Cellulitis and skin abscess: Epidemiology, microbiology, clinical manifestations, and diagnosis

INTRODUCTION — Cellulitis, abscess, or both are among the most common skin and soft tissue infections [1-3]. Cellulitis (which includes erysipelas) manifests as an area of skin erythema, edema, and warmth; it develops as a result of bacterial entry via breaches in the skin barrier [4]. A skin abscess is a collection of pus within the dermis or subcutaneous space. Misdiagnosis of these entities is common [5], and possible alternative diagnoses should be considered carefully (figure 1). (See 'Differential diagnosis' below.)

The epidemiology, microbiology, clinical manifestations, and diagnosis of cellulitis and skin abscess are reviewed here. Issues related to treatment of cellulitis and abscess are discussed separately. (See "Acute cellulitis and erysipelas in adults: Treatment".) (Related Pathway(s): Cellulitis and skin abscesses: Empiric antibiotic selection for adults.)

Issues related to skin and soft tissue infections associated with specific epidemiologic factors (such as diabetes, animal bites, and water exposure) are discussed separately. (See "Clinical manifestations, diagnosis, and management of diabetic infections of the lower extremities" and "Animal bites (dogs, cats, and other animals): Evaluation and management" and "Soft tissue infections following water exposure".)

Issues related to infection involving the gluteal area and perineum are discussed separately. (See "Pilonidal disease" and "Perianal and perirectal abscess".)

EPIDEMIOLOGY — Cellulitis is observed most frequently among middle-aged and older adults. Erysipelas occurs in young children and older adults [6,7]. The incidence of cellulitis is about 200 cases per 100,000 patient-years [8] and, in nontropical regions, has a seasonal predilection for warmer months [8-12].

Skin abscess may occur in healthy individuals with no predisposing conditions. The burden of skin abscess has varied. During the 1990s, the number of cases in the United States increased; this was attributed to the increasing prevalence of community-acquired methicillin-resistant Staphylococcus aureus strains (USA300 clone). In the 2000s, however, the incidence of skin abscess has plateaued [13-15].

Predisposing factors associated with risk of cellulitis and/or skin abscess include [16-25]:

●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, psoriasis)

●Edema due to impaired lymphatic drainage

●Edema due to venous insufficiency

●Obesity

●Immunosuppression (such as diabetes or HIV infection)

●Skin breaks between the toes ("toe web intertrigo"); these may be clinically inapparent

●Pre-existing skin infection (such as tinea pedis, impetigo, varicella)

●Prior saphenous vein harvesting for coronary artery bypass graft surgery

Lymphatic compromise may occur following surgical procedures (such as saphenous venectomy or lymph node dissection) or in the setting of congenital abnormalities. In a retrospective analysis of more than 165,000 hospital admissions for lymphedema in the United States between 2012 and 2017, most cases were associated with cellulitis (92 percent) [26]. (See "Early noncardiac complications of coronary artery bypass graft surgery", section on 'Post-venectomy cellulitis' and "Cellulitis following pelvic lymph node dissection".)

An additional risk factor for development of purulent skin and soft tissue infections is close contact with others with methicillin-resistant S. aureus infection or carriage. (See "Methicillin-resistant Staphylococcus aureus (MRSA) in adults: Epidemiology" and "Methicillin-resistant Staphylococcus aureus infections in children: Epidemiology and clinical spectrum", section on 'Epidemiology and risk factors'.)

MICROBIOLOGY

Cellulitis and erysipelas — The most common cause of cellulitis is beta-hemolytic streptococci (groups A, B, C, G, and F), most commonly group A Streptococcus or Streptococcus pyogenes; S. aureus (including methicillin-resistant strains) is a notable but less common cause [4,21,27-33]. Gram-negative aerobic bacilli are identified in a minority of cases.

The vast majority of erysipelas cases are caused by beta-hemolytic streptococci [7,27,34,35]. One study of nonpurulent cellulitis including 179 patients found that beta-hemolytic streptococci accounted for 73 percent of cases (diagnosed by positive blood culture results or serologic testing for anti-streptolysin-O and anti-DNase-B antibodies) [32]. No etiology was identified in 27 percent of cases, but the overall clinical response rate to beta-lactam therapy was 96 percent.

