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]

Synonyms and keywords:Skin abscess
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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.

Alexander Ogston, a scottish surgeon first described the pyogenic abscess in the late 19th century.^[1]

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 which are mostly due to staphylococcus aureus infection.

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]

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]

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]

• 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]

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

• Cutaneous abscess must be differentiated from other causes of lower limb edema like chronic venous insufficiency, acute deep venous thrombosis, lipedema, myxedema, lymphatic filariasis and causes of generalized edema.

Diseases	Symptoms							Signs	Gold standard Investigation to diagnose
	History	Onset	Pain	Fever	Laterality	Scrotal swelling	Symptoms of primary disease
(Cellulitis-erysipelas-skin abscess)	Acute painful swelling Fever	Acute	+	+	Unilateral	–	–	Tenderness, hotness, and may be fluctuation if abscess formed. Lymphangitis in nearby lymph nodes. Toxemia and fever in severe cases. Cellulitis involves the deeper dermis and erysipelas involves the upper dermis.[6]	Usually it doesn’t need any laboratory tests to diagnose.[9] Blood cultures are warranted for patients in the following circumstances:[10] Systemic toxicity Extensive skin or soft tissue involvement Underlying comorbidities persistent cellulitis In patients with recurrent cellulitis, serologic testing for beta-hemolytic streptococci is a good diagnostic tool.[11]
Lymphatic filariasis	History of living in endemic area or travelling to it	Chronic	+	+	Bilateral	+	–	Hepatomegaly Lymphedema Elephantiasis Lymphangitis Hydrocele Scrotal elephantiasis Lymphadenopathies Rhonchi may be present in patients with Pulmonary tropical eosinophilia syndrome.	Preparing blood smears Thick smears Thick smears consist of a thick layer of dehemoglobinized (lysed) red blood cells (RBCs). 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	History of untreated varicose veins Painful bilateral lower limb swelling that increases with standing and decreases by rest and leg elevation.	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.	Duplex ultrasound will demonstrate typical findings of venous valvular insufficiency
Acute deep venous thrombosis	History of prolonged recumbency Classic symptoms of DVT include acute unilateral swelling, pain, and erythema	Acute	+	–	Unilateral	–	May be associated with primary disease mandates recumbency for long duration	Dilated superficial veins Difference in calf diameter is twice as likely to have DVT(most impotant sign )[12] Calf pain on passive dorsiflexion of the foot (Homan’s sign) isn’t realiable sign.	Compression ultrasonography (CUS) with doppler is the diagnostic test of choice D-dimer level is used for unprobable cases
Lipedema	Family history especially in women; X-linked dominant or autosomal dominant condition.[13] Abnormal deposition of fat and edema and easy bruising.	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	History of untreated hypothyroidism. Infiltration of the skin with glycosaminoglycans with associated water retention.	Chronic	+	–	Bilateral	–	+ (hypothyroidism )	Pretibial myxedema	Thyroid function tests.
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]

• 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).

Men and women are affected equally.

It is more common among adults age 19 to 45 years.

Risk factors for developing cutaneous abscess include:^[23][24]

• 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

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

Recurrence may occur in 20% of patients^[26].

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]

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^[27]:

• 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

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)

The hallmark of the cutaneous abscess is painful, tender, indurated, and usually erythematous nodule.

Patients are usually well appearing.

Vital signs are within normal limits unless there is complication.

Indurated, tender and erythematous nodule with signs of local inflammation is the presenting feature.

Leukocytosis and increased level of acute phase reactants (ESR, CRP) are the most common laboratory findings.

Treatment is based on incision and drainage and sometimes antibiotic therapy is required. Cure rates with drainage alone are about 85% or higher.^[28][29]

Patients who require hospitalization for ICU admission, operating room surgical intervention, or death have one of the following six risk factors upon presentation^[27]:* abnormal cross-sectional imaging result* systemic inflammatory response syndrome* previous infection at the same location* infection involving the hand * diabetes* age >65 years

Antibiotic therapy is indicated in some circumstances that include and the duration based on severity and clinical response varies between 3 to 7 days:^[30][31][32]

• 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)

• 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

Incision and drainage is the preferred method of treatment for cutaneous abscesses.^[35] The following video, shows this procedure.{{#ev:youtube|MwgNdrA18fM}}

Avoid sharing personal hygiene items (razors, towels and brushes).^[30]

Decolonization of the index patient and of household contacts may be considered for patients with recurrent infections by using:^[30]

• Mupirocin
  • Apply 2% mupirocin ointment in nasal flares by using sterile applicators twice a day for 5 days.
  • Topical mupirocin applied to the nares.^[36] In this randomized controlled trial, patients used nasal mupirocin twice daily 5 days a month for 1 year.^[37] The does is about 1 centimeter of ointment on a swab applied to each nares.^[38]
• 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^[39]. To prevent recurrent infections due to Staphylococcus aureus, consider the following measures:

• • Chlorhexidine baths,^[40] 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.