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Cellulitis Clinical Presentation

  • Author: Thomas E Herchline, MD; Chief Editor: Michael Stuart Bronze, MD  more...
 
Updated: Aug 15, 2016
 

History

A directed history is vital to the proper care of a patient with cellulitis. The patient may or may not relate an episode of trauma that preceded symptoms; when cellulitis develops, it is usually several days after the inciting trauma. Rapid progression or significant pain is a concerning sign that may indicate a severe problem, such as necrotizing fasciitis, which should be managed promptly.

If the patient recalls an episode of trauma, the clinician should ask about circumstances surrounding the incident that may elicit clues to a particular etiology. For example, exposure to standing or brackish water could mean that Aeromonas or Vibrio is the cause of infection; or a cut that occurred while butchering may be an important clue to consider Erysipelothrix rhusiopathiae. Identifying the specific inciting cause helps the clinician identify the most likely pathogen, choose appropriate antibiotic therapy, and offer appropriate immunization, such as tetanus toxoid (Td or Tdap), if indicated.

The patient should also be questioned about the presence of other skin disorders, including various types of dermatitis and especially any preceding fungal infection, which may serve as a portal of entry for bacterial pathogens.[17]

The past medical history should focus on the presence of comorbid conditions that may increase the risk for cellulitis, with the most common ones being diabetes mellitus, human immunodeficiency virus (HIV) infection/acquired immunodeficiency syndrome (AIDS), chronic kidney disease, and chronic liver disease.

The surgical history may include a recent procedure that resulted in wound infection. For example, severe bacterial cellulitis may occur as a postsurgical complication following hip replacement[56] or liposuction. Alternatively, a remote surgical history involving lymph node dissection (eg, following either radical mastectomy or conservative breast surgery) may predispose to cellulitis, even years after the surgery, because of lymphatic occlusion.[57, 58, 59, 60] Impaired lymphatic drainage and edema are also considered predisposing factors to leg cellulitis following saphenous vein resection for coronary artery bypass.[22] In addition, the presence of foreign bodies, including indwelling IV catheters, external orthopedic pins, and other surgical devices, may predispose to infection.

Next

Physical Examination

The physical examination should first focus on the area of concern. Nonpurulent cellulitis is associated with 4 cardinal signs of infection: erythema, pain, swelling, and warmth. Several physical examination findings may help the clinician identify the most likely pathogen and assess the severity of the infection, thereby facilitating appropriate treatment. Those findings include the following:

  • The involved site(s)is/are red, hot, swollen, and tender
  • Unlike erysipelas, the borders are not elevated or sharply demarcated
  • The involved site is the leg, which is the most common site [46, 61]
  • Regional lymphadenopathy is present
  • Malaise, chills, fever, and toxicity are present
  • Skin infection without underlying drainage, penetrating trauma, eschar, or abscess is most likely caused by streptococci; on the other hand, S aureus, often community-acquired methicillin-resistant S aureus (CA-MRSA), is the most likely pathogen when these factors are present [1]
  • Perianal cellulitis is usually observed in children with perianal fissures; it is characterized by perianal erythema and pruritus, purulent secretions, painful defecation, and blood in the stools [62]
  • Cellulitis characterized by violaceous color and bullae suggests more serious or systemic infection with organisms such as V vulnificus (see the image below) or S pneumoniae
    Cellulitis due to documented Vibrio vulnificus inf Cellulitis due to documented Vibrio vulnificus infection. (Image courtesy of Kepler Davis.)
  • Lymphangitic spread (red lines streaking away from the area of infection), crepitus, and hemodynamic instability are indications of severe infection, requiring more aggressive treatment
  • Circumferential cellulitis or pain that is disproportional to examination findings should prompt consideration of severe soft-tissue infection

The IDSA indicates that the following are also signs/symptoms of potentially severe deep soft-tissue infection (Note: these frequently appear later in the course of necrotizing infections), which necessitate emergent surgical evaluation[2] :