Less common causes of cellulitis include Haemophilus influenzae type b (buccal cellulitis), clostridia and non-spore-forming anaerobes (crepitant cellulitis), Streptococcus pneumoniae, and Neisseria meningitidis [36-42]. In immunocompromised patients, the spectrum of potential pathogens is much broader, and infectious disease consultation is warranted.

Pathogens implicated in special clinical circumstances discussed in detail separately include:

●Pasteurella multocida and Capnocytophaga canimorsus (see "Animal bites (dogs, cats, and other animals): Evaluation and management")

●Aeromonas hydrophila and Vibrio vulnificus (see "Soft tissue infections following water exposure")

●Pseudomonas aeruginosa (see "Fever and rash in immunocompromised patients without HIV infection" and "Clinical manifestations, diagnosis, and management of diabetic infections of the lower extremities" and "Pseudomonas aeruginosa skin and soft tissue infections")

●Group B Streptococcus (see "Group B streptococcal infection in neonates and young infants", section on 'Other focal infection' and "Cellulitis following pelvic lymph node dissection", section on 'Streptococcal sex syndrome')

●Clostridium species (see "Clostridial myonecrosis")

●Erysipelothrix rhusiopathiae (see "Erysipelothrix infection")

●S. pneumoniae (see "Orbital cellulitis")

●Cryptococcus neoformans (see "Fever and rash in immunocompromised patients without HIV infection")

●Streptococcus iniae (see "Fever and rash in the immunocompetent patient")

●Helicobacter cinaedi (see "Fever and rash in patients with HIV")

●Mycobacterium abscessus (see "Rapidly growing mycobacterial infections: Mycobacteria abscessus, chelonae, and fortuitum")

Skin abscess — The most common cause of skin abscess is S. aureus (either methicillin-susceptible or methicillin-resistant S. aureus [MRSA]), which occurs in up to 75 percent of cases. Risk factors are summarized in the table (table 1); many patients with MRSA infection have no risk factors [3,43-48].

A skin abscess can be caused by more than one pathogen [44,49-51]; isolation of multiple organisms (including S. aureus together with S. pyogenes and gram-negative bacilli with anaerobes) is more common in patients with skin abscess involving the perioral, perirectal, or vulvovaginal areas [44]. Organisms of oral origin, including anaerobes, are seen most frequently among intravenous drug users [44].

Unusual causes of skin abscess include nontuberculous mycobacteria, blastomycosis, nocardiosis, and cryptococcosis (see related topics).

Most abscesses are due to infection. However, sterile abscesses can occur in the setting of injected irritants. Examples include injected drugs (particularly oil-based ones) that may not be fully absorbed and so remain at the site of injection, causing local irritation. Sterile abscesses can turn into hard, solid lesions as they scar.

CLINICAL MANIFESTATIONS — Patients with skin and soft tissue infection may present with cellulitis, abscess, or both [1-3,43].

Cellulitis and erysipelas — Cellulitis and erysipelas manifest as areas of skin erythema, edema, and warmth; they develop as a result of bacterial entry via breaches in the skin barrier (picture 1) [4]. Petechiae and/or hemorrhage can be seen in erythematous skin, and superficial bullae can occur. Fever and other systemic manifestations of infection may also be present. Cellulitis and erysipelas are nearly always unilateral, and the lower extremities are the most common site of involvement (picture 2 and picture 3 and picture 4); bilateral involvement should prompt consideration of alternative causes (figure 1) [4,6,52]. (See 'Differential diagnosis' below.)

Cellulitis involves the deeper dermis and subcutaneous fat; erysipelas involves the upper dermis and superficial lymphatics (figure 2). Cellulitis may present with or without purulence; erysipelas is nonpurulent [1-3]. Patients with cellulitis tend to have a more indolent course with development of localized symptoms over a few days.

Patients with erysipelas generally have acute onset of symptoms with systemic manifestations, including fever, chills, severe malaise, and headache; these can precede onset of local inflammatory signs and symptoms by minutes to hours. In erysipelas, there is clear demarcation between involved and uninvolved tissue [53]. There may be a raised, advancing border or erythema with central clearing. Classic descriptions of erysipelas note "butterfly" involvement of the face (picture 5). Involvement of the ear (Milian's ear sign) is a distinguishing feature for erysipelas, since this region does not contain deeper dermis tissue.

