base deficit of more than -2 mmol/ liter), and HbCO of more than 25%.19 Many hyperbaric physicians and toxicologists would also suggest that HBO2 therapy be considered in patients with any neurologic abnormality, patients with evidence of cardiac dysfunction, pregnant women with HbCO levels of more than 15%, patients with unresolved neurologic symptoms despite normobaric oxygen therapy, and patients with neuropsychometric deficits. Given the controversial aspects and indications for HBO2 therapy, it seems reasonable to seek guidance from a hyperbaric physician or a toxicologist who is familiar with the literature and the clinical application of HBO2. Air Embolism Air embolism occurs when bubbles of air are introduced into the circulatory system, either as Table 5. Management of adult patients with CO poisoning18 HBO2 is a therapeutic option for CO-poisoned patients No clinical variables, including HbCO levels, identify a subgroup of CO-poisoned patients for whom HBO2 therapy is most likely to provide benefit or cause harm a consequence of a dive-related accident or as the result of a medical procedure. Iatrogenic introduction of air into the circulatory system represents the most common cause of cerebral arterial gas embolism (CAGE).20 It has occurred in almost all medical specialties and settings including during cardiac bypass, cardiac catheterization, open lung procedures, craniotomy, head and neck surgeries, dialysis, relatively simple procedures such as the placement of a central line,21 and as the result of vaginal insufflation with air in pregnant women during oral sex.22 Air embolism can occur either on the venous side or the arterial side of the circulatory system. Additionally, a paradoxical arterial air embolism can develop when a venous air embolism travels to the arterial system by way of an intra-pulmonary shunt or through a patent foramen ovale. Venous Air Embolism A small venous air embolism or even a large volume of air delivered slowly (30 mL/minute) is likely to be filtered by the pulmonary system and remain asymptomatic.23 Large boluses of air introduced into the venous system all at once are capable of causing a complete obstruction of flow through the heart, resulting in immediate circulatory collapse.24 Between 100 and 300 mL of air is sufficient to cause cardiac arrest, and up to 100 mL per second of air can be injected through a 14-gauge needle.25 The mechanism by which the cardiovascular collapse develops begins with the arrival of the air bolus to into the right ventricle. It may remain in the right ventricle and cause a mechanical obstruction or move distally into the pulmonary vessels causing a progressive increase in pulmonary vascular resistance. This, in turn, leads to a decrease in pulmonary venous return and left ventricular preload. If the obstruction is large enough, cardiac output can drop to a level at which complete cardiovascular collapse could develop.20,24,25 Arterial Air Embolism It is estimated that up to 30% of otherwise healthy patients can have a patent foramen ovale.26 When air from the venous system is present in a large enough quantity, increased pressures in the right ventricular outflow tract can force air from the right side to the left side of the heart via the foramen ovale. Additionally, a massive volume of air delivered to the pulmonary vasculature can force air through other intrapulmonic shunts.20 This movement of venous air to the arterial side is called a paradoxical air embolism. Scuba diving accidents are a significant cause of arterial air embolism. As a scuba diver begins to ascend, the gas in his lungs expands. If the diver continues to breathe in and out during the assent, problems rarely develop. If, on the other hand, the diver takes a breath of air and holds it while Table 6. Indications for HBO2 therapy for acute CO poisoning — recommendations of the UHMS2 Recommended HBO2 therapy regardless of CO levels if: Consider HBO2 therapy if: Transient or prolonged unconsciousness Cardiovascular disfunction Severe metabolic acidosis Duration of exposure to CO is 24 hours or more, even if intermittent HbCO level 25% to 30% Neuropsychological test results are abnormal 15 Critical Decisions in Emergency Medicine continuing to ascend, the air will expand to exceed the maximum lung volume and eventually cause severe lung injury. Injuries can range from pneumothorax and pneumomediastinum to entry of the gas into the pulmonary venous system. This air is then delivered to the left ventricle and ultimately to the rest of the body. The consequences of an arterial gas embolism depend on which organs receive the gas and how well they tolerate an acute vascular occlusion. Muscle, connective tissue, and skin tolerate small emboli well; however, small bubbles of air entering the coronary arteries can precipitate an acute coronary syndrome. When air enters the carotid arteries and ultimately the brain, the symptoms that develop depend on which part of the brain is affected. Symptoms can include motor or sensory problems, confusion and altered mental status, hemiparesis, seizures, and coma.27 As little as 0.5 mL of blood-air foam arriving at the brainstem can be fatal.20 Bubbles produce injury by multiple mechanisms. The first, most obvious problem is acute arterial occlusion. Bubbles also cause damage to the endothelium of blood vessels. This can produce leukocyte activation, release of inflammatory mediators, and activation and aggregation of platelets.20 Additionally, a reperfusiontype injury can develop when the mechanical obstruction caused by the bubbles is relieved. A phenomenon called “no-reflow” can occur in which microvascular perfusion is impaired in the postischemic state. The cause of this is not well understood but is believed to involve factor VIII and an interaction with prostaglandins and leukocytes.28 CRITICAL DECISION What clinical presentations and signs