• Clinical science
  • Clinician

Skin and soft tissue infections

Summary

Skin and soft tissue infections (SSTIs) are a group of heterogeneous conditions affecting the epidermis, dermis, subcutaneous tissue, or superficial fascia. Uncomplicated infections are most commonly caused by gram-positive pathogens (Streptococcus, Staphylococcus) that infiltrate the skin after minor injuries (e.g., scratches, insect bites). Complicated infections have a higher tendency to be polymicrobial. SSTIs primarily manifest with painful, warm, erythematous skin lesions and may also lead to purulent fluid collections and/or necrosis of the affected tissue. Systemic symptoms like fever are usually a sign of more severe infections. Risk factors for developing SSTIs (or more severe forms of SSTIs) include diabetes mellitus, immunodeficiency, and chronic edema. Diagnosis is mostly clinical but some patients may require imaging or laboratory studies. Purulent infections, such as abscesses, are primarily treated with incision and drainage while nonpurulent infections (e.g., erysipelas, cellulitis) require antibiotic therapy. Necrotizing soft tissue infections (NSTIs) have a high mortality rate; they are a surgical emergency and require immediate wound debridement.

Overview

Overview of skin and soft tissue infections
Condition Most common pathogens Tissue involvement Clinical features
Impetigo

Staphylococcal scalded skin syndrome (generalized form of impetigo)

Nonpurulent SSTIs Erysipelas
Cellulitis
Purulent SSTIs Skin abscess
  • Deeper layers of the skin
  • Walled-off infection with a collection of pus
Folliculitis, furuncles, carbuncles
Necrotizing soft tissue infections


Tissue involvement of SSTI (from superficial to deep): impetigo (superficial epidermis), erysipelas (superficial dermis and lymphatic vessels), cellulitis (deep dermis and subcutaneous tissue), necrotizing fasciitis (superficial fascia)

Cardinal signs of inflammation

  • Rubor = redness
  • Calor = heat
  • Tumor = swelling/edema
  • Dolor = pain
  • Functio laesa = loss of function

Risk factors for skin and soft tissue infections [1]

Complications

  • Local spread of infection
  • Systemic involvement with fever and possible sepsis (see “Sepsis” for details on the management of severe infections)
  • Spread of infection to distant sites (see “Staphylococcal infections”)

Purulent skin and soft tissue infections

Folliculitis, furuncles, and carbuncles [3]

Facial furuncles can result in severe complications (e.g., periorbital cellulitis, cavernous sinus thrombosis).

Skin abscess [3][4]

In both scrotal abscess and epididymitis, the classic signs of inflammation are prominent and help to confirm the diagnosis.

Etiology [3]

Diagnostics [3][1]

Diagnosis is usually clinical. In patients with systemic symptoms, laboratory studies, cultures, and imaging may be indicated to assess severity and tailor treatment.

Treatment of purulent SSTIs

Incision and drainage; are the mainstay of treatment for purulent SSTIs and usually sufficient for mild infections. Patients with systemic signs of infections require empiric antibiotic therapy; and, in severe cases, hospitalization for intravenous therapy. If performed, microbiological studies can be used to tailor antibiotic regimens.

Interventional therapy [3][4]

Antibiotic therapy [3][4]

Mild purulent skin infections usually do not require systemic antibiotic treatment following drainage.

Supportive measures

  • Warm compresses (in folliculitis, furuncles, and carbuncles)
  • Rest and acute pain management as needed
  • Keep the affected area clean and dry. [11]
  • Consider MRSA decolonization for recurrent abscesses. [13]
  • Consider inpatient management for patients with systemic symptoms.
  • See “Sepsis” for more details on the management of severe infections.

Acute management checklist for moderate and severe purulent infections

  • Stabilize the patient as needed.
  • Complete labs and imaging (e.g., soft tissue ultrasound or CT) based on initial results, extension, and location.
  • Consider surgery consult if concern for large abscess or severe infection.
  • Incision and drainage if indicated; Consider sending fluid samples for Gram stains and cultures.
  • Start empiric antibiotic therapy according to recommendations for severity and risk factors (see “Empiric antibiotic therapy for skin and soft tissue infections”).
  • Provide symptomatic treatment (e.g., pain management, warm compresses).
  • Consider indications for admission/inpatient management.

