Cutaneous abscess
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor(s)-in-Chief: Seyedmahdi Pahlavani, M.D. [2]
Overview
Cutaneous abscess is defined as a collection of pus in skin layers and may occur in any body surface. Although, there is a rare type of sterile skin abscess that is secondary to injection mostly in diabetic patients who use insulin. diagnosis is clinical and consist of a painful, tender, indurated, and usually erythematous nodule or mass that is varying in size. Systemic sign and symptoms are rare except in sever and multiple abscess especially in immunocompromised patients. Treatment is based on incision and drainage associated with antibiotics.
Historical perspective
Alexander Ogston, a scottish surgeon first described the pyogenic abscess in the late 19th century.[1]
Classification
Cutaneous abscess may be classified as sterile abscess and infectious abscess.
- Sterile abscesses are mainly seen in diabetic patients secondary to insulin injection.
- Infectious abscesses are mostly secondary to staphylococcus aureus infection.
Pathophysiology
abscess is usually caused by staphylococcus aureus bacterial infection to an injured breast skin. Staphylococcus aureus could form abscess by secretion of several killing agents like enzymes and toxins. In a reaction to these bacterial substances, assembled white blood cells in this tissue produces anti-bacterial anti-bodies that help in killing the bacteria. However, these cells cause damage to the soft tissue contributing in the abscess formation.[2]
Pathogenesis
Skin serves as a barrier from pathogen entry. Breech in the skin surface allow the pathogen entry to cause local inflammation. PMNs are the first and the most important responding cells in abscess formation.[3] Neutrophils, are responsible for phagocytosis. Once the pathogen is opsonized by complement system, it will be recognized by neutrophils and the phagocytosis process will begin. After phagocytosis the bactricidal process will begin by producing superoxide radicals and other reactive oxygen species (ROS).[4]
Genetic factors
PMNs are the most important cellular defense. Genetic disorders that negatively affect PMN function may predispose persons to recurrent cutaneous abscess formation. For example, chronic granulomatous disease, which is a genetic disorder characterized by the inability of PMNs and other phagocytes to produce superoxide, often presents with severe and recurrent S. aureus infections.[5]
Causes
Common causes
- S. aureus (either methicillin-susceptible or methicillin-resistant S. aureus) is counting for 75% of cases.[6]
- Mixed flora (including S. aureus together with S. pyogenes and gram-negative bacilli with anaerobes)[7][8]
- Anaerobes, mostly seen in injecting drug users.[7]
Less common causes
Nontuberculous mycobacteria, blastomycosis, nocardiosis, and cryptococcosis.[7]
Differentiating cutaneous abscess from other Diseases
| Disease | Clinical features |
|---|---|
| Folliculitis | Hair follicle inflammation, presents as pruritic rash or pustule.[9][10] |
| Suppurative hydradenitis | Inflammation in intertriginous areas (axillae, inguinal area, inner thighs, perianal and perineal areas, mammary,..)
Presents as painful inflamed nodule, sinus tract and commedons. Associated with systemic symptoms. Needs surgical debridement and systemic antibiotic.[11] |
| Epidermoid cyst | Cyst or nodule presents with central punctum. May be secondarily infected.[12] |
| Nodular lymphangitis | Subcutaneous swelling along with lymphatics. mostly due to Sporothrix schenckii.[13] |
| Myiasis | Enlarging nodule secondary to insect bite and due to penetration of fly larvae into subdermal tissue. caused by Dermatobia hominis, the botfly and Cordylobia anthropophaga, the tumbu fly.[14] |
Epidemiology and Demographics
- It is estimated that 4% of children experience the cutaneous abscess.[15]
A national emergency department visit survey from 1996 to 2005 showed:
- Emergency department visits for abscesses more than doubled over the 10-year study period (1.2 million in 1996 to 3.28 million in 2005).
Gender
Men and women are affected equally.
Age
It is more common among adults age 19 to 45 years.
Risk Factors
Risk factors for developing cutaneous abscess include:[16][17]
- Skin barrier disruption due to trauma (such as abrasion, penetrating wound, pressure ulcer, venous leg ulcer, insect bite, injection drug use)
- Skin inflammation (such as eczema, radiation therapy)
- Edema due to impaired lymphatic drainage
- Edema due to venous insufficiency
- Obesity
- Immunosuppression (such as diabetes or HIV infection)
- Breaks in the skin between the toes ("toe web intertrigo"); these may be clinically inapparent
- Preexisting skin infection (such as tinea pedis, impetigo, varicella)
- Hemodialysis
Natural History, Complications and Prognosis
Natural History
If cutaneous abscess left untreated it may drain spontaneously or in severe cases may cause systemic spread and result in sepsis.[18]
Complications
A wide range of complications are possible in the course of skin abscess including: bacteremia, endocarditis, osteomyelitis, metastatic infection, sepsis, and toxic shock syndrome.[19]
Prognosis
Depending on the extent of the disease, the prognosis may vary. However, the prognosis is generally regarded as good.
