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NON PROFIT ORG US POSTAGE University Trauma Center PAID 200 Lothrop St. Pittsburgh, PA 15213-2582 PITTSBURGH, PA PERMIT NO. 3834 EMS NAVIGATOR The “must-have app” for EMS Responders in western Pennsylvania Trauma Rounds is published for emergency medicine and trauma professionals by UPMC. Executive Editor Andrew B. Peitzman, MD Thanks to a new, free app for Apple or Android mobile devices, it’s never been easier to access Pennsylvania EMS protocols, look up drug doses, or call in a response from a STAT MedEvac helicopter. Editor Louis Alarcon, MD The UPMC EMS Navigator app is a field guide created by UPMC Preshospital Care that features: U Interactive Pennsylvania statewide ALS and BLS protocols, 2011 edition — includes links to medication information, other protocols, 12:00 and tools Senior Manager, Outreach Services, Physician Relations J. Thomas Reiser, CRNP AM U Drug lookup and dose calculators — offering concise information for the most common medications, including route of administration, contraindications, and possible side effects Director, Prehospital Care Myron Rickens, EMT-P Managing Editor Kenneth B. Chiacchia, WEMT-B U Hospital directory for entire western Pennsylvania region U GPS locator and mapping tool — pinpoints your location with precise coordinates and integrated maps U Quick-call feature for response by STAT MedEvac U Continuing education calendar To get UPMC EMS Navigator for an Apple device, go to the Apple Store and search for “UPMC EMS,” or download from http://itunes.apple.com/us/app/upmc-ems-navigator/ id457603947?ls=1&mt=8 Critical Care Air Medical Transport 1-800-633-7828 UPMC is a member of the Center for Emergency Medicine of Western Pennsylvania, Inc. For Android devices, go to the Play Store and search for “UPMC EMS,” or download from https://play.google.com/store/apps/details?id=upmc.tdc.emsnavigator SYS405123 JAB/KC 05/12 © 2012 UPMC UPMC MedCall — 412-647-7000 or 1-800-544-2500 24-hour emergency consultation, referral, and transport arrangements UPMC is a $10 billion global health enterprise with more than 55,000 employees headquartered in Pittsburgh, Pa., and is transforming health care by integrating more than 20 hospitals, 400 doctors‘ offices and outpatient sites, a health insurance services division, and international and commercial services. Affiliated with the University of Pittsburgh Schools of the Health Sciences, UPMC is redefining health care by using innovative science, technology, and medicine to invent new models of accountable, cost-efficient, and patient-centered care. For more information on how UPMC is taking medicine from where it is to where it needs to be, go to UPMC.com. SPRING 2012 For emergency medicine and trauma professionals In This Issue 1 Necrotizing Soft Tissue Infections 2 Lactate Helps to Improve Prehospital Triage 7 Calendar of Events TRAUMA 8 EMS Navigator Necrotizing Soft Tissue Infections by Gina M. Howell, MD, and Matthew R. Rosengart, MD, MPH Necrotizing soft tissue infections (NSTIs) are infrequent but aggressive and rapidly spreading infections with potential for high morbidity and mortality. Though commonly called necrotizing fasciitis, this name refers only to a subset of NTSIs that invade the fascial layers. The basic pathophysiology involves the invasion and subsequent spread of bacteria into the subcutaneous tissue, where they release enzymes and toxins causing local tissue ischemia and necrosis. Associated stimulation of the production of inflammatory cytokines promotes systemic toxicity, shock, multisystem organ dysfunction, and death. The incidence of NSTI is approximately 500-1500 cases per year in the United States and is on the rise.1 Despite advances in medical care, mortality from NSTI remains as high as 35 percent.2 Early surgical debridement constitutes the mainstay of treatment, and has been shown in numerous studies to be the major determinant of survival. 