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The subcutaneous abscess: Beyond simple managementThe incidence of community-acquired methicillin-resistant Staphylococcus aureus is risingonly one fact that PAs must consider as they re-evaluate their approach to the patient with a subcutaneous abscess.Meredith F. Thompson, PA-C, MMSc; Michael Kramer, PA-C, MMScMeredith Thompson works at Eagles Landing Family Practice, Stockbridge, Ga. Michael Kramer is affiliated with the Emory University PA Program and the Rollins School of Public Health, Emory University, Atlanta, Ga. The authors have indicated no relationships to disclose relating to the content of this article.
A subcutaneous abscess, a type of skin and soft tissue infection (SSTI), is the diagnosis in 1% to 2% of patients who present to the emergency department (ED). A review of the key diagnostic and treatment considerations is therefore important for PAs working in the ED, and for other PAs who care for patients with abscess-related complaints. These may include complaints of a boil, a spider bite, oras commonly heard in the southern United Statesa risen. HistoryWhen evaluating a patient who may have a subcutaneous abscess, the clinician should obtain a thorough history to detect the infectious etiology. Questions should cover conditions associated with a break in the skin, such as trauma, bites (insect, spider, animal, or human), and eczema, as well as the subcutaneous form of drug abuse called skin-popping.
Physical examinationDuring the examination, look for serious systemic or bacteremic findings such as fever, chills, tachycardia, and hypotension. The skin examination may reveal diffuse, erythematous inflamed skin with poorly defined margins, lymphadenopathy, and lymphatic streaking (cellulitis) over a potentially draining fluctuant mass. However, fluctuance and/or cellulitis may not be present. Well-demarcated borders indicate erysipelas, a more superficial infection than cellulitis and one that typically does not coincide with an abscess. Two important diagnoses to consider during the skin examination are necrotizing fasciitis (NF) and deep vein thrombosis (DVT). NF manifests in its early stages very similarly to erythematous, inflamed SSTIs and can have a fatal outcome if the affected areas are not debrided promptly. DVT also can manifest with intensely painful lower-extremity and skin changes similar to those seen in cellulitis. Palpate the abscess for a thrill if it is located near a highly vascularized area. If it is near an extremity, assess for neurologic compromise and pain with active or passive motion, a sign of a deeper infection like tenosynovitis. The last aspect of the examination involves cardiac auscultation to assess for murmurs. Special considerationsNecrotizing fasciitis A subcutaneous abscess can look identical to early-stage NF, a skin condition associated with a 30% increased risk of death.1 Although only 500 to 1,500 cases of NF are reported in the United States annually, without early diagnosis and multiple surgical debridements, the condition is rapidly lethal.2 An early diagnosis can be complicated by the fact that NF manifests very similarly to an SSTI, with tenderness, erythema, and warmth. In a retrospective study of 89 patients with NF, the condition was suspected or diagnosed at the time of admission in only 14.6% (see Table 2).2 Of the remaining patients, all but 9% were initially thought to have either an abscess (18%) or cellulitis (58.4%).2
Endocarditis and abscess The first consideration in the relationship between endocarditis and abscess is bacteremia in the injection drug user (IDU). In fact, 5% of IDUs have bacteremia at the time of presentation.5 When assessing the patient for an abscess possibly caused by skin-popping (done when the IDU cannot access a vein), be aware of the possibility of infective endocarditis (IE) with accompanying fever and a systolic murmur. The diagnosis of endocarditis can be difficult. The Duke criteria, available at www.medcalc.com/endocarditis.html, provide data that correlate with good to excellent sensitivity in an infectious disease specialists clinical judgment.6 An echocardiogram and results from two separate blood cultures, preferably obtained 12 hours apart, are necessary to evaluate the patient for IE. If the first culture result is positive, the patient should be admitted for further evaluation to satisfy the Duke Criteria or to rule out IE. In a febrile IDU, however, fever alone dictates whether the patient should be admitted to the hospital to rule out IE or other possible infections.4
