Cutaneous abscess

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Cutaneous abscess
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]

Synonyms and keywords:Skin abscess
To return to abscess main page, click here.

Overview

Cutaneous abscess is defined as a collection of pus in the dermis or subcutaneous tissue and appears as a swollen, red, tender, and fluctuant mass, often with surrounding cellulitis and may occur in any part of the body. 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 for sever and multiple abscess especially in immunocompromised patients. Treatment is, 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.

Pathophysiology

Abscess is usually caused by staphylococcus aureus bacterial infection in an injured skin. Staphylococcus aureus could form abscess by secretion of several 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 bacterial elimination. 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. Polymorphonuclear cells (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

Less common causes

Nontuberculous mycobacteria, blastomycosis, nocardiosis, and cryptococcosis.[7]

Differentiating cutaneous abscess from other Diseases

Diseases Symptoms Signs Gold standard Investigation to diagnose
History Onset Pain Fever Laterality Scrotal swelling Symptoms of primary disease
(Cellulitis-erysipelas-skin abscess) Acute + + Unilateral - -
  • Usually it doesn't need any laboratory tests to diagnose.[9]
  • Blood cultures are warranted for patients in the following circumstances:[10]
  1. Systemic toxicity
  2. Extensive skin or soft tissue involvement
  3. Underlying comorbidities
  4. persistent cellulitis
Lymphatic filariasis
  • History of living in endemic area or travelling to it
Chronic + + Bilateral + -

Preparing blood smears

  • Thick smears
  1. Thick smears consist of a thick layer of dehemoglobinized (lysed) red blood cells (RBCs).
  2. Thick smears allow a more efficient detection of parasites (increased sensitivity).
  • Thin smears consist of blood spread in a layer such that the thickness decrease.

By the ultrasound, the following findings can be observed:

  • Dilated lymphatic channels
  • Living worms tend to be in motion which called "filarial dance" sign.
Chronic venous insufficiency Chronic + - Bilateral +

(If congenial)

-
  • Typical varicose veins
  • Skin change distribution correlate with varicose veins sites in the medial side of ankle and leg
  • Reduction of swelling with limb elevation.
Acute deep venous thrombosis Acute + - Unilateral - May be associated with primary disease mandates recumbency for long duration
Lipedema Chronic + - Bilateral - -
  • Tender with palpation
  • Negative Semmer sign to differentiate from lymphedema.[14]
  • Pinching the skin on the upper surface of the toes. If it is possible to grasp a thin fold of tissue then it is negative result.
  • In a positive result, it is only possible to grasp a lump of tissue.
  • MRI offers strong qualitative and quantitative parameters in the diagnosis of lipedema [15]
Myxedema Chronic + - Bilateral - +

(hypothyroidism )

Other causes of generalized edema
  • History of chronic general condition (cardiac-liver-renal)
Chronic - - Bilateral - +
  • According to the primary cause ( Echo- LFTs- RFT)


Disease Clinical features
Folliculitis Hair follicle inflammation, presents as pruritic rash or pustule.[16][17]
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.[18]

Epidermoid cyst Cyst or nodule presents with central punctum. May be secondarily infected.[19]
Nodular lymphangitis Subcutaneous swelling along with lymphatics. mostly due to Sporothrix schenckii.[20]
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.[21]

Epidemiology and Demographics

  • It is estimated that 4% of children experience the cutaneous abscess.[22]

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:[23][24]

Natural History, Complications and Prognosis

Natural History

If cutaneous abscess left untreated it may drain spontaneously. However, in severe cases it may cause systemic spread and result in sepsis.[25]

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.[9]

Prognosis

Depending on the extent of the disease, the prognosis may vary. However, the prognosis is generally regarded as good.