3-6 Microbiology Three basic microbial subtypes of NSTI are described. Type I, or polymicrobial, NSTI is the most common form of disease, constituting 55 to 75 percent of all NSTI.4, 7-9 These infections tend to occur in the perineal and trunk region, and are often diagnosed in patients with known risk factors or immune compromise. Type II infections are monomicrobial infections caused by Group A Streptococcus (GAS), either alone or in association with Staphylococcus aureus, and as such can be associated with toxic shock syndrome. Despite its notoriety in the lay press as “flesh-eating” bacteria, Type II infections are a much less common form of NSTI. These infections classically occur on the extremities, and are more likely to be diagnosed in otherwise young, healthy hosts. GAS can be an especially virulent pathogen, causing rapidly progressive disease due to a variety of unique virulence factors.10,11 Type III NSTI, also known as myonecrosis or “gas gangrene,” is primarily caused by Clostridium perfringens, and is much less common than types I or II NTSIs. An emerging cause of NSTI is community-acquired methicillin-resistant S. aureus (CA-MRSA), which is present in cultures of one-quarter to one-third of cases of NTSI. This has important implications in the antibiotic management of NSTI, because many of the recommended antibiotic regimens may not provide adequate coverage for MRSA. (Continued on page 4) http://www.upmc.com/Services/EmergencyMedicine/ prehospital-care/Pages/TraumaRounds.aspx UPMC MedCall: 1-800-544-2500 2 TR AUMA RO U NDS Lactate Helps to Improve Prehospital Triage by Francis X. Guyette, MD The Problem Shock has been defined by the American College of Surgeons as “the presence of inadequate tissue perfusion and oxygenation” and, better still, by Gross as “the rude unhinging of the machinery of life.” Prehospital triage helps us to identify patients in shock who need of lifesaving interventions (LSIs) — tasks done in the field or hospital to prevent death. LSIs may include prehospital hemorrhage control, airway management, or fluid resuscitation. In addition, once the patient is brought to an emergency department, further action may be necessary to prevent death, including emergent operation, resuscitation with fluid or blood products, or definitive airway management. As prehospital providers, our role is to identify those patients who need LSIs and determine how to get them to the best care available. when their vital signs are normal.7,8 A new generation of handheld, point-of-care (POC) lactate analyzers is now available for use in EMS. They work much like a standard glucometer..9 Importance High lactate identifies patients who have a higher risk of death, need for surgery, need for blood transfusions, and rate of ICU admission following ED presentation. Lactate may be added to vital signs and mechanism of injury to develop better triage criteria for trauma patients. In the near future, lactate levels may help direct transport to regionalized trauma centers for more aggressive early resuscitation. Ultimately, prehospital protocols might use lactate to determine who might benefit from treatment with fluids or medications. Traditional trauma triage depends on vital signs and mechanism of injury, which often do not predict need for LSIs or injury severity.1,2 Mechanisms of injury are not accurate, and tend to send many uninjured people to the hospital while adding little benefit. A recent study suggests that a high heart rate (HR) and field hypotension (systolic blood pressure õ 90 mmHg) predicts an increased risk of death but may miss many serious injuries. 3,4,5 Blood pressure and heart rate may change late in shock, and only when the body can no longer compensate for blood loss. Furthermore, patients with head injuries, the very old or very young, and those being treated with certain medications (for example, beta blockers) may not exhibit hypotension or tachycardia in response to traumatic injury. Experience from Iraq and Afghanistan has taught us that very fit persons may be able to keep near normal heart rates and blood pressures despite life-threatening injuries. This type of “compensated shock” is not easily recognized, and may lead to triage of some patients away from specialized trauma centers and delayed resuscitation, which is strongly associated with death.3,4,5 If paramedics cannot rely on mechanism of injury and vital signs, what other tools can help them to identify shock in trauma patients? One answer may be lactic acid, or lactate. Serum lactate is a byproduct of anaerobic metabolism; we have all felt that our muscles “burn” after hard exercise. Lactate is a circulating biomarker of poor organ oxygen supply or high demand, and is directly related to death in patients with sepsis, myocardial infarction, and trauma.6,7 Following lactate levels can help us to identify patients who are not getting enough oxygen to tissues, even Lactate meter. The Evidence