  • Violaceous bullae
  • Cutaneous hemorrhage
  • Skin sloughing
  • Skin anesthesia
  • Rapid progression
  • Gas in the tissue
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Contributor Information and Disclosures
Author

Thomas E Herchline, MD Professor of Medicine, Wright State University, Boonshoft School of Medicine; Medical Director, Public Health, Dayton and Montgomery County, Ohio

Thomas E Herchline, MD is a member of the following medical societies: Alpha Omega Alpha, Infectious Diseases Society of Ohio, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Coauthor(s)

Pranatharthi Haran Chandrasekar, MBBS, MD Professor, Chief of Infectious Disease, Program Director of Infectious Disease Fellowship, Department of Internal Medicine, Wayne State University School of Medicine

Pranatharthi Haran Chandrasekar, MBBS, MD is a member of the following medical societies: American College of Physicians, American Society for Microbiology, International Immunocompromised Host Society, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Subramanian Swaminathan, DNB, MD Fellow, Department of Infectious Diseases, Detroit Medical Center, Wayne State University School of Medicine

Subramanian Swaminathan, DNB, MD is a member of the following medical societies: American College of Physicians, Infectious Diseases Society of America, International AIDS Society, HIV Medicine Association

Disclosure: Nothing to disclose.

Chief Editor

Michael Stuart Bronze, MD David Ross Boyd Professor and Chairman, Department of Medicine, Stewart G Wolf Endowed Chair in Internal Medicine, Department of Medicine, University of Oklahoma Health Science Center; Master of the American College of Physicians; Fellow, Infectious Diseases Society of America

Michael Stuart Bronze, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, Oklahoma State Medical Association, Southern Society for Clinical Investigation, Association of Professors of Medicine, American College of Physicians, Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Acknowledgements

Barry E Brenner, MD, PhD, FACEP Professor of Emergency Medicine, Professor of Internal Medicine, Program Director, Emergency Medicine, Case Medical Center, University Hospitals, Case Western Reserve University School of Medicine

Barry E Brenner, MD, PhD, FACEP is a member of the following medical societies: Alpha Omega Alpha, American Academy of Emergency Medicine, American College of Chest Physicians, American College of Emergency Physicians, American College of Physicians, American Heart Association, American Thoracic Society, Arkansas Medical Society, New York Academy of Medicine, New York Academy ofSciences,andSociety for Academic Emergency Medicine

Disclosure: Nothing to disclose.

David F Butler, MD Professor of Dermatology, Texas A&M University College of Medicine; Chair, Department of Dermatology, Director, Dermatology Residency Training Program, Scott and White Clinic, Northside Clinic

David F Butler, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, American Society for MOHS Surgery, Association of Military Dermatologists, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Dennis Cunningham, MD Assistant Professor of Pediatrics, Section of Infectious Diseases, Children's Hospital, Ohio State College of Medicine

Disclosure: Nothing to disclose.

Danny Lee Curtis, MD Clinical Assistant Professor of Medicine, University of South Florida College of Medicine; Consulting Staff, James A Haley Veterans Hospital

Danny Lee Curtis, MD is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Vinod K Dhawan, MD, FACP, FRCP(C), FIDSA Professor, Department of Clinical Medicine, University of California, Los Angeles, David Geffen School of Medicine; Chief, Division of Infectious Diseases, Rancho Los Amigos National Rehabilitation Center

Vinod K Dhawan, MD, FACP, FRCP(C), FIDSA is a member of the following medical societies: American College of Physicians, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, and Royal College of Physicians and Surgeons of Canada

Disclosure: Pfizer Inc Honoraria Speaking and teaching

Robert Edelman, MD Professor, Associate Director for Clinical Research, Department of Medicine, Division of Geographic Medicine, Center for Vaccine Development, University of Maryland School of Medicine

Disclosure: Nothing to disclose.