and symptoms should raise suspicion for air embolism? Because the symptoms can mimic an acute cerebrovascular accident, 16 epilepsy, or any other acute neurologic condition, CAGE can be difficult to diagnose if taken out of clinical context. A diver who surfaces with immediate neurologic symptoms should be assumed to have CAGE until it is proved otherwise. Air embolism with paradoxical passage of venous air into the arterial side of the system should be strongly considered in patients who develop CNS symptoms in the context of a new central line placement or who have a complication of an existing central line. The development of an acute coronary syndrome in these contexts also suggests arterial air embolism, although the usual causes of acute coronary syndrome must still be considered. Acute coronary syndrome developing concomitantly with CAGE in the appropriate context very strongly suggests an air embolism. During the workup for arterial embolism, a CT scan of the brain might occasionally show air in the cerebral vessels; however this finding is variable and can be difficult to recognize. Imaging with CT or MRI may be useful in some, less clear-cut cases to help exclude a cerebrovascular accident or intracerebral hemorrhage that developed via the usual mechanisms. CRITICAL DECISION What treatments should be undertaken as soon as the diagnosis of air embolism is suspected? Primary treatments for venous embolism may include aspiration of large air pockets in the ventricle, treatment with oxygen, and hemodynamic support. Immediately placing patients in the left-lateral decubitus position is advocated for patients with venous air embolism with the goal of trapping air in the right ventricle and decreasing the risk of paradoxical embolization and passage more distally into the lungs. This is usually ineffective by the time the patient is seen in the emergency department, because venous air has already been distributed to the lungs and through any shunts and may be gone from the right ventricle. In cases of venous air embolism, HBO2 therapy is usually considered an adjunctive therapy, unless a paradoxical arterial air embolism develops concomitantly. HBO2 therapy may be useful for patients with venous gas embolism who remain symptomatic, especially with pulmonary edema.20,28 The only definitive treatment for an acute arterial embolism is recompression in a hyperbaric chamber.20,21,23,27-29 The faster the patient receives HBO2 therapy, the more likely the chance for complete neurologic recovery. For this reason, rapid recognition of an arterial gas embolism as the cause of the patient’s symptoms is essential. When arterial gas embolism is suspected, the patient should be immediately placed on oxygen at the highest possible concentration. A tight-fitting nonrebreathing mask with a reservoir, on 15 L of oxygen per minute will typically deliver about 72% oxygen. High-flow oxygen serves to not only treat hypoxia but also to help create a diffusion gradient across existing bubbles that favors the movement of inert gases (nitrogen) out of the bubble and back into solution, thereby reducing bubble size.20,21,23,27-29 If the head-down position is used for a short time, the patient should be returned to the supine position, which will be more helpful in resuscitative efforts.29 Although there are no data in humans, multiple animal studies have shown that the administration of lidocaine seems to improve cerebral blood flow, reduce infarct size and edema, and lower intracranial pressure in CAGE. Given the low risk of lidocaine use and the potential benefit, it is recommended in cases of CAGE at the dose of 1.5 mg/kg bolus, followed by infusion at typical cardiac dosing of 2 to 4 mg/minute.20,21,29,32,33 Patients should be transferred as quickly as possible to a hyperbaric chamber for immediate July 2009 • Volume 23 • Number 11 recompression therapy. The current recommendations from the UHMS in the Hyperbaric Oxygen Therapy Committee Report are for patients to be treated using the US Navy recommendations (Figure 2). This treatment regimen involves compression with 100% oxygen at pressures between 2 ATA to 2.82 ATA with at least 60 minutes spent at 2.82 ATA. Time extensions at both the higher and lower pressures can be added depending on the patient’s response to the treatment. Some patients will require additional treatments in the hyperbaric chamber to facilitate more complete resolution of symptoms. Decompression Sickness Decompression sickness develops from the formation of bubbles of inert gases (mainly nitrogen) in the tissues and/or blood in volumes large enough to impair organ function.3-5,34-38 Bubbles can form when the ascent from diving (or from a compressed air environment) is too rapid and/ or when unpressurized flying takes place soon after a patient surfaces from a dive.34 It is necessary to discuss the basic properties of gases, the physiology of diving, and the mechanism by which bubble formation occurs to understand the pathophysiology of decompression sickness. of taking on more nitrogen with increased depth is called “ongassing” or supersaturation.34,35 As a diver ascends, the ambient pressure decreases and the partial pressure of the inspired nitrogen is less than the partial pressure of nitrogen dissolved in the blood. Because gases move from areas of higher concentration to areas of lower concentration, the nitrogen accumulated in the body tissues during descent begins to move from the tissue to the blood and from the blood out through the lungs. This is called off-gassing.34,35 Bubble Formation During a proper ascent, nitrogen should remain in solution as it moves from the tissues to the blood stream and should not reform into the gaseous phase until it reaches the lungs.34 The reformation of gaseous nitrogen in tissues and/or blood (prior to arrival at the lungs) causes bubbles to develop in the blood and