Previous studies have demonstrated that lactate can predict severe bleeding after trauma and is associated with need for hospital admission, ICU admission, emergent intervention, and death.10,11 Trauma surgeons at the University of Alabama, Birmingham, note that standard blood pressure and heart rate monitoring underestimate the severity of hemorrhage. Among patients with systolic blood pressure under 110 mmHg, an increase in lactate was associated with the need for massive transfusion (more than six units of blood). They showed that lactate was better than blood pressure alone for the identification of shock. Prehospital continuing education test at http://www.upmc.com/Services/EmergencyMedicine/prehospital-care/Pages/TraumaRounds.aspx UPMC In another study, trauma patients with high prehospital lactate were more likely get admitted to the hospital and twice as likely to die even when their vital signs were normal.12 The authors concluded that lactate is better than all prehospital vital signs for the prediction of death and need for hospital admission.13 References Point-of-care lactate also has been used in a large air medical system to identify shock.11,14 In this study, 400 trauma patients underwent continuous vital sign monitoring and both prehospital and emergency department lactate sampling. Those patients with prehospital lactate levels >4 mmol/L had greater need for emergent operation, intubation, and vasopressors. Lactate better predicted death and surgery even when age, GCS, and initial vital signs were taken into account.14 Among the 265 3. Lipsky AM, Gausche-Hill M, Henneman PL, et al. (2000) “Prehospital hypotension is a predictor of the need for an emergent, therapeutic operation in trauma patients with normal systolic blood pressure in the emergency department.” J Trauma 65(5):1228-1233. patients with normal vital signs, those with lactates >4 mmol/L were five times as likely to need surgery (odds ratio [OR] 5, confidence interval [CI] 1.5–16.2) and 3.5 times as likely to die (OR 3.5, CI 1.3–9.7) compared with those with a lactate <4 mmol/L. Prehospital lactate strongly predicts death and the need for emergent surgery among trauma patients with normal vital signs.11,14 The Next Step Although lactate is better than vital signs alone for identifying critical trauma patients, we do not know if it is better than the overall result of current paramedic triage (vitals, mechanism, and gut feeling). EMS services in western Pennsylvania are part of a large multicenter study to evaluate the ability of prehospital lactate to triage patients that could not be otherwise identified by abnormal vital signs. In addition, a combination of lactate and vital-sign criteria may give advance warning in patients with life threatening hemorrhage. Lactate also may identify patients with more severe conditions who could potentially benefit from lifesaving interventions and new treatments. Francis X. Guyette, MD, is an assistant professor of emergency medicine, University of Pittsburgh School of Medicine, and associate medical director, STAT MedEvac. 1. McGee S, Abernethy WB 3rd, Simel DL (1999) “The rational clinical examination: is this patient hypovolemic?” JAMA 281(11):1022-1029. 2. Brasel KJ, Guse C, Gentilello LM, et al. (2007) “Heart rate: is it truly a vital sign?” J Trauma 62(4):812-817. 4. Claridge JA, Crabtree TD, Pelletier SJ, et al. (2000) “Persistent occult hypoperfusion is associated with a significant increase in infection rate and mortality in major trauma patients.” J Trauma 48(1):8-14; discussion 14-15. 5. Crowl AC, Young JS, Kahler DM, et al. (2000) “Occult hypoperfusion is associated with increased morbidity in patients undergoing early femur fracture fixation.” J Trauma 48(2):260-267. 6. Shapiro NI, Howell MD, Talmor D, et al. (2005) “Serum lactate as a predictor of mortality in emergency department patients with infection.” Ann Emerg Med 45(5):524-528. 7. Jansen TC, van Bommel J, Mulder PG, et al. (2008) “The prognostic value of blood lactate levels relative to that of vital signs in the pre-hospital setting: A pilot study.” Crit Care 12(6):R160. 8. Abramson D, Scalea TM, Hitchcock R, et al. (1993) “Lactate clearance and survival following injury.” J Trauma 35:584-588. 9. Asimos AW, Gibbs MA, Marx JA, et al. (2000) “Value of point-of-care blood testing in emergent trauma management.” J Trauma 48:11011108. 