The brown recluse spider bite misdiagnosis When patients present with a subcutaneous abscess, the pain and appearance of the skin often lead them to believe that a spider bit them. Clinicians also commonly misdiagnose an abscess as a spider bite, even labeling it as a brown recluse bite (see Figure 2.9 These bites should be considered in regions of the United States where the brown recluse spider is endemic (southeastern Nebraska through Texas to Georgia and southernmost Ohio).9 However, the key to this diagnosis is identifying the spider (see Figure 3). One brown recluse expert who writes of erroneous diagnoses of brown recluse spider bites suggests that the diagnosis be ruled out if the patient is not in an endemic area, unless the spider can be recovered from the scene of the bite.10-13 Additionally, he suggests that even in endemic areas, the spider should be positively identified before the diagnosis can be considered confident. Other diagnoses, such as Lyme disease and MRSA infections, should also be considered. In a patient with an MRSA-infected skin lesion, a misdiagnosis could result in possible complications, recurrent infections, and person-to-person transmission. Awareness of community-acquired MRSAAntibiotic resistance should play a major role in the decision of how to treat a subcutaneous abscess. Many antibiotics have become ineffective secondary to bacterial overexposure, and scientists are constantly researching new options. It is the PAs duty to the patient and to the world to recognize a potentially resistant infection and to provide the most effective treatment. An increase in SSTIs caused by MRSA concerns the scientific and medical communities. MRSA was once largely confined to hospitals and other inpatient facilities and to patients who had had procedures such as surgery or dialysis. Since 1980, however, a genetically distinct, community-acquired (CA) strain has existed,14 and awareness has increased in the past 10 years as outbreaks of SSTIs due to CA-MRSA have occurred among prisoners, military personnel, and members of sports teams.9,15-17 The clinician most commonly will find CA-MRSA associated with SSTI infections such as cellulitis and abscesses, but it also causes more serious conditions such as osteomyelitis, sepsis, septic arthritis, and complicated pneumonia (often with empyema).
Screening for MRSA risk factors is essential. A patient with established risk factors gives the clinician the information needed to make an educated empiric choice. Although these infections have also been found in children with no identified predisposing risk,18 the prevalence of MRSA among persons without risk factors remains low (0.24%).19 Distinction between the CA- and hospital-acquired (HA) strains is also essential because CA-MRSAunlike the nosocomial strainfrequently remains sensitive to the oral agents trimethoprim-sulfamethoxazole (TMP-SMX), clindamycin, minocycline, and linezolid.20 The CDC says that a CA-MRSA infection is likely when all of the following criteria are met:21
Needle biopsy Consider performing a needle aspiration biopsy when the presence of an abscess is questionablefor example, when the location is deep below the skin surface. Not only does the biopsy provide the diagnosis, but if purulent material is present, biopsy also produces a culture sample. Swabbed samples favor skin flora contamination and are not recommended. Culture There is controversy in the literature over routine wound culture, especially with a smaller abscess in the healthy patient.22 However, considering the rise in SSTIs caused by CA-MRSA and the possible presence of atypical organisms such as Mycobacterium tuberculosis,23 ordering a culture in all patients may be a reasonable practice. In the ED, a culture serves to supplement the hospital antibiogram data, which assists clinicians in choosing the appropriate antibiotic. In the outpatient or inpatient setting, culture results allow the provider to make appropriate antibiotic adjustments