Additional manifestations of cellulitis and erysipelas include lymphangitis and enlargement of regional lymph nodes. Edema surrounding the hair follicles may lead to dimpling in the skin, creating an appearance reminiscent of an orange peel texture ("peau d'orange"). Vesicles, bullae, and ecchymoses or petechiae may be observed (picture 6 and figure 1). Cutaneous hemorrhage can occur in the setting of significant inflammation in the skin. Crepitant and gangrenous cellulitis are unusual manifestations of cellulitis due to clostridia and other anaerobes. Severe manifestations with systemic toxicity should prompt investigation for additional underlying sources of infection. (See "Invasive group A streptococcal infection and toxic shock syndrome: Epidemiology, clinical manifestations, and diagnosis" and "Staphylococcal toxic shock syndrome".)

The interdigital toe spaces should be examined for fissuring or maceration; minimizing these conditions may reduce the likelihood of recurrent lower-extremity cellulitis.

Other forms of cellulitis include orbital cellulitis, abdominal wall cellulitis (in patients with morbid obesity), buccal cellulitis (due to S. pneumoniae and, prior to the conjugate vaccine era, H. influenzae type b) and perianal cellulitis (due to group A beta-hemolytic Streptococcus) [54,55]. Rarely, infections involving the medial third of the face (ie, the areas around the eyes and nose) can be complicated by septic cavernous thrombosis, since the veins in this region are valveless (figure 3). (See "Orbital cellulitis" and "Septic dural sinus thrombosis".)

Laboratory findings are nonspecific and may include leukocytosis and elevated inflammatory markers such as erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) [4,56].

Skin abscess — A skin abscess is a collection of pus within the dermis or subcutaneous space (picture 7 and figure 2). It manifests as a painful, fluctuant, erythematous nodule, with or without surrounding cellulitis [44]. Spontaneous drainage of purulent material may occur. Regional adenopathy may be observed. Fever, chills, and systemic toxicity are unusual.

A skin abscess may develop via deep infection of a hair follicle (known as a furuncle or boil), which reflects extension of purulent material through the dermis into the subcutaneous tissue. Multiple furuncles can coalesce to form carbuncles (picture 8), which may be associated with systemic symptoms. Common areas of involvement include the back of the neck, face, axillae, and buttocks.

Complications — Complications of cellulitis and abscess include bacteremia, endocarditis, septic arthritis or osteomyelitis, metastatic infection, sepsis, and toxic shock syndrome [4].

DIAGNOSIS — The diagnosis of cellulitis, erysipelas, and skin abscess is usually based upon clinical manifestations. Cellulitis and erysipelas manifest as areas of skin erythema, edema, and warmth (figure 1). Erysipelas lesions are raised above the level of surrounding skin with clear demarcation between involved and uninvolved tissue. A skin abscess manifests as a painful, fluctuant, erythematous nodule, with or without surrounding cellulitis (picture 7).

Laboratory testing is not required for patients with uncomplicated infection in the absence of comorbidities or complications.

Patients with drainable abscess should undergo incision and drainage [57,58]. Routine culture of debrided material is not necessary in healthy patients who do not receive antibiotics.

Cultures of debrided material and blood cultures (prior to addition of antibiotic therapy) are warranted in the following circumstances [59,60]:

●Severe local infection (eg, extensive cellulitis)

●Systemic signs of infection (eg, fever)

●History of recurrent or multiple abscesses

●Failure of initial antibiotic therapy

●Extremes of age (young infants or older adults)

●Presence of underlying comorbidities (lymphedema, malignancy, neutropenia, immunodeficiency, splenectomy, diabetes)

●Special exposures (animal bite, water-associated injury)

●Presence of indication for prophylaxis against infective endocarditis

●Community patterns of S. aureus susceptibility are unknown or rapidly changing

Positive blood cultures can impact antibiotic selection or prompt evaluation for additional infections (eg, osteomyelitis, endocarditis). Overall, blood cultures are positive in less than 10 percent of cellulitis cases, but certain populations may have higher rates of culture positivity [61-63]. For example, one observational study found that positive blood cultures occurred in 25 percent of older (≥65 years) individuals who were hospitalized for cellulitis, erysipelas, or skin abscess [64]. A skin biopsy may be warranted if the diagnosis is uncertain; cultures of skin biopsy specimens yield a pathogen in 20 to 30 percent of cases [65-68]. Cultures of swabs from intact skin are not helpful and should not be performed [2,3].

