Learning Objectives: After reading this article, the physician should be able to:
1. Identify and treat MRSA as the dominant pathogen in community-acquired skin and soft tissue infections presenting to the emergency department.
2. Explain the evidence for increased mortality associated with nesiritide therapy and how to avoid its use except in special circumstances.
3. Describe the ACC/AHA guidelines to the risk stratification and treatment of unstable angina and acute coronary syndrome in the emergency department, with consideration of patient factors and local constraints.
Release Date: September 2008
High Prevalence of Methicillin-Resistant Staphylococcus Aureus in Emergency Department Skin and Soft Tissue Infections
Frazee BW, et al
Ann Emerg Med
Antimicrobial resistance plays an increasingly important role in selecting empiric antibiotic therapy; resistance may result in delayed healing, repeat visits to the ED, or permanent disability or death. S. aureus, a common source of skin and soft-tissue infections, has a long history of antibiotic resistance. As early as the 1960s, methicillin-resistant strains of S. aureus (MRSA) were described as nosocomial pathogens, and by the 1980s, outpatients also had MRSA infections.
Over the past eight years, community-acquired MRSA (CA-MRSA) has become known as a distinct bacteriologic entity, with a special genome encoding the Panton-Valentine leukocidin that conveys greater virulence and predilection for abscess formation and necrotizing pneumonia. Athletes sharing equipment, injection drug users, and prisoners are known to be at risk for CA-MRSA infections, but overall prevalence has not been determined.
The authors enrolled 137 subjects with skin and soft tissue infections presenting to an urban ED. They cultured the infection site and nares of all patients, and collected extensive clinical and demographic information. Excluding 18 patients with cellulitis who had only nasal cultures taken, 119 patients had wound cultures done. Of those, 61 (51%) grew MRSA, 18 grew methicillin-sensitive S. aureus (MSSA), 14 grew a non-staphylococcal pathogen, and 26 had no growth.
Of the 66 abscesses cultured, 31 (47%) grew MRSA, while 19 of 20 infections identified as furuncles grew MRSA (95%). Pooled results from nares and wound cultures indicated that 75 percent of all S. aureus isolates in this population were found to be MRSA; genotyping indicated CA-MRSA in 99 percent of those. In vitro antimicrobial susceptibility testing of the MRSA isolates showed 100% susceptibility to vancomycin and trimethoprim/sulfamethoxazole, 94% susceptibility to clindamycin, 86% to tetracycline, and only 57% to levofloxacin.
The authors concluded that CA-MRSA has become the dominant organism in skin and soft tissue infections in their outpatient population, and advocated empiric therapy active against MRSA, alone or in combination with beta-lactam therapy. Their choice of empiric therapy was IV vancomycin for severe infections, oral trimethoprim/sulfamethoxazole and cephalexin for moderate infections, oral doxycycline for mild infections, and clindamycin for children or patients with allergies to other agents.
Short-term Risk of Death after Treatment with Nesiritide for Decompensated Heart Failure
Sackner-Bernstein JD, et al
Nesiritide, a polypeptide diuretic, vasodilator, and inotropic agent derived from brain natriuretic peptide (BNP), was initially hailed as a more effective diuretic and vasodilator for acute decompensated heart failure. Reports of worsening renal function associated with it, however, have called into question its safety, especially in comparison with traditional agents such as nitroglycerin and furosemide that have track records of safety. The authors performed a meta-analysis of nesiritide trials to assess its relative safety.
After searching the literature, they identified three double-blinded, randomized studies of acute decompensated heart failure comparing nesiritide with vasodilators and diuretics only (no inotropic agents), which reported mortality data at 30 days. These were the NSGET, VMAC, and PROACTION trials, pub lished between 2000 and 2003. Together they included 862 patients with decompen sated heart failure, either as inpatients or ED patients, of whom 485 randomly received nesiritide and 377 received control therapy. Fifteen (4%) patients treated with the control therapy died within 30 days, compared with 35 (7.2%) treated with nesiritide. This was statistically significant (p=0.04), and the calculated hazard ratio (relative risk of death) was 1.86, implying an 86 percent greater chance of death at 30 days with nesiritide. For every 31 patients treated with nesiritide, one excess death could be expected.