if necessary. If the needle-aspiration biopsy is unproductive, educate the patient about using warm compresses, provide antibiotics for cellulitis, admit to the hospital if necessary, and follow up. The abscess may require a future I&D unless it is small, in which case it may resolve spontaneously. After I&D, see the patient in 48 hours to remove packing, give wound care instructions, assess for improvement, and redirect treatment from the culture results as necessary. Antibiotic therapyIn a healthy person without systemic complications who presents with a small abscess, I&D may be all that is needed. However, antibiotics should be prescribed for an MRSA infection regardless of abscess size.24 One study of 69 healthy children with abscesses smaller than 5 cm and CA-MRSA present found a low clinical failure rate when antibiotics were not prescribed;25 however, the benefits of I&D without antibiotics cannot outweigh the risk of peripheral spread of MRSA. Other reasons to use antibiotics in patients with a small abscess include poorly controlled diabetes, immunocompromise, infectious disease, cancer, malnutrition, smoking, habitual alcohol use, advanced age, and chronic medical illness such as chronic obstructive pulmonary disease or chronic renal failure.8 What drug to use Hot packs, I&D, and TMP-SMX are recommended for patients with CA-MRSA infection, large and/or multiple abscesses, or fever. TMP-SMX appears to be the safest current choice for treating CA-MRSA.26 Clindamycin can be used in penicillin-allergic patients, but be aware of the possibility that erythromycin-resistant S aureus may be resistant to clindamycin.27 Some hospitals use the D test to assess for clindamycin-resistant organisms.27 Never use erythromycin and other macrolides because of resistance.22 Fluoroquinolones, especially the older agent ciprofloxacin, should be second-line drugs because of the possibility that rapid resistance will develop and because of their unnecessarily broad spectrum of activity.22 If anaerobic bacteria are a concern, as with patients who are IDUs, provide coverage with clindamycin. A beta-lactam antibiotic like a first-generation cephalosporin can be prescribed for the patient with no MRSA risk factors; however, the culture results must be pursued since CA-MRSA shows up in healthy patients without risk factors. Treat patients for 10 to 14 days or until all symptoms resolve. A recurring infection may indicate an MRSA-colonized nasal passage. Note that treatment with mupirocin promotes the development of further resistance; in the outpatient setting, use it only with recurrent infections. New antibiotics The newer agents developed to address resistant S aureus and enterococci are in use as second-line agents. Linezolid, quinupristin-dalfopristin, daptomycin, and now moxifloxacin and gatifloxacin are FDA-approved for treating uncomplicated SSTIs, and they can be used as alternatives to vancomycin. Scientists have already begun to detect resistance to these agents, however, so do not use them as first-line treatments. Resistance of S aureus to vancomycin in SSTIs is rare, and the drug is the standard IV treatment for HA-MRSA infections. For outpatients, linezolid is the only new antibiotic with 100% oral availability.28 Linezolid is expensive, however, and can be reserved for converting from IV to oral treatment in order to facilitate the discharge process. ConclusionWhen evaluating and managing a seemingly simple subcutaneous abscess, clinicians should be alert for NF in its early stages, avoid making a brown recluse spider bite diagnosis without proper identification, be aware of the increased incidence of CA-MRSA and its risk factors, recognize the link between endocarditis and an abscess, know their limitations before performing an I&D, and be able to make an educated choice regarding treatment. REFERENCES 1. Brook I, Frazier EH. Clinical and microbiological features of necrotizing fasciitis. J Clin Microbiol. 1995;33(9):2382-2387. 2. Wong CH, Chang HC, Pasupathy S, et al. Necrotizing fasciitis: clinical presentation, microbiology, and determinants of mortality. J Bone Joint Surg Am. 2003;85-A(8):1454-1460. 3. Valeriano-Marcet J, Carter JD, Vasey FB. Soft tissue disease. Rheum Dis Clin North Am. 2003;29(1):77-88, vi. 4. Calder KK, Severyn FA. Surgical emergencies in the intravenous drug user. Emerg Med Clin North Am. 2003;21(4)1089-1116. 