Radiographic examination can be useful to determine whether a skin abscess is present (via ultrasonography) (see "Techniques for skin abscess drainage", section on 'Bedside ultrasonography') and for distinguishing cellulitis from osteomyelitis (via magnetic resonance imaging) [69]. Radiographic evaluation may be warranted in patients with underlying immunosuppression, diabetes, venous insufficiency, or lymphedema and in patients with persistent systemic symptoms. Radiographic examination cannot reliably distinguish cellulitis from necrotizing fasciitis or gas gangrene; if there is clinical suspicion for these entities, radiographic imaging should not delay surgical intervention [70,71]. (See "Necrotizing soft tissue infections" and "Clostridial myonecrosis".)

In patients with recurrent cellulitis, serologic testing for beta-hemolytic streptococci may be a useful diagnostic tool. Assays include the anti-streptolysin-O (ASO) reaction, the anti-deoxyribonuclease B test (anti-DNAse B), the anti-hyaluronidase test (AHT), or the Streptozyme antibody assay [28]. Anti-DNase B and AHT responses are more reliable than the ASO response following group A streptococcal skin infections. (See "Acute cellulitis and erysipelas in adults: Treatment", section on 'Recurrent infection'.)

DIFFERENTIAL DIAGNOSIS

Cellulitis and erysipelas — Cellulitis is often confused with other infections or noninfectious illnesses [72,73].

Rapidly progressive erythema with signs of systemic toxicity should prompt consideration of severe infection, including:

●Necrotizing fasciitis – Necrotizing fasciitis is a deep infection that results in progressive destruction of the muscle fascia. The affected area may be erythematous, swollen, warm, and exquisitely tender. Pain out of proportion to exam findings may be observed. The diagnosis is established surgically with visualization of fascial planes. (See "Necrotizing soft tissue infections".)

●Toxic shock syndrome – Toxic shock syndrome typically presents with pain that precedes physical findings. Clinical signs of soft tissue infection consist of local swelling and erythema followed by ecchymoses and sloughing of skin. Fever is common. Patients may be normotensive on presentation but subsequently become hypotensive. (See "Invasive group A streptococcal infection and toxic shock syndrome: Epidemiology, clinical manifestations, and diagnosis".)

●Gas gangrene or myonecrosis – Gas gangrene should be suspected in the setting of fever and severe pain in an extremity, particularly in the setting of recent surgery or trauma. The presence of tissue crepitus favors clostridial infection. Gas gangrene can also be detected radiographically. (See "Clostridial myonecrosis".)

Cellulitis must be distinguished from other infections including:

●Erythema migrans – Erythema migrans is an early manifestation of Lyme disease; it consists of a region of erythema at the site of a tick bite, often with central clearing and a necrotic center (picture 9). The diagnosis is established based on serologic testing, although sensitivity in early disease is low. A similar lesion may occur in patients with Southern tick–associated rash illness. (See "Clinical manifestations of Lyme disease in adults" and "Southern tick-associated rash illness (STARI)".)

●Herpes zoster – The rash of herpes zoster begins as erythematous papules that evolve into grouped vesicles (picture 10). The rash is generally limited to one dermatome but can affect two or three neighboring dermatomes. The diagnosis is established by polymerase chain reaction (See "Epidemiology, clinical manifestations, and diagnosis of herpes zoster".)

●Septic arthritis – Cellulitis may overlie a septic joint. Clinical manifestations include joint pain, swelling, warmth, and limited range of motion. The diagnosis of septic arthritis is established based on synovial fluid examination. (See "Septic arthritis in adults".)

●Septic bursitis – Cellulitis may precede or accompany septic bursitis. Distinguishing cellulitis with and without bursitis depends on skilled palpation. Radiographic imaging is warranted if septic bursitis is suspected. (See "Septic bursitis".)

●Osteomyelitis – Osteomyelitis may underlie an area of cellulitis. It is prudent to pursue imaging for assessment of bone involvement in the setting of chronic soft tissue infection that fails to improve with appropriate antibiotic therapy. (See "Nonvertebral osteomyelitis in adults: Clinical manifestations and diagnosis".)