10. Vandromme M (2010) “Lactate is a better predictor than systolic blood pressure for determining blood requirement and mortality: Could prehospital measures improve trauma triage?” J Am Coll Surgeons [Trauma] 210(5):861-867. 11. Guyette F (2009) “Identification of occult shock using out-of-hospital lactate.” Ann Emerg Med 54(3):S142. 12. Gunnerson KJ (2008) “Prehospital lactate levels are better predictors of mortality and hospital admission than traditional vital signs.” Circulation 120(S):S1459. 13. Gunnerson KJ (2008) “Prehospital point of care lactate does not correlate with initial hemodynamic variables.” Chest [Abstract] 138(Oct.):65003. 14. Castillo. (2009) “The role of prehospital lactate as a predictor of outcomes in trauma patients.” J Trauma [Abstract]. UPMC MedCall: 1-800-544-2500 3 4 TR AUMA RO U NDS (Continued from page 1) Diagnosis cases, the diagnosis of NTSI is best made on the basis of clinical The diagnosis of NTSI is often delayed due to the lack of exam and findings at surgical debridement. recognition and the paucity of early clinical findings. One should utilize a high index of suspicion and maintain a low threshold for operative intervention in cases of suspected NSTI. This is particularly relevant in managing patients with known risk factors: diabetes mellitus, intravenous drug use, HIV, obesity, ethanol Treatment Rapid and simultaneous resuscitation, operative debridement, and antibiotics are critical. Most patients with NTSI should be rapidly triaged to a tertiary care center. abuse, and recent trauma or surgery.12 However, a significant number of NSTIs occur in otherwise healthy, immunocompetent patients without these risk factors. Table 2: The Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) Score Variable Partial Score Clinical findings suggestive of NSTI include pain out of proportion to exam, tense edema, ecchymoses, bullae, crepitus, local C-reactive protein (mg/L) anesthesia, systemic toxicity, and disease progression despite <150 0 antibiotic therapy.13 Radiographic imaging in the form of plain film, >150 4 CT, or MRI may reveal soft tissue gas, enhancement or thickening of involved fascia, and/or associated abscesses.14 However, soft WBC (cells/mm3) tissue gas may be absent on x-ray in two-thirds of patients and on <15 0 CT in a quarter of patients with documented NTSI; thus the 15-25 1 >25 2 absence of gas on imaging does NOT exclude the diagnosis of NTSI. Furthermore, surgical consultation and treatment should NOT be delayed in order to obtain imaging such as MRI. In many Table 1: Group A Streptococcus Virulence Factors Hemoglobin (g/dL) >13.5 0 11-13.5 1 2 Virulence Factor Function <11 M protein Surface proteins. Facilitate attachment to host cells, inhibit phagocytosis. M1 and M3 are most virulent subtypes. Sodium (mmol/L) Streptolysin O, S Beta-hemolysis. Streptokinase Activates plasminogen. Exotoxins Damages endothelium, causes loss of microvascular integrity, stimulates release of cytokines. Exotoxin A may be important mediator of toxic shock syndrome. >135 0 <135 2 Creatinine (mcg/L) Superantigens Directly stimulates T-cell activation, causing massive release of systemic cytokines. Hyaluronidase Degrades hyaluronic acid. <141 0 >141 2 Glucose (mmol/L) <10 0 >10 1 Add partial scores for total LRINEC score; sum of >6 has a high correlation with necrotizing infection, with a positive predictive value of 92 percent and a negative predictive value 96 percent. Prehospital continuing education test at http://www.upmc.com/Services/EmergencyMedicine/prehospital-care/Pages/TraumaRounds.aspx UPMC Table 3. Recommended Antibiotic Regimens for NSTI Surgery The most important determinant of survival in NSTI is prompt surgical debridement. Several studies have shown that delay of debridement beyond 24 hours after presentation is associated Monotherapy Agents with increased mortality. 