5. Blick PW, Flowers MW, Marsden AK, et al. Antibiotics in surgical treatment of acute abscesses. Br Med J. 1980;281(6233):111-112. 6. Sekeres MA, Abrutyn E, Berlin JA, et al. An assessment of the usefulness of the Duke criteria for diagnosing active infective endocarditis. Clin Infect Dis. 1997;24(6):1185-1190. 7. Dajani AS, Taubert KA, Wilson W, et al. Prevention of bacterial endocarditis: recommendations by the American Heart Association. Circulation. 1997;96(1):358-366. 8. Babcock MD, Grekin RC. Antibiotic use in dermatologic surgery. Dermatol Clin. 2003;21(2):337-348. 9. Dominguez TJ. Its not a spider bite, its community-acquired methicillin-resistant Staphylococcus aureus. J Am Board Fam Pract. 2004;17(3):220-226. 10. Vetter RS. Brown recluse spider bite diagnoses and lawsuits [comment]. Pediatr Emerg Care. 2003;19(4):291-292. 11. Vetter RS. Myth: idiopathic wounds are often due to brown recluse or other spider bites throughout the United States [see comment]. West J Med. Nov 2000;173(5):357-358. 12. Vetter RS, Bush SP. Reports of presumptive brown recluse spider bites reinforce improbable diagnosis in regions of North America where the spider is not endemic. Clin Infect Dis. 2002;35(4):442-445. 13. Vetter RS, Cushing PE, Crawford RL, Royce LA. Diagnoses of brown recluse spider bites (loxoscelism) greatly outnumber actual verifications of the spider in four western American states. Toxicon. 2003;42(4):413-418. 14. Purcell K, Fergie JE. Exponential increase in community-acquired methicillin-resistant Staphylococcus aureus infections in South Texas children. Pediatr Infect Dis J. 2002;21(10):988-989. 15. Outbreaks of community-associated methicillin-resistant Staphylococcus aureus skin infections. Los Angeles County, California, 2002-2003. MMWR Morb Mortal Wkly Rep. 2003;52(5):88. 16. Lindemayer JM, Schoenfeld S, OGrady R, Carney JK. Methicillin-resistant Staphylococcus aureus in a high school wrestling team and the surrounding community. Arch Intern Med. 1998;158(8):895-899. 17. Methicillin-resistant Staphylococcus aureus skin and soft tissue infections in a state prisonMississippi, 2000. MMWR Morb Mortal Wkly Rep. 2001;50(42):919-922. 18. Herold BC, Immergluck LC, Maranan MC, et al. Community-acquired methicillin-resistant Staphylococcus aureus in children with no identified predisposing risk [see comment]. JAMA. 1998;279(8):593-598. 19. Salgado CD, Farr BM, Calfee DP. Community-acquired methicillin-resistant Staphylococcus aureus: a meta-analysis of prevalence and risk factors. [see comment]. Clin Infect Dis. 2003;36(2):131-139. 20. Gilbert DN, Moellering RC, Eliopoulous GM, Sande MA, eds. The Sanford Guide to Antimicrobial Therapy. Sperryville, Va: Antimicrobial Therapy Inc; 2004. 21. Community-associated MRSA information for clinicians. Available at: http://www.cdc.gov/ncidod/dhqp/ar_mrsa_ca_clinicians.html. Accessed April 3, 2006. 22. Fung HB, Chang JY, Kuczynski S. A practical guide to the treatment of complicated skin and soft tissue infections. Drugs. 2003;63(14):1459-1480. 23. Garcea G, Lloyd T, Jacobs M, et al. Role of microbiological investigations in the management of non-perineal cutaneous abscesses. Postgrad Med J. 2003;79(935):519-521. 24. Eron LJ, Lipsky BA, Low DE, et al. Managing skin and soft tissue infections: expert panel recommendations on key decision points. J Antimicrob Chemother. 2003;52(suppl 1):i3-17. 25. Lee MC, Rios AM, Aten MF, et al. Management and outcome of children with skin and soft tissue abscesses caused by community-acquired methicillin-resistant Staphylococcus aureus [see comment]. Pediatr Infect Dis J. 2004;23(2):123-127. 26. Eady EA, Cove JH. Staphylococcal resistance revisited: community-acquired methicillin resistant Staphylococcus aureusan emerging problem for the management of skin and soft tissue infections. Curr Opin Infect Dis. 2003;16(2):103-124. 27. Frank AL, Marcinak JF, Mangat PD, et al. Clindamycin treatment of methicillin-resistant Staphylococcus aureus infections in children. Pediatr Infect Dis J. 2002;21(6):530-534. 28. Schweiger ES, Weinberg JM. Novel antibacterial agents for skin and skin structure infections. J Am Acad Dermatol. 2004;50(3):331-340; quiz 341-332. |