Nonpurulent skin and soft tissue infections

Definitions [3][4]

Clinical features [3][4]

  • Local signs: erythema, edema, warmth, tenderness
    • Specific to erysipelas: raised, sharply demarcated lesion
    • Specific to cellulitis: poorly defined lesion with induration
  • Cutaneous lymphatic edema (historically referred to as “peau d'orange”)
  • Common locations: lower limbs, face
  • Possible additional features
  • Systemic symptoms (in moderate/severe infections): fever, chills, confusion, nausea, headache, muscle and joint pain

Pathophysiology [3][4]

  • Entry is commonly via a minor skin injury ; erysipelas can consequently spread via superficial lymphatic vessels.
  • May also be secondary to a systemic infection

In both erysipelas and cellulitis, the most common point of entry for the pathogen is a small skin lesion (e.g., interdigital tinea pedis).

Etiology [3][4]

GAS is the most common cause of nonpurulent skin and soft tissue infections (i.e., erysipelas, cellulitis).

Diagnostics [3][8]

Diagnosis is usually clinical. In patients with systemic symptoms, laboratory studies, cultures, and imaging may be indicated to assess severity and tailor treatment.

Treatment of nonpurulent SSTIs [3][1][14]

Empiric antibiotic therapy active against streptococci and S. aureus is the mainstay of treatment for nonpurulent SSTIs. Patients with systemic symptoms often require hospitalization and parenteral antibiotic therapy. Treatment should also include the control of any predisposing factors (e.g., edema, fungal infections).

Antibiotic therapy

Antibiotics should be targeted against gram-positive pathogens and provide broad-spectrum coverage in severe cases. [4]

Supportive care

  • Elevation of the affected limbs
  • Rest and acute pain management as needed
  • See “Sepsis” for more details on the management of severe infections.

Acute management checklist for nonpurulent SSTI

Subtypes and variants

Complications [3][4]

Necrotizing soft tissue infections

Definitions [3][4]

Etiology [3][4]

The only way to definitively establish the causative pathogen is by obtaining a deep tissue culture (i.e., during surgical exploration). Clinical features alone are not reliable enough to distinguish between pathogens.

Clinical features [3][4]

Necrotizing fasciitis first spreads along the fascia before spreading to the superficial cutaneous tissue. Local findings may, therefore, be unremarkable, with patients experiencing a disproportionate level of pain.

Red flags that suggest necrotizing deep tissue infection include the presence of crepitus, bullous lesions, skin necrosis, and signs of systemic toxicity (especially altered mental status).

Diagnostics [3]

Definitive diagnosis usually made during the visualization of the tissue during surgery. If there is concern for necrotizing SSTI the patient should be referred to surgery immediately.

Imaging and laboratory studies should not delay surgery.

  • Laboratory studies
  • Microbiology
    • Blood cultures (2 sets)
    • Gram stain and cultures from deep tissue [3]
  • Imaging: not routinely indicated and should not delay treatment [8][4]
    • CT/MRI with/without IV contrast [4]
      • Gas in soft tissue
      • Fascial thickening and edema
      • Lack of contrast enhancement (confirms necrosis)
      • Fluid collections on deep fascial planes
      • Intermuscular septal edema
    • X-ray [4]
      • May detect gas in soft tissue
      • The absence of gas does not rule out NSTI.
    • Ultrasound: can identify fluid accumulation and diffuse thickening of the deep tissue [4]

Superficial wound cultures may not accurately represent the pathogens found in deep tissue and should not be used to guide management.

Management [3][4]

  • If clinical features suggest NSTI, start immediate surgical and medical treatment.
  • Patients often require hemodynamic and respiratory support and typically require admission to the ICU; (see “Sepsis” for more recommendations on the management of severe infections).