Dirk M Elston, MD Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Eric S Halsey, MD Head, Virology Department, Naval Medical Research Center Detachment-Peru (NMRCD-Peru); Assistant Professor of Medicine, Uniformed Services University of the Health Sciences

Eric S Halsey, MD is a member of the following medical societies: Armed Forces Infectious Diseases Society, HIV Medicine Association of America, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

Isaac P Humphrey, MD Assistant Professor of Internal Medicine, Uniformed Services University of the Health Sciences; Clinical Assistant Professor of Internal Medicine, Wright State University Boonshoft School of Medicine

Isaac P Humphrey, MD is a member of the following medical societies: American College of Physicians

Disclosure: Nothing to disclose.

William D James, MD Paul R Gross Professor of Dermatology, Vice-Chairman, Residency Program Director, Department of Dermatology, University of Pennsylvania School of Medicine

William D James, MD is a member of the following medical societies: American Academy of Dermatology and Society for Investigative Dermatology

Disclosure: Elsevier Royalty Other

Sungnack Lee, MD Vice President of Medical Affairs, Professor, Department of Dermatology, Ajou University School of Medicine, Korea

Sungnack Lee, MD is a member of the following medical societies: American Dermatological Association

Disclosure: Nothing to disclose.

Fred A Lopez, MD Associate Professor and Vice Chair, Department of Medicine, Assistant Dean for Student Affairs, Louisiana State University School of Medicine

Fred A Lopez, MD is a member of the following medical societies: Alpha Omega Alpha, American College of Physicians-American Society of Internal Medicine, Infectious Diseases Society of America, and Louisiana State Medical Society

Disclosure: Nothing to disclose.

Mark Louden, MD, FACEP Assistant Medical Director, Emergency Department, Duke Raleigh Hospital

Mark Louden, MD, FACEP is a member of the following medical societies: American Academy of Emergency Medicine and American College of Emergency Physicians

Disclosure: Nothing to disclose.

Giuseppe Micali, MD Head, Professor, Department of Dermatology, University of Catania School of Medicine, Italy

Giuseppe Micali, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Christen M Mowad, MD Associate Professor, Department of Dermatology, Geisinger Medical Center

Christen M Mowad, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Maria R Nasca, MD, PhD Assistant Professor, Department of Dermatology, University of Catania School of Medicine, Italy

Disclosure: Nothing to disclose.

Charles V Sanders, MD Edgar Hull Professor and Chairman, Department of Internal Medicine, Professor of Microbiology, Immunology and Parasitology, Louisiana State University School of Medicine at New Orleans; Medical Director, Medicine Hospital Center, Charity Hospital and Medical Center of Louisiana at New Orleans; Consulting Staff, Ochsner Medical Center

Charles V Sanders, MD is a member of the following medical societies: Alliance for the Prudent Use of Antibiotics, Alpha Omega Alpha, American Association for the Advancement of Science, American Association of University Professors, American Clinical and Climatological Association, American College of Physician Executives, American College of Physicians, American Federation for Medical Research, American Foundation for AIDS Research, AmericanGeriatricsSociety, American Lung Association, American Medical Association, American Society for Microbiology, American Thoracic Society, American Venereal Disease Association, Association for Professionals in Infection Control and Epidemiology, Association of American Medical Colleges, Association of American Physicians, Association of Professors of Medicine, Infectious Disease Society for Obstetrics and Gynecology, InfectiousDiseases Societyof America, Louisiana State Medical Society, Orleans Parish Medical Society, Royal Society of Medicine, Sigma Xi, Society of General Internal Medicine, Southeastern Clinical Club, Southern Medical Association, Southern Society for Clinical Investigation, and Southwestern Association of Clinical Microbiology

Disclosure: Baxter International and Johnson & Johnson Royalty Other

Barry J Sheridan, DO Chief Warrior in Transition Services, Brooke Army Medical Center

Barry J Sheridan, DO is a member of the following medical societies: American Academy of Emergency Medicine