tissues. This forms the basis for the problems seen in decompression sickness.3-5,34-38 Bubbles can be generated if the ascent is too rapid for the given amount of dissolved nitrogen to move from the tissues to the lungs before returning to the gaseous phase.4,34-36 When the diver surfaces, the amount of nitrogen in the body is still elevated, and off-gassing is still taking place, although not in the form of pathologic bubbles.3,34 For this reason, air travel shortly after diving can be problematic. Most commercial aircraft are pressurized to the ambient pressure at 8,000 feet (2,440 m) (about 0.73 atmospheres), not to the pressure found at sea level. A diver’s continued rapid ascent to this new, lower ambient pressure can further facilitate the formation of bubbles in the blood and tissue that were previously off-gassing well, resulting in an increased chance of decompression sickness.34,35,37 Some newer aircraft and most private jets now pressurize to sea level, eliminating this concern. When a diver follows the standard US Navy dive tables or uses a dive computer, the maximum depth allowed and the length of time at that depth do not usually allow for enough nitrogen to accumulate to cause nitrogen bubble formation (Table 7). Figure 2. US Navy recommendations for duration of HBO2 therapy following dives at various depths (US Navy Diving Manual, Volume 5, Table 6) Diving Physiology As a diver descends under water, the ambient pressure increases and it becomes harder for the diver to expand his/her chest. Scuba gear is designed to address this problem by sensing the external pressure and delivering air through the regulator at the ambient pressure so as to overcome the increased work of breathing.34 A rise in air pressure increases the total pressure of the inspired gas and thereby the partial pressures of the component gasses (nitrogen and oxygen). As the partial pressure of nitrogen rises, the amount dissolved in the blood and transferred to the tissues also rises. This concept 17 Critical Decisions in Emergency Medicine Mechanism of Damage There are two major mechanisms by which the bubbles in blood/tissues cause decompression sickness. The first is mechanical occlusion of vessels causing tissue hypoxia and prevention of further off-gassing. The second is the blood-bubble interaction that can damage endothelium, resulting in leakage of plasma into tissues, activation of clotting factors and cytokines, and platelet aggregation.5,35 These serve to worsen tissue hypoxia.5 The blood-bubble interactions can be the most detrimental factors in patients with decompression sickness because the effect can continue long after the removal of the bubbles from tissues. Tissue hypoxia and inflammation cause the symptoms of decompression illness.5,35 Table 7. Time and depth limits at which decompression is not required Depth (Feet) 10 15 20 25 30 35 40 50 60 70 80 90 100 110 120 130 140 150 160 170 180 190 18 (Meters) 3.0 4.6 6.1 7.6 9.1 10.7 12.2 15.2 18.2 21.3 24.4 27.4 30.5 33.5 36.6 39.6 42.7 45.7 48.8 51.8 54.8 59.9 Time (Minutes) 310 200 100 60 50 40 30 25 20 15 10 10 5 5 5 5 5 CRITICAL DECISION What signs and symptoms should prompt an emergency physician to consider decompression sickness? Decompression sickness is a clinical diagnosis. The history and physical examination will usually make the diagnosis. Most patients will present with sensory symptoms that began within 1 to 3 hours after they surfaced from a dive.36 One study reports that 50% of patients will have symptoms within 10 minutes of surfacing, 85% within 1 hour, and 90% within the first 24 hours.35 It is unlikely for symptoms to arise after 24 hours.4 Joint pain and paresthesias are the most common complaints, occurring in 40% of patients with decompression sickness.35 Symptoms occur along a spectrum and can range from a simple rash to shock and cardiopulmonary arrest.35,36 Once decompression sickness has been considered as the cause of a patient’s symptoms, a detailed history of the dive should be obtained, including the maximum depth, length of time at that depth, characteristics of the ascent, and any increase in altitude shortly after surfacing.3,5,36 The maximum depth and length of time spent at that depth are used to determine if the diver exceeded depth/time limits. The risk of decompression sickness in divers who exceed depth and time limits approaches 100%.35 It is important to note however, that decompression sickness can still occur in divers who adhere strictly to decompression tables.3 The type of dive is also important.3 Decompression sickness is less likely in breath-holding dives than in dives in which scuba gear is used and on-gassing (supersaturation) takes place.34,35 The physical examination should focus on vital signs and cardiopulmonary, skin, and neurologic examinations. The cardiopulmonary examination can reveal signs of pneumothorax, pneumomediastinum, or subcutaneous emphysema, all of which can be present. The presence of pneumothorax is especially important, as it will require management prior to any definitive treatment in a hyperbaric chamber. The skin should be thoroughly examined for rashes. The most common rash is a marbled, pruritic rash also known as cutis marmorata.4 A complete neurologic examination should be done, including assessment of sensory/motor/cerebellar function. The neurologic examination can often reveal subtle deficits that the patient may not have noticed. CRITICAL DECISION How does the physician distinguish between type I and type II decompression sickness? Decompression sickness is categorized by symptoms into type I (mild) and type II (serious).4 Patients can, however, have both types concurrently. Type I decompression sickness is characterized by pain, itching, fatigue, pitting edema, and skin rash.3,34,36 Pain in or near a joint is often referred to as the “bends.” Pruritus or “skin bends” can also manifest as