Necrotizing soft tissue infections are a surgical emergency.

Surgical exploration and debridement

  • Procedure [4]
    • Extensive exploration with surgical debridement (removal of necrotic tissue)
    • Obtain deep tissue samples for Gram stain, cultures, and histopathology.
    • Tissue with uncertain perfusion may be left for reassessment on a second intervention.
    • Reexploration every 12–36 hours until there is no evidence of necrotic tissue
  • Supportive findings
    • Fascia appears swollen
    • Dull gray fascia; areas of necrosis may be visible
    • Possible brown exudate (no pus)
    • Easy dissection of tissue planes with a blunt instrument or gloved finger

Surgical exploration provides diagnostic confirmation and allows for surgical treatment. It should not be delayed if NSTI is suspected!

Antibiotic therapy [3][4]

Supportive care [3][4]

  • Hemodynamic support: aggressive fluid resuscitation and/or vasopressor support
  • Patients typically require admission to the ICU; (see “Sepsis” for more recommendations on the management of severe infections).
  • Consider adjuvant therapy on an individual basis (e.g., hyperbaric oxygen, negative pressure wound therapy, intravenous immunoglobulin therapy).

Acute management checklist for necrotizing SSTI

Complications

Differential diagnoses

Antibiotic therapy for skin and soft tissue infections

Severity of SSTI [3]

SSTI severity grading [3]
Grade Characteristics

Mild SSTI

  • Locally confined
Moderate SSTI
  • Systemic symptoms
Severe SSTI

Necrotizing infections are always considered severe!

Empiric antibiotic therapy [3]

Empiric antibiotic therapy for skin and soft tissue infections (based on the 2014 IDSA guidelines) [3][1][4]

Mild infection

Moderate infection

Severe infection

Purulent SSTI

Nonpurulent SSTI

Necrotizing SSTI

  • Necrotizing infections are always considered severe.

Differential diagnoses

Ecthyma gangrenosum

Erysipeloid

  • Definition: cellulitis caused by Erysipelothrix rhusiopathiae
  • Pathogen: Erysipelothrix rhusiopathiae, a gram-positive, capsulated bacilli that is found in a variety of animals including fish, shellfish, pigs, and birds
  • Pathophysiology: infection usually acquired occupationally by contact with infected meat (enters through abrasions in the hand)
  • Clinical features: warm, tender, well-demarcated, erythematous plaques (most commonly affects the hands)
  • Treatment: penicillin
  • Complications: sepsis, endocarditis

Other

The differential diagnoses listed here are not exhaustive.