3-6 Radical excision of all devitalized imipenem/cilastatin meropenem ertapenem tissue should be performed until healthy, bleeding tissue is piperacillin-tazobactam encountered. Surgical findings consistent with NSTI include: tigecycline gray necrotic fascia, loss of resistance to blunt finger dissection (i.e., the “finger test”), lack of bleeding tissue, and the presence of foul-smelling “dishwater” fluid. Serial debridements spaced Multidrug Regimens 12 to 36 hours apart are generally the rule, because infections penicillin or cephalosporin PLUS aminoglycoside or fluoroquinolone are rarely eradicated after the initial debridement. Initially, as with PLUS clindamycin or metronidazole all infected wounds, they should be left open and packed with add vancomycin, linezolid, or daptomycin for MRSA coverage if indicated wet-dry dressings. Once infection is controlled, the patient may benefit from negative-pressure wound therapy to assist with add protein synthesis inhibitor in severe or rapidly progressive infections (clindamycin, linezolid) granulation and wound closure15, though larger wounds may ultimately require skin grafting. Antibiotics Impaired delivery of antibiotics to necrotic infected tissue can limit their effectiveness locally, but antibiotics remain critical in restricting bacterial spread and ameliorating systemic sepsis. Empiric broad-spectrum antibiotic therapy directed against Gram-positive cocci, Gram-negative rods, and anaerobes should be instituted immediately. There is no single regimen that has been advocated in the literature to date, and many single and 7,12 multidrug regimens have shown to be efficacious. Hyperbaric Oxygen Therapy Hyperbaric oxygen (HBO) therapy has been proposed as an adjunct to surgery and antibiotics in the treatment of NSTI. The technique involves the administration of 100 percent oxygen at a pressure greater than 1 atmosphere absolute (ATA), resulting in a dramatic increase in oxygen tension.16 Typical HBO therapy involves administration at 2 to 3 ATA for 90 minutes three times in the first 24 hours, then twice daily thereafter, though no standard regimen has been established. Special consideration should be given to antimicrobial coverage of GAS and MRSA. Many would advocate the addition of clindamycin to any empiric regimen, especially for coverage of GAS.11 Because MRSA appears to be evolving as a significant pathogen in NSTI, empiric therapy should include vancomycin, daptomycin, or linezolid.12 Regardless of the initial regimen, antibiotic therapy should be appropriately tailored to final microbiological speciation and antibiotic sensitivity. Current guidelines recommend continuing treatment until no further surgical debridement is necessary and the patient’s physiology has normalized — typically a 10- to 14-day course.12 The proposed benefits of HBO include suppression of clostridial њ-toxin production and generalized bacterial growth, enhancement of leukocyte-killing activity and antibiotic effects, promotion of tissue repair and wound closure, and bacteriocidal effects on anaerobic organisms.16 Despite the physiologic rationale behind its use, clinical human studies are limited mostly to case series and retrospective analyses, and the data from these are inconsistent17-20. However, many authors argue that the purported theoretical benefits and relatively few major risks may support its use as an adjunct to standard therapy. UPMC MedCall: 1-800-544-2500 5 6 TR AUMA RO U NDS Intravenous Immunoglobulin Intravenous immunoglobulin (IVIG) is another adjunctive measure that has been studied in patients with NSTI, primarily in those with GAS or staphylococcal infections. Patients with NTSI are deficient in antibodies recognizing streptococcal cell wallattachment proteins, which theoretically would be replaced with pooled IVIG.10 Some small studies suggest a mortality benefit for patients with NTSI treated with IVIG. While it is difficult to form solid conclusions, some experts support the use of IVIG as an 6. Elliott DC et al. (1996) “Necrotizing soft tissue infections. Risk factors for mortality and strategies for management.” Ann Surg 224:672-683. 7. Elliott D et al. (2000) “The microbiology of necrotizing soft tissue infections.” Am J Surg 179:361-366. 8. Sarani B et al. (2009) “Necrotizing fasciitis: current concepts and review of the literature.” J Am Coll Surg 208(2):279-288. 9. Cainzos M et al. (2007) “Necrotizing soft tissue infections.” Curr Opin Crit Care 13:433-439. adjunct to surgery and antibiotics in critically ill patients with NSTI secondary to streptococcal or staphylococcal species. Conclusion Though relatively uncommon, NSTIs are rapidly progressive soft tissue infections that threaten both life and limb of affected patients. Clearly, the major determinant of outcomes is the rapidity with which the disease is diagnosed and surgical debridement performed. Early, aggressive surgical debridement, broad-spectrum antibiotics, and resuscitation form the cornerstone of management. Most of these patients should be triaged to a tertiary care facility that can provide the surgical and critical care resources necessary to manage them. Adjunctive therapies such as HBO, IVIG, and others may have real promise and the potential to improve outcomes. Gina M. Howell, MD, is a surgical resident, and Matthew R. Rosengart, MD, MPH, is an associate professor of surgery and critical care medicine at the University of Pittsburgh School of Medicine. References 1. Ellis Simonsen SM et al. (2006) “Cellulitis incidence in a defined population.” Epidemio Infect 134:293-299. 