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Medscape Salary Employment

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Mild cellulitis with a fine lacelike pattern of erythema. This lesion was only slightly warm and caused minimal pain, which is typical for the initial presentation of mild cellulitis.
Swelling seen in cellulitis involving the hand. In a situation with hand cellulitis, always rule out deep infection by imaging studies or by obtaining surgical consultation.
Severe cellulitis of the leg in a woman aged 80 years. The cellulitis developed beneath a cast and was painful and warm to the touch. Significant erythema is evident. The margins are irregular but not raised. An ulcerated area is visible in the center of the photograph.
Burns complicated by cellulitis. The larger lesion is a second-degree burn (left), and the smaller lesion is a first-degree burn (right), each with an expanding zone of erythema consistent with cellulitis.
Cellulitis due to documented Vibrio vulnificus infection. (Image courtesy of Kepler Davis.)
A case of cellulitis without associated purulence in an infant. Note the presence of lymphedema, a risk factor for cellulitis.(Photo courtesy of Amy Williams.)
Patient with cellulitis of the left ankle. This cellulitis was caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA). (Photo courtesy of Texas Dept. of Public Health.)
Abscess and associated cellulitis caused by community-acquired methicillin-resistant Staphylococcus aureus (CA-MRSA). (Photo courtesy of Texas Dept. of Public Health.)
Guidelines for the management of patients who require hospitalization for cellulitis or cutaneous abscess. AFB = acid-fast bacilli; BID = twice daily; CRP = C reactive protein; CT = computed tomography scanning; DS = double strength; DM = diabetes mellitus; ESR = erythrocyte sedimentation rate; ESRD = end-stage renal disease; HIV = human immunodeficiency virus; ICU = intensive care unit; I&D = incision and drainage; ID = infectious disease; IDU = injection drug user; IV = intravenous; LRINEC = Laboratory Risk Indicator for Necrotizing Fasciitis; MRI = magnetic resonance imaging; MSRA = methicillin-resistant Staphylococcus aureus; NSAIDS = nonsteroidal anti-inflammatory drugs; PO = by mouth; SSTI = skin and soft-tissue infections; TID = 3 times daily. Adapted from Jenkins TC, Knepper BC, Sabel AL, et al. Decreased antibiotic utilization after implementation of a guideline for inpatient cellulitis and cutaneous abscess. Arch Intern Med. 2011;171(12):1072-9.
A male patient with orbital cellulitis with proptosis, ophthalmoplegia, and edema and erythema of the eyelids. The patient also exhibited pain on eye movement, fever, headache, and malaise.
A male patient with orbital cellulitis with proptosis, ophthalmoplegia, and edema and erythema of the eyelids. The patient also exhibited chemosis and resistance to retropulsion of the globe.
Gross photograph of complicated cellulitis. Instead of the presence of yellow fat, the tissue is hemorrhagic and necrotic.
Hematoxylin and eosin (H&E) stain, high power. This image shows deeper subcutaneous tissue involved in a case of cellulitis, with acute inflammatory cells and fat necrosis.
Hematoxylin and eosin (H&E) stain, high power. This image shows cellulitis caused by herpes simplex virus, with the multinucleated organism in the center of the picture.
Table 1. Empiric Antibiotic Therapy for Cellulitis by Etiology and Anatomic Location
Location Likely Organisms Other Organisms Complication/ Discussion Antibiotic Regimen -- Oral/ Outpatient Indication for Hospitalization Antibiotic Regimen -- Parenteral/ Hospitalized
Uncomplicated cellulitis Group A streptococci much more likely than Staphylococcus aureus     Cephalexin or dicloxacillin



or clindamycin



  Cefazolin or oxacillin



or nafcillin



Cellulitis, concern for methicillin-resistant S aureus is a concern Group A streptococci and S aureus     [(Cephalexin or dicloxacillin or clindamycin) plus trimethoprim/ sulfamethoxazole]



or



Clindamycin



  Vancomycin



Daptomycin



Ceftaroline



Dog bite Pasteurella species (50% of wounds)



S aureus



Streptococcus pyogenes



Staphylococci, streptococci



Aerobes --Moraxella and Neisseria



Anaerobes --Fusobacterium, Bacteroides, Porphyromonas, and Prevotella



Capnocytophaga canimorsus may cause sepsis in patients with asplenia/hepatic disease.