  • 1. Ramakrishnan K, Salinas RC, Agudelo Higuita NI. Skin and Soft Tissue Infections. Am Fam Physician. 2015; 92(6): pp. 474–83. pmid: 26371732.
  • 2. Mermel LA, Allon M, Bouza E, et al. Clinical practice guidelines for the diagnosis and management of intravascular catheter-related infection: 2009 Update by the Infectious Diseases Society of America. Clin Infect Dis. 2009; 49(1): pp. 1–45. doi: 10.1086/599376.
  • 3. Stevens DL, Bisno AL, Chambers HF, et al. 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. 2014; 59(2): pp. e10–52. doi: 10.1093/cid/ciu444.
  • 4. Sartelli M, Guirao X, Hardcastle TC, et al. 2018 WSES/SIS-E consensus conference: recommendations for the management of skin and soft-tissue infections. World Journal of Emergency Surgery. 2018; 13(1). doi: 10.1186/s13017-018-0219-9.
  • 5. Miller LG, Quan C, Shay A, et al. A Prospective Investigation of Outcomes after Hospital Discharge for Endemic, Community-Acquired Methicillin-Resistant and -Susceptible Staphylococcus aureus Skin Infection. Clinical Infectious Diseases. 2007; 44(4): pp. 483–492. doi: 10.1086/511041.
  • 6. Klevens RM, Morrison MA, Nadle J, et al. Invasive methicillin-resistant Staphylococcus aureus infections in the United States. JAMA. 2007; 298(15): pp. 1763–71. doi: 10.1001/jama.298.15.1763.
  • 7. Summanen PH, Talan DA, Strong C, et al. Bacteriology of Skin and Soft-Tissue Infections: Comparison of Infections in Intravenous Drug Users and Individuals with No History of Intravenous Drug Use. Clinical Infectious Diseases. 1995; 20(Supplement_2): pp. S279–S282. doi: 10.1093/clinids/20.supplement_2.s279.
  • 8. Expert Panel on Musculoskeletal Imaging:., Beaman FD, von Herrmann PF, et al. ACR Appropriateness Criteria® Suspected Osteomyelitis, Septic Arthritis, or Soft Tissue Infection (Excluding Spine and Diabetic Foot). J Am Coll Radiol. 2017; 14(5S): pp. S326–S337. doi: 10.1016/j.jacr.2017.02.008.
  • 9. Talan DA, Moran GJ, Krishnadasan A, et al. Subgroup Analysis of Antibiotic Treatment for Skin Abscesses. Ann Emerg Med. 2018; 71(1): pp. 21–30. doi: 10.1016/j.annemergmed.2017.07.483.
  • 10. Daum RS, Miller LG, Immergluck L, et al. A Placebo-Controlled Trial of Antibiotics for Smaller Skin Abscesses. N Engl J Med. 2017; 376(26): pp. 2545–2555. doi: 10.1056/nejmoa1607033.
  • 11. Walls R, Hockberger R, Gausche-Hill M. Rosen's Emergency Medicine. Philadelphia, PA: Elsevier Health Sciences; 2018.
  • 12. Gottlieb M, DeMott JM, Hallock M, Peksa GD. Systemic Antibiotics for the Treatment of Skin and Soft Tissue Abscesses: A Systematic Review and Meta-Analysis. Ann Emerg Med. 2019; 73(1): pp. 8–16. doi: 10.1016/j.annemergmed.2018.02.011.
  • 13. Liu C, Bayer A, Cosgrove SE et al. 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. 2011; 52(3): pp. e18–55. doi: 10.1093/cid/ciq146.
  • 14. Chitalia VC, Kothari J, Wells EJ, et al. Cost-benefit analysis and prediction of 24-hour proteinuria from the spot urine protein-creatinine ratio. Clin Nephrol. 2001; 55(6): pp. 436–47. pmid: 11434354.
  • 15. Brook I, Frazier EH. Clinical and microbiological features of necrotizing fasciitis. J Clin Microbiol. 1995; 33(9): pp. 2382–7. doi: 10.1128/JCM.33.9.2382-2387.1995.
  • 16. Jameson JL, Fauci AS, Kasper DL, Hauser SL, Longo DL, Loscalzo J. Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2). McGraw-Hill Education / Medical; 2018.
  • Fitch MT, Manthey DE, McGinnis HD, Nicks BA, Pariyadath M. Abscess Incision and Drainage. N Engl J Med. 2007; 357(19): p. e20. doi: 10.1056/nejmvcm071319.
  • O’Malley GF, Dominici P, Giraldo P, et al. Routine Packing of Simple Cutaneous Abscesses Is Painful and Probably Unnecessary. Academic Emergency Medicine. 2009; 16(5): pp. 470–473. doi: 10.1111/j.1553-2712.2009.00409.x.
  • Chinnock B, Hendey GW. Irrigation of Cutaneous Abscesses Does Not Improve Treatment Success. Ann Emerg Med. 2016; 67(3): pp. 379–383. doi: 10.1016/j.annemergmed.2015.08.007.
  • Herold G. Internal Medicine. Cologne, Germany: Herold G; 2014.
last updated 11/16/2020
{{uncollapseSections(['jTa_qP', 'lqXvA_', 'PFcWRV0', '3FcS3V0', 'BhczTX0', 'jFc_3V0', 'yhcdgX0'])}}