The authors acknowledged their study was limited by differences in methodology and patient population across the three studies and because the original studies were not meant to report 30-day mortality. Even using assumptions that favored nesiritide when necessary, the mortality data clearly favored control therapy in this meta-analysis. The authors concluded that larger, prospective, randomized studies are needed to confirm or deny this troubling finding regarding nesiritide. For clinicians, this means nesiritide probably should not be used where nitroglycerin, furosemide, ACE inhibitors, and other traditional agents would suffice unless part of an investigational protocol or as ordered by a cardiologist.
Practical Implementation of the Guidelines for Unstable Angina/Non-ST-Segment Elevation Myocardial Infarction in the Emergency Department
Gibler WB, et al
Ann Emerg Med
Are We Putting the Cart Ahead of the Horse: Who Determines the Standard of Care for the Management of Patients in the Emergency Department?
Fesmire FM, Jagoda A
Ann Emerg Med
Approximately 1.4 million hospitalizations occur annually in the United States from acute coronary syndrome, making it the leading cause of hospitalization via the ED and the leading cause of death in this country. It is not surprising that acute coronary syndrome (ACS) is the most common subject of new guidelines and practice standards for physicians. The authors describe the American College of Cardiology and American Heart Association's guidelines for managing ACS patients.
The recommended initial approach stratifies risk as follows:
▪ Low Risk: Patients had a brief period of chest pain that resolved, a nondiagnostic EKG, normal initial troponin, and no high-risk features. These patients are typically observed and receive stress testing if they have coronary risk factors, but require no therapy other than aspirin.
▪ Intermediate Risk: These patients have typical symptoms lasting greater than 10 minutes, EKGs with T-wave inversions consistent with ischemia, slightly elevated troponin, and/or very high likelihood of ACS based on historical features. They do not, however, have any high-risk features. These patients generally should be treated aggressively, but do not necessarily benefit from early coronary angiography (early conservative management).
▪ High Risk: These are patients who have high-risk features, defined as elevated troponin, new ST depression, refractory-recurrent angina, new heart failure-decreased ejection fraction, hemodynamic instability, sustained ventricular tachycardia, or recent stent or CABG procedure. These patients are to be treated aggressively, and benefit from early coronary angiography (early invasive management).
Treatment strategy is based on risk assessment:
▪ Early Conservative: Aspirin is indicated for all patients except those with true allergy, and all should receive bed rest, oxygen, cardiac monitoring, nitrates, and morphine. Beta-blockers should be administered if no contraindications exist, and ACE inhibitors and nondihydropyridine calcium-channel blockers may be added for blood pressure control. Clopidogrel is now recommended for all intermediate- and high-risk ACS patients and in all with true aspirin allergy. Anticoagulation with heparin or low-molecular-weight heparin (enoxaparin) is also recommended. Antiplatelet therapy (eptifibatide, GP IIb/IIIa inhibitors tirofiban) should be considered if ischemia is refractory.
▪ Early Invasive: The same interventions apply except clopidogrel may be withheld until after coronary angiography to avoid giving it to patients requiring CABG surgery. Additionally, antiplatelet therapy should be started prior to catheterization.
The accompanying editorial contests the strength of recommendations applied to the interventions; they are not necessarily ED-specific and in some cases are based on expert consensus rather than randomized trials. In particular, the editorial takes issue with the application of “Class I” recommendations for using ACE inhibitors, clopidogrel, and IIb/IIIa platelet glycoprotein inhibitors in the ED. In applying these recommendations, it is important to remember specialist- and institution-specific constraints and preferences as well as individual patient factors and to adjust treatment accordingly.