2. Anaya DA et al. (2005) “Predictors of mortality and limb loss in necrotizing soft tissue infections.” Arch Surg 140:151-158. 3. Mok MY et al. (2006) “Necrotizing fasciitis in rheumatic disease.” Lupus 15:380-383. 4. Wong CH et al. (2003) “Necrotizing fasciitis: clinical presentation, microbiology, and determinants of mortality.” J Bone Joint Surg Am 85:1454-1460. 10. Johansson L et al. (2010) “Getting under the skin: the immunopathogenesis of Streptococcus pyogenes deep tissue infection.” Clin Infect Dis 51:58-65. 11. Mulla ZD. (2004) “Treatment options in the management of necrotizing fasciitis caused by Group A Streptococcus.” Expert Opin Pharmocother 5(8):1695-1700. 12. May AK et al. (2009) “Treatment of complicated skin and soft tissue infections.” Surgical Infections 10(5):467-499. 13. Anaya DA et al. (2007) “Necrotizing soft tissue infection: Diagnosis and management.” Clin Infect Dis 44:705-710. 14. Struk DW et al. (2001) “Imaging of soft tissue infections.” Radiol Clin North Am 39:277-303. 15. Huang WS et al. (2006) “Use of vacuum-assisted wound closure to manage limb wounds in patients suffering from acute necrotizing fasciitis.” Asian J Surg 29:135-139. 16. Kaide CG et al. (2008) “Hyperbaric oxygen: Applications in infectious disease.” Emerg Med Clin N Am 26:571-595. 17. Jallali N et al. (2005) “Hyperbaric oxygen as adjuvant therapy in the management of necrotizing fasciitis.” Am J Surg 189:462-466. 18. Wilkinson D et al. (2004) “Hyperbaric oxygen treatment and survival from necrotizing soft tissue infection.” Arch Surg 139:1339-1345. 19. Escobar SH et al. (2005) “Adjuvant hyperbaric oxygen therapy for treatment of necrotizing fasciitis reduces mortality …” Undersea Hyperb Med 32:437-443. 20. George ME et al. (2009) “Hyperbaric oxygen does not improve outcomes in patients with necrotizing soft tissue infection.” Surg Infect 10(1):21-28. 5. Voros D et al. (1993) “Role of early and extensive surgery in the treatment of severe necrotizing soft tissue infection.” Br J Surg 80:1190-1191. Prehospital continuing education test at http://www.upmc.com/Services/EmergencyMedicine/prehospital-care/Pages/TraumaRounds.aspx UPMC CALENDAR OF EVENTS Continuing Education Classes Name Date Time Location Cost Cadaver Lab May 31 6 to 8 p.m. Ross West View EMS 5325 Perry Highway Pittsburgh, PA 15229 None AMLS Provider Course Two days May 31 & June 1 8 a.m. to 4 p.m. (Both days) Murrysville Medic One 3237 Sardis Road Murrysville, PA 15668 UPMC/CMC Command providers $15.00 all other providers: $50.00 ACLS/PALS Renewal June 6 8 a.m. to 4 p.m. Uniontown Firemen’s Ambulance 84 N. Beeson Blvd. Uniontown, PA 15401 UPMC/CMC Command providers $5.00 per discipline all other providers: $45.00 per discipline Advanced Burn Life Support June 27 8 a.m. to 4 p.m. UPMC Mercy Sr. M. Ferdinand Clark Auditorium 1400 Locust St. Pittsburgh, PA 15219 $25 Fire Fighter Rehab July 18 6 to 9 p.m. Uniontown Firemen’s Ambulance 84 N. Beeson Blvd. Uniontown, PA 15401 None Advanced Burn Life Support Sept. 14 8 a.m. to 4 p.m. UPMC Mercy Sr. M. Ferdinand Clark Auditorium 1400 Locust St. Pittsburgh, PA 15219 $25 Advanced Trauma Life Support 2011 June 18-19 July 19-20 Nov. 12-13 Dec. 3-4 June 19 (re-verification) July 19 (re-verification) Nov. 13 (re-verification) Dec. 4 (re-verification) For more information about ATLS courses, email [email protected] or call 412-647-8115. For a list of nationally available ATLS courses, see http://web2.facs.org/atls/ATLSSearch.cfm?Search=USA. Consider the opportunity to earn continuing education credits by reading Trauma Rounds and completing the corresponding continuing education test. After reading, log on to http://www.upmc.com/Services/EmergencyMedicine/prehospital-care/Pages/TraumaRounds.aspx. On the Trauma Rounds website, you can print the test and mail the completed version back to UPMC, or you can take the test online through the Pennsylvania Department of Health’s online testing program. UPMC MedCall: 1-800-544-2500 7