a burning sensation and rash. The pitting edema is often painless and is a sign of lymphatic involvement.3,34,36 Type II decompression sickness is characterized by central nervous system (CNS) dysfunction, cardiopulmonary symptoms, or any symptoms of type I decompression sickness occurring while the diver is still under water.3,34 The CNS symptoms can include loss of consciousness, ataxia, paresthesias, paresis, paralysis, urinary/bowel incontinence, and mental status changes.3,4,36 The pulmonary symptoms are also referred to as the “chokes” and include burning with inspiration, nonproductive cough, and respiratory distress. Cardiac effects include vasomotor instability and shock.3,4,36 July 2009 • Volume 23 • Number 11 CRITICAL DECISION What therapies should be initiated in patients with decompression sickness? As with all emergency department patients, care should be taken to address any cardiopulmonary instability by ensuring the patient’s airway is intact. Some patients may require intubation if they are obtunded or cannot protect their airway. Supplemental oxygen should be given at the highest attainable concentration.5,38 All patients should be hydrated, given aspirin, and transferred to a hyperbaric facility as soon as possible.5 Although patients with type I or mild type II illness may dramatically improve with 100% oxygen, this should not prevent their transfer to a hyperbaric facility; these patients will often have recurrence of symptoms and worse outcomes if HBO2 therapy is delayed. Recompression using HBO2 therapy is the only definitive treatment for decompression sickness.3-5,34-38 HBO2 therapy reduces bubble size by compressing the gas in the bubble, facilitating its passage to more distal parts of the circulation. Also, by increasing the pressure gradient, oxygen diffuses into the bubble and causes nitrogen to diffuse out and back into the plasma and into solution. Finally, tissue hypoxia is corrected, reperfusion injury is blunted, and cerebral edema is reduced. All these actions result in reversal of the mechanical cause of decompression sickness and amelioration of the resultant tissue injury.5,36,37 Aspirin prevents platelet aggregation that is caused by interaction of bubbles with endothelium. There are no studies regarding the dose of aspirin, although cardiac dosing is commonly used.5 The use of early steroids in decompression sickness has only been shown to be useful in those patients with evidence of spinal cord ischemia and injury. The recommended dose is methylprednisolone 30 mg/kg within the first 8 hours of injury.5,38 It is essential to understand that patients who seem to experience only mild type I symptoms could manifest concomitant type II symptoms that initially might be very subtle. Some of these patients will develop full-blown type II decompression sickness over time. For this reason, all patients who develop decompression sickness of any kind should be evaluated for immediate recompression in a hyperbaric chamber. Transport to a hyperbaric facility can often entail travel of some distance. In these cases, patients should be transported via ground to avoid worsening of their condition by altitude. If the patient must go by air, he or she should be transported in an aircraft that can be pressurized to sea level or by helicopter with flight level below 300 m.3,5 Case Resolutions n Case One The pregnant 28-year-old woman responded to high-flow normobaric oxygen with improving mental status. The obstetrics service was immediately consulted, and fetal monitoring was initiated demonstrating decreased short-term and long-term heart rate variability suggestive of fetal hypoxia. A decision was made to treat with HBO2 at 3 ATA. After completion of the treatment, repeat fetal monitoring demonstrated good tracing. The patient was admitted to the obstetrical service and monitored overnight. She did well and eventually delivered a healthy baby at 39 weeks by cesarean section. n Case Two On arrival of the hyperbaric physician, the patient’s vital signs had stabilized. The patient was immediately placed in the supine position and taken out of Trendelenburg position. The patient still remained comatose and made no effort at movement. The history, laboratory findings, and imaging were reviewed. A second look at the patient’s head CT demonstrated intracranial air. This finding is virtually pathognomonic for CAGE. The patient was given 100 mg of lidocaine (approximately 1.5 mg/ kg). The hyperbaric physician performed a bilateral myringotomy. The patient was transported to the hyperbaric department (adjacent to the emergency department) and was placed in the monoplace hyperbaric chamber with cardiac monitor, IV access, and arterial line in place. She was connected to the hyperbaric ventilator. Treatment was initiated following the US Navy Treatment Table 6 protocol. During the first hour of treatment at 2.8 ATA, the patient became agitated and developed a brief tonic-clonic seizure. She received 2 mg of lorazepam intravenously, and a 1 mg/kg bolus of propofol was delivered followed by a continuous infusion. The patient’s agitation was controlled, and no further complications developed. The patient awoke during the last 30 minutes of the treatment and was following commands. She was transported to the ICU where she remained in stable condition. She was extubated the following morning. She made two additional trips to the hyperbaric chamber for residual neurologic symptoms. After her third treatment was completed, she appeared to have returned to baseline neurologic function. Detailed cognitive testing revealed some mild deficits with regard to memory and mathematical processing. A echocardiogram with a bubble study performed during her hospitalization revealed a patent foramen ovale. n Case Three The patient was presumed to have decompression sickness type II precipitated by altitude closely following