●Mycotic aneurysm – Mycotic aneurysm should be suspected in the setting of erythema, swelling, and tenderness at an intravenous drug injection site such as antecubital fossa [74]. The diagnosis is established via ultrasonography. (See "Overview of infected (mycotic) arterial aneurysm".)

Noninfectious masqueraders of cellulitis (unilateral) include:

●Contact dermatitis – Contact dermatitis may be distinguished from cellulitis in that the contact dermatitis lesions are pruritic. Clinical features include erythema, edema, vesicles, bullae, and oozing. The reaction is generally limited to the site of contact and is associated with burning, stinging, or pain. (See "Irritant contact dermatitis in adults".)

●Acute gout – Acute gouty arthritis consists of severe pain, warmth, erythema, and swelling overlying a single joint. The diagnosis can be established by synovial fluid analysis, which should demonstrate the characteristic urate crystals of gout or the calcium pyrophosphate crystals of pseudogout. Additional clues suggestive of gout include involvement of the first metatarsophalangeal joint, prior self-limited attacks of arthritis, and presence of tophi. (See "Clinical manifestations and diagnosis of gout".)

●Drug reaction – A drug reaction presents with an erythematous maculopapular rash that involves the trunk and proximal extremities. It may be accompanied by pruritus, low-grade fever, and mild eosinophilia. The diagnosis is suspected in a patient receiving drug treatment who presents with a rash of recent onset. The clinical suspicion can be substantiated by histopathologic examination of a skin biopsy. (See "Exanthematous (maculopapular) drug eruption".)

●Vasculitis – The morphology of cutaneous lesions of vasculitis is variable. Macular and papular (including palpable purpura) lesions are characteristically nonblanchable due to the presence of extravasated erythrocytes in the dermis, which occurs as a result of damaged vessel walls. The diagnosis is established by skin biopsy. (See "Evaluation of adults with cutaneous lesions of vasculitis".)

●Insect bite – An insect bite triggers an inflammatory reaction at the site of the punctured skin, which appears within minutes and consists of pruritic local erythema and edema. In some cases, a local reaction is followed by a delayed skin reaction consisting of local swelling, itching, and erythema. (See "Insect and other arthropod bites".)

●Deep venous thrombosis – Findings suggestive of cellulitis involving the lower extremity should prompt consideration of deep venous thrombosis; the evaluation consists of ultrasound evaluation. (See "Clinical presentation and diagnosis of the nonpregnant adult with suspected deep vein thrombosis of the lower extremity".)

●Panniculitis – Panniculitis refers to inflammation of subcutaneous fat and may have many causes, both infectious and noninfectious (table 2). The diagnosis is confirmed via biopsy. (See "Panniculitis: Recognition and diagnosis".)

●Vaccination site reaction – A local reaction to vaccination manifests with erythema, swelling, and tenderness at the injection site; these are typically self-limited. (See "Allergic reactions to vaccines", section on 'Delayed vaccine reactions' and "Allergic reactions to vaccines", section on 'Reactions to COVID-19 vaccines'.)

●Erythema ab igne - Erythema ab igne is an erythematous pigmented dermatosis resulting from repeated exposures to moderate heat or infrared radiation. The diagnosis is established clinically and may be confirmed by biopsy. (See "Acquired hyperpigmentation disorders", section on 'Erythema ab igne'.)

Noninfectious masqueraders of cellulitis (bilateral) include:

●Stasis dermatitis – Stasis dermatitis is an inflammatory dermatosis of the lower extremities that occurs in patients with chronic venous insufficiency. It is usually bilateral but can be unilateral in the setting of anatomic asymmetry. The diagnosis is usually established clinically (figure 1). (See "Stasis dermatitis" and "Clinical manifestations of lower extremity chronic venous disease".)

●Lipodermatosclerosis – Lipodermatosclerosis is a fibrosing panniculitis of the subcutaneous tissue that can develop in the setting of chronic venous insufficiency following severe cases of deep venous thrombosis or associated with lymphatic compromise. Typically the overlying skin is heavily pigmented and bound down to the subcutaneous tissues. (See "Clinical manifestations of lower extremity chronic venous disease", section on 'Lipodermatosclerosis (C4b)'.)