Patients who require hospitalization for ICU admission, operating room surgical intervention, or death have one of the following six risk factors upon presentation[26]:

  • abnormal cross-sectional imaging result ("air or gas, abscess or fluid collection, osteomyelitis, or suspicion of osteomyelitis")
  • systemic inflammatory response syndrome
  • previous infection at the same location
  • infection involving the hand * diabetes* age >65 years

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:

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 (ESR, CRP) 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.[27][28]

Patients who require hospitalization for ICU admission, operating room surgical intervention, or death have one of the following six risk factors upon presentation[26]:* abnormal cross-sectional imaging result* systemic inflammatory response syndrome* previous infection at the same location* infection involving the hand * diabetes* age >65 years

Medical therapy

Antibiotic therapy is indicated in some circumstances that include and the duration based on severity and clinical response varies between 3 to 7 days:[29][30][31]

Antibiotic therapy[32][33][28]

  • 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.[34] The following video, shows this procedure.{{#ev:youtube|MwgNdrA18fM}}

Prevention

Primary prevention

Avoid sharing personal hygiene items (razors, towels and brushes).[29]

Secondary prevention

Decolonization of the index patient and of household contacts may be considered for patients with recurrent infections by using:[29]

  • Mupirocin
    • Apply 2% mupirocin ointment in nasal flares by using sterile applicators twice a day for 5 days.
    • Topical mupirocin applied to the nares.[35] In this randomized controlled trial, patients used nasal mupirocin twice daily 5 days a month for 1 year.[36] The does is about 1 centimeter of ointment on a swab applied to each nares.[37]
  • Chlorhexidine
    • Apply 4% Chlorhexidine gluconate solution for all body parts except for face, mucus membranes and open wounds followed by rinsing daily for 5 days.

A more intensive regimen, although not used in this setting, has been described[38]. To prevent recurrent infections due to Staphylococcus aureus, consider the following measures:

    • Chlorhexidine baths,[39] in a randomized controlled trial, nasal recolonization with S. aureus occurred at 12 weeks in 24% of nursing home residents receiving mupirocin ointment alone (6/25) and in 15% of residents receiving mupirocin ointment plus chlorhexidine baths daily for the first three days of mupirocin treatment (4/27). Although these results did not reach statistical significance, the baths are easy to do.

References

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  2. 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.
  3. 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.
  4. 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.
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  27. 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.
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  29. 29.0 29.1 29.2 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.
  30. 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.
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  33. 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.
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  35. van Rijen M, Bonten M, Wenzel R, Kluytmans J (2008). "Mupirocin ointment for preventing Staphylococcus aureus infections in nasal carriers". Cochrane Database Syst Rev (4): CD006216. doi:10.1002/14651858.CD006216.pub2. PMID 18843708.
  36. Raz R, Miron D, Colodner R, Staler Z, Samara Z, Keness Y (1996). "A 1-year trial of nasal mupirocin in the prevention of recurrent staphylococcal nasal colonization and skin infection". Arch Intern Med. 156 (10): 1109–12. PMID 8638999.
  37. Harbarth S, Dharan S, Liassine N, Herrault P, Auckenthaler R, Pittet D (1999). "Randomized, placebo-controlled, double-blind trial to evaluate the efficacy of mupirocin for eradicating carriage of methicillin-resistant Staphylococcus aureus". Antimicrob. Agents Chemother. 43 (6): 1412–6. PMC 89288. PMID 10348762. Unknown parameter |month= ignored (help)
  38. Huang SS, Singh R, McKinnell JA, Park S, Gombosev A, Eells SJ; et al. (2019). "Decolonization to Reduce Postdischarge Infection Risk among MRSA Carriers". N Engl J Med. 380 (7): 638–650. doi:10.1056/NEJMoa1716771. PMID 30763195.
  39. Watanakunakorn C, Axelson C, Bota B, Stahl C (1995). "Mupirocin ointment with and without chlorhexidine baths in the eradication of Staphylococcus aureus nasal carriage in nursing home residents". Am J Infect Control. 23 (5): 306–9. PMID 8585642.