Clinical Decision Making
Chapman DM, et al
Rosen's Emergency Medicine: Concepts and Clinical Practice
6th ed. St. Louis: Mosby, 2006
The authors describe the cognitive processes that occur in emergency physicians' clinical decision-making. They also note the common errors associated with the various diagnostic approaches, and give some general recommendations on avoiding or reducing errors and adverse events in the ED.
Diagnosis of a new patient proceeds along one of three cognitive routes. Pattern-recognition is used for familiar situations conforming to past similar presentations, and is most commonly used by experienced clinicians to reach the correct diagnosis quickly and easily, sometimes known as a “doorway diagnosis.”
Rule-using is employed in situations where enough information exists to apply explicit or implicit clinical decision rules, such as algorithms and scoring systems. This requires more cognitive effort than pattern recognition, but can be used to simplify complex or error-prone clinical situations.
The hypothetico-deductive process is the most time- and effort-intensive because it involves making educated guesses about unfamiliar situations and using tests to confirm or refute those guesses. With time and experience, clinicians rely less and less on this latter model and more on the former two.
Analysis of these main cognitive processes in making diagnoses leads to a framework for analyzing common errors in decision-making. These are classified into several categories, such as lapses in judgment, memory, or concentration; misapplication or misinterpretation of clinical decision rules; and errors in hypothesis generation and verification. Observation of these leads to several heuristics for avoiding error in the ED.
▪ Generate and exclude life-threatening diagnostic hypotheses first.
▪ Only do testing that affects disposition or diagnostic hypotheses; use decision rules to avoid or reduce diagnostic testing.
▪ Take two or three minutes to process each patient mentally.
▪ Avoid inheriting others' thinking or previous diagnoses.
▪ Pay attention to past history, risk factors, and nurses' notes for clues.
▪ Avoid premature closure, and enlist the patient in diagnostic uncertainty (follow-up arrangements, return precautions).
▪ Beware of high-risk times (sign-out, high volume, personal fatigue) and high-risk patients (hostile, violent, alcohol or drug abuse, psychiatric, return visits).
▪ Beware of high-risk diagnoses: MI, PE, subarachnoid hemorrhage, tendon or nerve injuries, retained foreign bodies, ectopic pregnancy, appendicitis, meningitis, testicular torsion, vascular catastrophes in the elderly, and ICH with intoxication.
▪ Beware of the nonfit, when symptoms, signs, and tests do not match the presumptive diagnosis. Stop and re-evaluate or refine diagnostic hypotheses.
About the LLSA
As part of its continuous certification program, the American Board of Emergency Medicine has developed the Lifelong Learning and Self-Assessment (LLSA) program to promote continuous education of diplomates. Each year, beginning in 2004, 16 to 20 articles are chosen based on the Emergency Medicine Model. A list of these articles can be found on the ABEM web site, www.abem.org.
ABEM is not authorized to confer CME credit for the successful completion of the LLSA test, but it has no objection to physicians participating in such activities. EMN's CME activity, Living with the LLSA, is not affiliated with ABEM's LLSA program, and reading this article and completing the quiz does not count toward ABEM certification. Rather, participants may earn 1 CME credit from the Lippincott Continuing Medical Education Institute, Inc., for each completed EMN quiz.
CME Participation Instructions
To earn CME credit, you must read the article in Emergency Medicine News, and complete the quiz, answering at least 80 percent of the questions correctly. Mail the completed quiz with your check for $10 payable to the Lippincott Continuing Medical Education Institute, Inc., 770 Township Line Road, Suite 300, Yardley, PA 19067. Only the first entry will be considered for credit, and must be received by Lippincott Continuing Medical Education Institute, Inc., by September 30, 2009. Acknowledgement will be sent to you within six to eight weeks of participation.
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Lippincott Continuing Medical Education Institute, Inc., designates this educational activity for a maximum of 1 AMA PRA Category 1 Credit™. Physicians should only claim credit commensurate with the extent of their participation in the activities.