Diagnosis
History and symptoms
History
A detailed history must be taken from all patients. Specific area of focus when obtaining a history from the patient include:
- Recent trauma
- Recent weight change
- Recent immunosuppresive drugs
- Underlying comorbidities (lymphedema, malignancy, neutropenia, immunodeficiency, splenectomy, diabetes)
Symptoms
The hallmark of the cutaneous abscess is painful, tender, indurated, and usually erythematous nodule.
Physical examination
Appearance of the Patient
Patients are usually well appearing.
Vital signs
Vital signs are within normal limits unless there is complication.
Skin
Indurated, tender and erythematous nodule with signs of local inflammation is the presenting feature.
Laboratory findings
Leukocytosis and increased level of acute phase reactants are the most common laboratory findings.
Treatment
Treatment is based on incision and drainage and sometimes antibiotic therapy is required. Cure rates with drainage alone are about 85% or higher.[20][21]
Medical therapy
Antibiotic therapy is indicated in some circumstances that include:[22][23][24]
- Single abscess ≥2 cm
- Multiple lesions
- Extensive surrounding cellulitis
- Associated immunosuppression or other comorbidities
- Systemic signs of toxicity (fever >100.5°F/38°C, hypotension, or sustained tachycardia)
- Inadequate clinical response to incision and drainage alone
- Presence of an indwelling medical device (such as prosthetic joint, vascular graft, or pacemaker)
- High risk for transmission of S. aureus to others (such as in athletes, military personnel)
Antibiotic therapy[25][21]
- Preferred regimen: Trimethoprim-sulfamethoxazole one or two double strength doses (160 mg of trimethoprim and 800 mg of sulfamethoxazole) PO twice daily
- Alternative regimen (1): Clindamycin 300-450 mg PO three to four times daily
- Alternative regimen (2): Doxycycline 100 mg PO twice daily
- Alternative regimen (3): Minocycline 200 mg PO once, then 100 mg PO twice daily
- Alternative regimen (4): Linezolid 600 mg PO twice daily
- Alternative regimen (5): Tedizolid 200 mg PO once daily
Surgery
Incision and drainage is the preferred method of treatment for cutaneous abscesses.[26] The following video, shows this procedure.{{#ev:youtube|MwgNdrA18fM}}
References
- ↑ "Classics in infectious diseases. "On abscesses". Alexander Ogston (1844-1929)". Rev. Infect. Dis. 6 (1): 122–8. 1984. PMID 6369479.
- ↑ Kobayashi SD, Malachowa N, DeLeo FR (2015). "Pathogenesis of Staphylococcus aureus abscesses". Am J Pathol. 185 (6): 1518–27. doi:10.1016/j.ajpath.2014.11.030. PMC 4450319. PMID 25749135.
- ↑ Kolaczkowska E, Kubes P (2013). "Neutrophil recruitment and function in health and inflammation". Nat. Rev. Immunol. 13 (3): 159–75. doi:10.1038/nri3399. PMID 23435331.
- ↑ Quinn MT, Gauss KA (2004). "Structure and regulation of the neutrophil respiratory burst oxidase: comparison with nonphagocyte oxidases". J. Leukoc. Biol. 76 (4): 760–81. doi:10.1189/jlb.0404216. PMID 15240752.
- ↑ Bieluch VM, Tally FP (1983). "Pathophysiology of abscess formation". Clin Obstet Gynaecol. 10 (1): 93–103. PMID 6872404.
- ↑ Stevens DL, Bisno AL, Chambers HF, Dellinger EP, Goldstein EJ, Gorbach SL, Hirschmann JV, Kaplan SL, Montoya JG, Wade JC (2014). "Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the infectious diseases society of America". Clin. Infect. Dis. 59 (2): 147–59. doi:10.1093/cid/ciu296. PMID 24947530.
- ↑ 7.0 7.1 7.2 Summanen PH, Talan DA, Strong C, McTeague M, Bennion R, Thompson JE, Väisänen ML, Moran G, Winer M, Finegold SM (1995). "Bacteriology of skin and soft-tissue infections: comparison of infections in intravenous drug users and individuals with no history of intravenous drug use". Clin. Infect. Dis. 20 Suppl 2: S279–82. PMID 7548575.
- ↑ Moran GJ, Krishnadasan A, Gorwitz RJ, Fosheim GE, McDougal LK, Carey RB, Talan DA (2006). "Methicillin-resistant S. aureus infections among patients in the emergency department". N. Engl. J. Med. 355 (7): 666–74. doi:10.1056/NEJMoa055356. PMID 16914702.
- ↑ Luelmo-Aguilar J, Santandreu MS (2004). "Folliculitis: recognition and management". Am J Clin Dermatol. 5 (5): 301–10. PMID 15554731.
- ↑ Laureano AC, Schwartz RA, Cohen PJ (2014). "Facial bacterial infections: folliculitis". Clin. Dermatol. 32 (6): 711–4. doi:10.1016/j.clindermatol.2014.02.009. PMID 25441463.