a dive, which clearly violated the “no decompression” dive limits. She was placed on 100% oxygen and given intravenous 19 Critical Decisions in Emergency Medicine fluids and 325 mg of aspirin. Because of the neurologic deficits and concern for spinal cord injury, methylprednisolone (30 mg/kg IV) was given. The local hyperbaric center was contacted, and she was transported via ambulance to that facility. She was immediately placed in a hyperbaric chamber and treated using US Navy Treatment Table 6 protocol. Her leg pain completely resolved after the first treatment, and she was able to stand; however she continued to have some leg weakness. She received two additional treatments, after which her weakness completely resolved. Summary HBO2 therapy has 13 approved applications recommended by the Undersea and Hyperbaric Medical Society. Of these, CO poisoning, gas embolism, and decompression illness are most likely to be encountered in emergency medicine. CO poisoning must be considered in patients who present with loss of consciousness and acute neurologic deficits from environments with potential exposure to CO. Although HBO2 treatment in CO poisoning is controversial, we feel that there is ample evidence to justify treatment of selected individuals. At the least, a referral or consultation should be made to a knowledgeable hyperbaric physician or toxicologist. HBO2 treatment in air embolism cases can be life-saving. The diagnosis of air embolism is difficult; it should be considered in divers and those undergoing venous or arterial vessel manipulation who suffer a cardiovascular or neurologic event. HBO2 therapy is the only definitive treatment for decompression sickness. The symptoms of decompression sickness are varied, and emergency physicians must maintain a high degree of suspicion for the diagnosis when confronted with a patient who has recently been diving. 2. Gesell LB, ed. Hyperbaric Oxygen Therapy Indications. 12th ed. Durham, NC: Undersea and Hyperbaric Medical Society; 2008. References 14. Thom SR. Carbon monoxide-mediated brain lipid peroxidation in the rat. J Appl Physiol. 1990;68:997-1003. 1. Kindwall E. A history of hyperbaric medicine. In: Kindwall EP, Wheelan HT, eds. Hyperbaric Medicine Practice. 3rd ed. Flagstaff, AZ: Best Publishing Company; 2008:5-22. 3. Schockley LW. Scuba diving and dysbarism. Marx JA, Hockberger RS, Walls RM, eds. Rosen’s Emergency Medicine: Concepts and Clinical Practice. 6th ed. St Louis, MO: Mosby; 2006:2279-2295. 4. Kindwall EP, Wheelan HT. Hyperbaric Medicine Practice, 3rd ed. Flagstaff, AZ: Best Publishing Company; 2008. (Comprehensive review.) 5. Tetzlaff K, Shank ES, Muth CM. Evaluation and management of decompression illness—an intensivist’s perspective. Intensive Care Med. 2003:29:2128-2136. 6. Gasman JD, Varon J, Gardner JP. Revenge of the barbecue grill. Carbon monoxide poisoning. West J Med. 1990;153: 656-657. 7. Thom SR, Keim LW. Carbon monoxide poisoning: a review epidemiology, pathophysiology, clinical features, and treatment options including hyperbaric therapy. J Toxicol Clin Toxicol. 1989;27:141-156. 8. Coburn RF. The carbon monoxide body stores. Ann NY Acad Sci. 1970;174:11-22. 9. Anderson GK. Treatment of carbon monoxide poisoning with hyperbaric oxygen. Mil Med. 1978;143:538-541. 10. Farrow JR, Davis GJ, Roy TM, et al. Fetal death due to nonlethal maternal carbon monoxide poisoning. J Forensic Sci. 1990;35:1448-1452. 11. Longo LD, Hill EP. Carbon monoxide uptake and elimination in fetal and maternal sheep. Am J Physiol. 1977;232:H324-H330. 12. Hardy KR, Thom SR. Pathophysiology and treatment of carbon monoxide poisoning. J Toxicol Clin Toxicol. 1994;32:613-629. 13. Zhang J, Piantadosi CA. Mitochondrial oxidative stress after carbon monoxide hypoxia in the rat brain. J Clin Invest. 1992;90:1193-1199. 15. Thom SR. Leukocytes in carbon monoxide-mediated brain oxidative injury. Toxicol Appl Pharmoacol. 1993;123:234-247. 16. Penny DG. Acute carbon monoxide poisoning: animal models: a review. Toxicology. 1990;62:123-160. Pearls and Pitfalls • HBO2 therapy should not be given to patients with untreated pneumothorax or patients with current or recent (within 7 days) doxorubicin treatment. • CO poisoning can be subtle, manifesting only as a headache, with minimal additional symptoms. • When patients present with headache, vomiting, lethargy, confusion, nonspecific dizziness, or afebrile viral-like illnesses lacking symptoms of an upper respiratory infection, this should trigger the question, “Why isn’t this CO poisoning?” • Although controversy exists with HBO2 treatment in CO poisoning, we feel that there is ample evidence to justify treatment of selected individuals. At the least, a referral or consultation should be made to a knowledgeable hyperbaric physician or toxicologist. • Air embolism should be considered in patients who have just completed a scuba dive and in those who have had procedures involving access to the pulmonary or venous system who develop sudden cardiovascular collapse or severe CNS problems. • Although the patient may be placed in the headdown position initially, the value of the Trendelenburg 20 • • • • position is refuted by studies suggesting it does little to prevent or ameliorate the symptoms of CAGE and may even promote cerebral edema. The only definitive treatment for an acute arterial embolism is recompression in a hyperbaric chamber. The faster the patient receives HBO2 therapy, the more likely the chance for complete neurologic recovery. The diagnosis of decompression sickness should be considered in any patient with acute onset of pain, paresthesias, or loss of consciousness who has recently been diving. Diagnostic testing in patients with possible decompression sickness should be minimal, as definitive HBO2 therapy should not be delayed. Patients should be stabilized, placed on the highest amount of oxygen available, receive a chest radiograph (to rule out pneumothorax), and transferred to a hyperbaric facility as soon as possible. Do not withhold HBO2 therapy from patients with decompression sickness who improve with 100% oxygen. These patients may develop more serious problems (type II) or have a recurrence if they do not receive HBO2 therapy. July 2009 • Volume 23 • Number 11 17. Thom SR. Dehydrogenase conversion to oxidase and lipid peroxidation in brain after carbon monoxide poisoning. J Appl Physiol. 