●Lymphedema – Lymphedema is abnormal accumulation of interstitial fluid resulting from injury or anatomic abnormality of the lymphatic system. The diagnosis is usually established clinically. (See "Clinical features and diagnosis of peripheral lymphedema".)

Skin abscess — Skin lesions that should be distinguished from skin abscess include:

●Epidermoid cyst – An epidermoid cyst is a skin-colored cutaneous nodule. The diagnosis is usually clinical, based on the clinical appearance of a discrete cyst or nodule, often with a central punctum, that is freely movable on palpation. Epidermoid cysts may become secondarily infected. (See "Overview of benign lesions of the skin", section on 'Epidermoid cyst'.)

●Folliculitis – Folliculitis refers to inflammation of one or more hair follicles. The diagnosis is often established clinically; rarely, Gram stain and culture or skin biopsy may be warranted to differentiate folliculitis from other conditions. (See "Infectious folliculitis".)

●Hidradenitis suppurativa – Hidradenitis suppurativa is a chronic suppurative process involving the skin and subcutaneous tissue of intertriginous skin. The diagnosis is usually established clinically. (See "Hidradenitis suppurativa: Pathogenesis, clinical features, and diagnosis".)

●Nodular lymphangitis – Nodular lymphangitis presents as nodular subcutaneous swellings along the course of the lymphatic channels. The differential diagnosis is broad and is summarized separately. (See "Lymphangitis", section on 'Nodular lymphangitis'.)

●Botryomycosis – Botryomycosis is a chronic, suppurative infection characterized by a granulomatous inflammatory response to S. aureus and other bacteria; it occurs most commonly in immunocompromised patients. The diagnosis is established via Gram stain, culture, or examination of pus for granules. (See "Botryomycosis".)

●Myiasis – Myiasis presents as an enlarging nodular mass associated with an insect bite; it is caused by penetration of fly larvae into subdermal tissue. The diagnosis is established via clinical manifestations in the setting of epidemiologic exposure to tropical and subtropical areas. (See "Skin lesions in the returning traveler", section on 'Myiasis'.)

The differential diagnosis for skin and soft tissue infections in immunocompromised patients is summarized separately. (See "Clinical manifestations, diagnosis, and grading of acute graft-versus-host disease", section on 'Differential diagnosis'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Skin and soft tissue infections".)

SUMMARY AND RECOMMENDATIONS

●Risk factors – These include skin barrier disruption, edema, venous insufficiency, and immunosuppression. However, healthy individuals with no risk factors may also develop these infections. (See 'Epidemiology' above.)

●Microbiology – The most common microbiologic cause of cellulitis is beta-hemolytic streptococci (groups A, B, C, G, and F), usually group A Streptococcus or Streptococcus pyogenes; Staphylococcus aureus (including methicillin-resistant strains) is a notable but less common cause. The vast majority of erysipelas cases are caused by beta-hemolytic streptococci. The most common microbiologic cause of skin abscess is S. aureus; a skin abscess can be caused by more than one pathogen. (See 'Microbiology' above.)

●Clinical manifestations – Cellulitis and erysipelas manifest as areas of skin erythema, edema, and warmth. Erysipelas lesions are raised above the level of surrounding skin with clear demarcation between involved and uninvolved tissue. Cellulitis and erysipelas are nearly always unilateral, and the lower extremities are the most common site of involvement (figure 1). A skin abscess manifests as a painful, fluctuant, erythematous nodule, with or without surrounding cellulitis. (See 'Clinical manifestations' above.)

●Diagnosis – The diagnosis of cellulitis, erysipelas, and skin abscess is usually based upon clinical manifestations. Cultures should be obtained from skin abscesses, and blood cultures are warranted for patients in the circumstances described above. (See 'Diagnosis' above.)

•Differential diagnosis – Misdiagnosis of these entities is common, and possible alternative diagnoses should be considered carefully (figure 1). (See 'Differential diagnosis' above.)

•Role of imaging – Ultrasound can be useful to determine whether skin abscess is present. Imaging studies cannot reliably distinguish cellulitis from necrotizing fasciitis or gas gangrene; if there is clinical suspicion for these entities, imaging should not delay surgical intervention. (See 'Diagnosis' above.)