- ↑ Revuz J (2009). "Hidradenitis suppurativa". J Eur Acad Dermatol Venereol. 23 (9): 985–98. doi:10.1111/j.1468-3083.2009.03356.x. PMID 19682181.
- ↑ Zuber TJ (2002). "Minimal excision technique for epidermoid (sebaceous) cysts". Am Fam Physician. 65 (7): 1409–12, 1417–8, 1420. PMID 11996426.
- ↑ Kostman JR, DiNubile MJ (1993). "Nodular lymphangitis: a distinctive but often unrecognized syndrome". Ann. Intern. Med. 118 (11): 883–8. PMID 8480962.
- ↑ Arosemena R, Booth SA, Su WP (1993). "Cutaneous myiasis". J. Am. Acad. Dermatol. 28 (2 Pt 1): 254–6. PMID 8432924.
- ↑ Holsenback H, Smith L, Stevenson MD (2012). "Cutaneous abscesses in children: epidemiology in the era of methicillin-resistant Staphylococcus aureus in a pediatric emergency department". Pediatr Emerg Care. 28 (7): 684–6. doi:10.1097/PEC.0b013e31825d20e1. PMID 22743746.
- ↑ McNamara DR, Tleyjeh IM, Berbari EF, Lahr BD, Martinez J, Mirzoyev SA, Baddour LM (2007). "A predictive model of recurrent lower extremity cellulitis in a population-based cohort". Arch. Intern. Med. 167 (7): 709–15. doi:10.1001/archinte.167.7.709. PMID 17420430.
- ↑ Gordon RJ, Lowy FD (2005). "Bacterial infections in drug users". N. Engl. J. Med. 353 (18): 1945–54. doi:10.1056/NEJMra042823. PMID 16267325.
- ↑ Llera JL, Levy RC, Staneck JL (1984). "Cutaneous abscesses: natural history and management in an outpatient facility". J Emerg Med. 1 (6): 489–93. PMID 6444142.
- ↑ Raff AB, Kroshinsky D (2016). "Cellulitis: A Review". JAMA. 316 (3): 325–37. doi:10.1001/jama.2016.8825. PMID 27434444.
- ↑ Rajendran PM, Young D, Maurer T, Chambers H, Perdreau-Remington F, Ro P, Harris H (2007). "Randomized, double-blind, placebo-controlled trial of cephalexin for treatment of uncomplicated skin abscesses in a population at risk for community-acquired methicillin-resistant Staphylococcus aureus infection". Antimicrob. Agents Chemother. 51 (11): 4044–8. doi:10.1128/AAC.00377-07. PMC 2151464. PMID 17846141.
- ↑ 21.0 21.1 Schmitz GR, Bruner D, Pitotti R, Olderog C, Livengood T, Williams J, Huebner K, Lightfoot J, Ritz B, Bates C, Schmitz M, Mete M, Deye G (2010). "Randomized controlled trial of trimethoprim-sulfamethoxazole for uncomplicated skin abscesses in patients at risk for community-associated methicillin-resistant Staphylococcus aureus infection". Ann Emerg Med. 56 (3): 283–7. doi:10.1016/j.annemergmed.2010.03.002. PMID 20346539.
- ↑ Liu C, Bayer A, Cosgrove SE, Daum RS, Fridkin SK, Gorwitz RJ, Kaplan SL, Karchmer AW, Levine DP, Murray BE, J Rybak M, Talan DA, Chambers HF (2011). "Clinical practice guidelines by the infectious diseases society of america for the treatment of methicillin-resistant Staphylococcus aureus infections in adults and children". Clin. Infect. Dis. 52 (3): e18–55. doi:10.1093/cid/ciq146. PMID 21208910.
- ↑ Stevens DL, Bisno AL, Chambers HF, Dellinger EP, Goldstein EJ, Gorbach SL, Hirschmann JV, Kaplan SL, Montoya JG, Wade JC (2014). "Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America". Clin. Infect. Dis. 59 (2): e10–52. doi:10.1093/cid/ciu444. PMID 24973422.
- ↑ Talan DA, Mower WR, Krishnadasan A, Abrahamian FM, Lovecchio F, Karras DJ, Steele MT, Rothman RE, Hoagland R, Moran GJ (2016). "Trimethoprim-Sulfamethoxazole versus Placebo for Uncomplicated Skin Abscess". N. Engl. J. Med. 374 (9): 823–32. doi:10.1056/NEJMoa1507476. PMC 4851110. PMID 26962903.
- ↑ Talan DA, Krishnadasan A, Gorwitz RJ, Fosheim GE, Limbago B, Albrecht V, Moran GJ (2011). "Comparison of Staphylococcus aureus from skin and soft-tissue infections in US emergency department patients, 2004 and 2008". Clin. Infect. Dis. 53 (2): 144–9. doi:10.1093/cid/cir308. PMID 21690621.
- ↑ Singer AJ, Talan DA (2014). "Management of skin abscesses in the era of methicillin-resistant Staphylococcus aureus". N. Engl. J. Med. 370 (11): 1039–47. doi:10.1056/NEJMra1212788. PMID 24620867.