1992;73:1584-1589. 18. Wolf SW, Lavonas EJ, Sloan EP, et al. Clinical policy: critical issues in the management of adult patients presenting to the emergency department with acute carbon monoxide poisoning. Ann Emerg Med. 2008;51:138-152. 19. Weaver LK, Hopkins RO, Chan KJ, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med. 2002;347:1057-1067. 20. Kindwall EP. Gas Embolism. In: Kindwall EP, Wheelan HT, eds. Hyperbaric Medicine Practice, 3rd ed. Flagstaff, AZ: Best Publishing Company; 2008:519-534. 21. Muth CM; Shank ES. Gas Embolism. N Engl J Med. 2000;342:476-482. 22. Fyke FE 3rd, Kamier FJ, Harms RW. Venous air embolism: life-threatening complication of orogenital sex during pregnancy. Am J Med. 1985;78:333-336. 23. Van Allen CM, Hrdina LS, Clark J. Air embolism from the pulmonary vein. Arch Surg. 1929;19:567-599. 24. Durant TM, Long J, Oppenheimer MJ. Pulmonary (venous) air embolism. Am Heart J. 1947;33:269-81. 25. Palmon SC, Moore LE, Lundberg J, et al. Venous air embolism: a review. J Clin Anesth. 1997;9:251-257. 26. Lynch JJ, Schuchard GH, Gross CM, et al. Prevalence of right-to-left atrial shunting in a healthy population: detection by Valsalva maneuver contrast echocardiography. Am J Cardiol. 1984;53:1478-1480. 27. Smith RM, Van Hoesen KB, Neuman TS. Arterial gas embolism and hemoconcentration. J Emerg Med. 1994;12:147-153. 28. Francis TJ, Mitchell SJ. Pathophysiology of decompression sickness. In Bove AA, ed. Bove and Davis’ Diving Medicine. 4th ed. Philadelphia, PA: Elsevier; 2004:164-183. (Comprehensive review of dive medicine.) 29. Moon RE. Treatment of decompression illness. In Bove AA, ed. Bove and Davis’ Diving Medicine. 4th ed. Philadelphia, PA: Elsevier; 2004:195-223. 30. Van Liew HD, Conkin J, Burkard ME. The oxygen window and decompression bubbles: estimates and significance. Aviat Space Environ Med. 1993;64:859-865. 31. Butler BD, Laine GA, Leiman BC, et al. Effects of Trendelenburg position on the distribution of arterial air emboli in dogs. Ann Thorac Surg. 1988;45:198-202. 32. Fukaya E, Hopf HW. HBO and gas embolism. Neurol Res. 2007;29:142-145. 33. McDermott JJ, Dutka AJ, Evans DE, et al. Treatment of experimental cerebral air embolism with lidocaine and hyperbaric oxygen. Undersea Biomed Res. 1990;17:525-534. 34. Bookspan J. Diving Physiology in Plain English. Kensington, MD: Undersea and Hyperbaric Medical Society, Inc; 1995. 35. Bove AA, ed. Bove and Davis’ Diving Medicine. 4th ed. Philadelphia, PA: Elsevier; 2004. 36. Freiberger JJ, Lyman SJ, Denoble PJ, et.al. Consensus factors used by experts in the diagnosis of decompression illness. Aviat Space Environ Med. 2004;75(12):1023-1028. (Study about factors used to make diagnosis of DCS.) 37. Freiberger JJ, Denoble PJ, Pieper CF, et al. The relative risk of decompression sickness during and after air travel following diving. Aviat Space Environ Med. 2002;73:980-984. (Risk of flying after diving.) 38. Moon RE. Treatment of diving emergencies. Crit Care Clin. 1999;15:429-456. The Critical Image A previously healthy 40-year-old man presenting with a 4-week history of cough, sputum production, subjective fever, and mild dyspnea. He had been seen 2 weeks previously in the emergency department and treated with moxifloxacin for a possible atypical pneumonia. A chest x-ray was performed (B). The patient was diagnosed by the emergency physician with bronchitis and discharged. A B C This case illustrates several important points: • When prior x-rays are available, always compare them with the current x-ray to detect subtle changes. • In this case, comparison of the current x-ray (B) with the one obtained 2 weeks previously (A) would have revealed an increase in heart size to more than half of the right-left chest diameter. In addition, an increase in pulmonary vascular markings in the upper lung fields is notable. This redistribution of vascular markings is called cephalization and is an early finding of pulmonary edema. The patient returned again 7 days later (20 days after his initial presentation), and another chest x-ray was obtained (C). He continued to complain of cough, and his vital signs were notable for tachycardia to 130 and a temperature of 38.3°C (100.9°F). On this visit, the emergency physician noted an interval increase in heart size on the chest x-ray, and a viral cardiomyopathy was suspected. Within days, the patient required a left ventricular assist device. He underwent heart transplant surgery and recovered. Feature Editor: Joshua S. Broder, MD, FACEP Images courtesy of Emergency Medicine Picture Archiving & Communication System (www.empacs.org). 21 Critical Decisions in Emergency Medicine CME Questions Qualified, paid subscribers to Critical Decisions in Emergency Medicine may receive CME certificates for up to 5 ACEP Category I credits, 5 AMA PRA Category I Credits™, and 5 AOA Category 2-B credits for answering the following questions. To receive your certificate, go to www.acep.org/criticaldecisionstesting and submit your answers online. You will immediately receive your score and printable CME certificate. You may submit the answers to these questions at any time within 3 years of the publication date. You will be given appropriate credit for all tests you complete and submit within this time. Answers to this month’s questions will be published in next month’s issue. 1. Which radiologic study is most sensitive for NSTI? A. CT scan B. MRI C. plain films D. ultrasonography E. V/Q scan 2. For suspected necrotizing fasciitis, which of the following antibiotic combinations is recommended? A. clindamycin, piperacillin/tazobactam B. imipenem C. vancomycin, clindamycin, piperacillin/tazobactam D. vancomycin, piperacillin/tazobactam E. vancomycin, rifampin, piperacillin/tazobactam 3. A 35-year-old woman presents with warmth, swelling, and erythema at the site of her incision from a recent cesarean section. Crepitus is present. What is the next step in her care? A. emergent gynecology consultation B. MRI C. radiographs D. transfer to a center for hyperbaric oxygen E. ultrasonography 4. A 23-year-old woman presents with severe buttock pain after a fall from standing 3 days ago. She is febrile, hypotensive, and has necrotic-appearing skin over her left buttock and into her vulva that is draining foul-smelling fluid. There is no crepitus. What is the most likely causative organism? A. Escherichia coli B. Haemophilus C. Neisseria D. Streptococcus E. Vibrio 5. The mortality rate for NSTI treated only with antibiotics is: A. 15% B. 25% C. 50% D. 75% E. approaching 100% 6. Which of the following is an advantage of CT over ultrasonography in assessing suspected NSTI that involves the trunk? A. can be performed at bedside B. can always be performed more quickly C. may show an intraabdominal source D. may show fluid along the deep fascia E. may show subcutaneous gas 22 7. A 70-year-old man with peripheral vascular disease develops NSTI at the site of an existing skin ulcer. What is the most likely causative organism? A. Candida B. a mixture of aerobic and anaerobic bacteria C. Pseudomonas D. Streptococcus E. Vibrio 8. In what subset of patients with NSTI might IVIG be useful? A. patients with Fournier gangrene B. patients with group A streptococcus infection and shock C. patients with high fever D. patients with NSTI of the head and neck E. young adult patients 9. What is the role of radiologic studies in evaluating NSTI? A. assist surgeon with operative approach B. confirm a clinical diagnosis C. accurately evaluate the extent of disease D. expedite care for patients with a paucity of clinical findings E. identify drainable fluid collections 10. Which of the following antibiotics inhibits protein synthesis and, therefore, toxin production in bacteria causing NSTI? A. ciprofloxacin B. clindamycin C. penicillin D. tobramycin E. vancomycin 11. A diver presents, having just surfaced from a 37-meter dive that lasted for 29 minutes, complaining of intense right foot pain and itching along his abdomen. He states that the symptoms started halfway through his ascent. He has a marbling rash over the epigastric area of his abdomen and a normal neurologic examination. This patient has which of the following conditions? A. air embolism B. allergic reaction and musculoskeletal pain C. barotrauma D. decompression sickness type I E. decompression sickness type II 12. Which of the following factors makes it less likely that a patient’s symptoms are caused by decompression sickness? A. breath-holding dive B. exceeding depth and time limits for a given dive C. flying within the first 24 hours after surfacing from a dive D. rapid ascent E. scuba diving July 2009 • Volume 23 • Number 11 13. Which of the following patients is most likely to benefit from acute hyperbaric oxygen treatment? A. a patient presenting with an itchy skin rash 3 days after a scuba diving trip B. a patient with a sudden collapse after a central line placement who recovers to a normal blood pressure over 15 minutes with no neurologic deficits C. a patient who develops sudden hemiparesis immediately after an open lung biopsy D. a scuba diver who lost consciousness immediately after making a rapid emergency ascent from 45 feet while holding his breath. He has been in cardiopulmonary arrest with ACLS in progress for 1 hour E. an 80-year-old hypertensive scuba diver with an acute intraventricular hemorrhage on cranial CT 14. Which of the following statements best characterizes the role of HBO2 therapy in patients presenting with an acute venous air embolism? A. it is a first-line therapy and should be initiated immediately in all patients in whom the diagnosis of venous air embolism is considered B. it is a first-line therapy in patients with venous embolism who present with hypotension, hypoxia, and a new focal neurological deficit C. it is an unproven therapy in all cases of venous air embolism D. it is most effective in venous air embolism when delivered at an Fio2 of 21% at 3 ATA for 60 minutes E. it should be initiated only after definitive confirmation of a paradoxical arterial embolism in a patient with a suspected venous air embolism 15. Which of the following is a contraindication to HBO2 therapy? A. a history of a traumatic pneumothorax, 3 years ago B. a history of a pneumothorax with a chest tube in place C. a small apical pneumothorax less than 15% D. a history of severe claustrophobia E. chemotherapy with rituximab 1 year ago 16. Tissue hypoxia from CO is a result of competitive binding of hemoglobin. This shifts the oxyhemoglobin dissociation curve to: A. downward B. the left C. no shift; CO affects oxygenation via a different mechanism D. the right E. upward 17. A CO level that is not fatal in an adult can be deadly in a fetus because: A. CO binds less tightly to fetal hemoglobin; more free CO causes more damage to tissues B. CO binds less tightly to fetal hemoglobin, shifting the oxyhemoglobin dissociation curve farther to the left C. CO binds more tightly to fetal hemoglobin; less free CO causes more damage to tissues D. CO binds more tightly to fetal hemoglobin, shifting the oxyhemoglobin dissociation curve farther to the left E. CO binds more tightly to fetal hemoglobin, shifting the oxyhemoglobin dissociation curve farther to the right 18. The most common cause of air embolism is: A. introduction of air during a case of untreated tension pneumothorax B. introduction of air during an invasive surgical or medical procedure C. introduction of air from oral-vaginal sexual activity D. introduction of air via a scuba diving accident E. introduction of air via explosive decompression in a compromised aircraft at altitude 19. Bubbles cause injury to tissues by all of the following mechanisms except: A. activation and aggregation of platelets B. damage to the endothelium of blood vessels producing leukocyte activation, release of inflammatory mediators C. hypoxia from acute arterial occlusion D. initiation of secondary reperfusion injury E. maximal distention of arterioles and capillaries producing vascular burst phenomena 20. Which of the following patients with CO exposure has the best indication for HBO2 therapy? A. a patient with a CO level of 20 and a severe headache B. a patient with chest pain, ST-segment depression, and a CO level of 29 C. a pregnant smoker with a CO level of 10 D. a smoker with headache, cough, muscle aches, fever, and a CO level of 7 E. an unresponsive patient pulled from a house fire 30 minutes ago on oxygen via nonrebreathing mask with a CO level of 6 and coma Answer key for June 2009, Volume 23, Number 10 1 C 2 B 3 B 4 E 5 D 6 A 7 C 8 D 9 C 10 B 11 B 12 B 13 A 14 E 15 B 16 A 17 C 18 A 19 B 20 E The American College of Emergency Physicians makes every effort to ensure that contributors to College-sponsored publications are knowledgeable authorities in their fields. Readers are nevertheless advised that the statements and opinions expressed in this series are provided as guidelines and should not be construed as College policy unless specifically cited as such. The College disclaims any liability or responsibility for the consequences of any actions taken in reliance on those statements or opinions. The materials contained herein are not intended to establish policy, procedure, or a standard of care. 23 NONPROFIT U.S. POSTAGE P A I D DALLAS, TX PERMIT NO. 1586 July 2009 • Volume 23 • Number 11 Critical Decisions in Emergency Medicine is the official CME publication of the American College of Emergency Physicians. Additional volumes are available to keep emergency medicine professionals up-to-date on relevant clinical issues. Editor-in-Chief Louis G. Graff IV, MD, FACEP Professor of Traumatology and Emergency Medicine, Professor of Clinical Medicine, University of Connecticut School of Medicine; Farmington, Connecticut Section Editor J. Stephen Bohan, MS, MD, FACEP Executive Vice Chairman and Clinical Director, Department of Emergency Medicine, Brigham & Women’s Hospital; Instructor, Harvard Medical School, Boston, Massachusetts Feature Editors Michael S. Beeson, MD, MBA, FACEP Program Director, Department of Emergency Medicine, Summa Health System, Akron, Ohio; Professor, Clinical Emergency Medicine, Northeastern Ohio Universities College of Medicine, Rootstown, Ohio The Critical ECG A 63-year-old woman with generalized weakness. Joshua S. Broder, MD, FACEP Assistant Clinical Professor of Surgery, Associate Residency Program Director, Division of Emergency Medicine, Duke University Medical Center, Durham, North Carolina Amal Mattu, MD, FACEP Program Director, Emergency Medicine Residency Training Program, Co-Director, Emergency Medicine/Internal Medicine Combined Residency Training Program, University of Maryland School of Medicine, Baltimore, Maryland Associate Editors Daniel A. Handel, MD, MPH Director of Clinical Operations, Department of Emergency Medicine, Oregon Health & Science University, Portland, Oregon Frank LoVecchio, DO, MPH, FACEP Research Director, Maricopa Medical Center Emergency Medicine Program; Medical Director, Banner Poison Control Center, Phoenix, Arizona; Professor, Midwestern University/Arizona College of Osteopathic Medicine, Glendale, Arizona. Sharon E. Mace, MD, FACEP Associate Professor, Department of Emergency Medicine, Ohio State University School of Medicine; Faculty, MetroHealth Medical Center/Cleveland Clinic Foundation Emergency Medicine Residency Program; Director, Pediatric Education/Quality Improvement and Observation Unit, Cleveland Clinic Foundation, Cleveland, Ohio Robert A. Rosen, MD, FACEP Medical Director, Culpeper Regional Hospital, Culpeper, Virginia George Sternbach, MD, FACEP Sinus rhythm with second-degree atrioventricular block type 1 (Mobitz I, Wenckebach), rate 80. This is an example of a slowly progressing Mobitz I rhythm with only one nonconducted P wave on the ECG. The P-P intervals remain constant, and there is very slight PR-interval prolongation from one complex to the next, although the PR-interval prolongation becomes more evident just prior to the nonconducted P wave. Feature Editor: Amal Mattu, MD, FACEP From: Mattu A, Brady W. ECGs for the Emergency Physician. London: BMJ Publishing; 2003:100,140. Available at www.acep.org/bookstore. Reprinted with permission. Clinical Professor of Surgery (Emergency Medicine), Stanford University Medical Center, Stanford, California Editorial Staff Mary Anne Mitchell, ELS Managing Editor Mike Goodwin Creative Services Manager Mary Hines Editorial Assistant Lilly E. Friend CME and Subscriptions Coordinator Marta Foster Director and Senior Editor Educational and Professional Publications Critical Decisions in Emergency Medicine is a trademark owned and published monthly by the American College of Emergency Physicians, PO Box 619911, Dallas TX 75261-9911. Send address changes to Critical Decisions in Emergency Medicine, PO Box 619911, Dallas TX 75261-9911, or to [email protected]. Copyright 2009 © by the American College of Emergency Physicians. All rights reserved. No part of this publication may be reproduced, stored, or transmitted in any form or by any means, electronic or mechanical, including storage and retrieval systems, without permission in writing from the Publisher. Printed in the USA. [email protected]