Avoid first-generation cephalosporins/ erythromycin/ dicloxacillin.



High likelihood of infection –



Prophylactic antibiotics indicated for the following wounds: deep puncture, hands, requiring surgical repair, immunocompromised host, venous or lymphatic compromise, crush injury.



Requires close follow-up care within 24-48 h.



Amoxicillin/ clavulanate



Penicillin allergic:



Moxifloxacin



Deep wounds or severe wounds;



infections not responding to oral antibiotics



Third-generation cephalosporin (ceftriaxone [Rocephin]) plus metronidazole



or



beta-lactam/beta-lactamase inhibitor (eg, ampicillin/sulbactam) or



fluoroquinolone plus metronidazole



or



carbapenem (ertapenem)



Human bite Eikenella corrodens (gram-negative facultative anaerobe, 29% of wounds)



Aerobic gram-positive cocci, anaerobes



  Clenched fist lacerations over metacarpophalangeal joints should be considered human bites; anesthetize wounds and irrigate; reevaluate within 24-48 h.



Intercanine distance >3 cm is likely bite from adult; if wound to child, consider abuse.



Amoxicillin/ clavulanate



Penicillin allergic:



Moxifloxacin



or



(Clindamycin or metronidazole) plus (doxycycline or cefuroxime or trimethoprim/ sulfamethoxazole)



  Third-generation cephalosporin (Rocephin) plus metronidazole



or



beta-lactam/beta-lactamase inhibitor (eg, ampicillin/sulbactam)



or



fluoroquinolone plus metronidazole



or



carbapenem (ertapenem)



Cat bite Pasteurella multocida and P septica (75% of wounds) Staphylococci, streptococci, Bacteroides, Peptostreptococcus, Actinomyces, Fusobacterium, Porphyromonas, and Veillonella parvula Avoid first-generation cephalosporins/ erythromycin/ dicloxacillin



High likelihood of infection -- Prophylactic antibiotics indicated for the following wounds: deep puncture, hands, requiring surgical repair, immunocompromised host, venous or lymphatic compromise.



Requires close follow-up care within 24-48 h.



Amoxicillin/ clavulanate



Penicillin allergic --



Moxifloxacin



or



(Clindamycin or metronidazole) plus



(doxycycline or cefuroxime or trimethoprim/ sulfamethoxazole)



Deep wounds or severe wounds; infections not responding to oral antibiotics Third-generation cephalosporin (Rocephin) plus metronidazole



or



beta-lactam/beta-lactamase inhibitor (eg, ampicillin/sulbactam) or



fluoroquinolone plus metronidazole



or



carbapenem (ertapenem)



Preseptal (periorbital) cellulitis Haemophilus influenzae type b, Streptococcus pneumoniae, S aureus, other streptococcal species, and anaerobes Nocardia brasiliensis, Bacillus anthracis, Pseudomonas aeruginosa, Neisseria gonorrhoeae, Proteus species, Pasteurella multocida, Mycobacterium tuberculosis Largest study indicates that H influenzae type b and S pneumoniae not diminished in facial cellulitis as a result of immunizations[25] Amoxicillin-clavulanate, cefpodoxime, cefdinir Age < 1 y/ more severe disease require intravenous antibiotic Third-generation cephalosporin (Rocephin)
Lower extremity --



Complicating saphenous venectomy site after coronary bypass grafting



No pathogen identifiable in most infections, but it is likely to be streptococcal (> staphylococcal)



Non-group A beta-hemolytic streptococci most likely organism; S aureus less common



  Recurrent episodes common; may be associated with rigors, extreme fatigue, myalgias, and hypotension; some associated with tinea pedis (toe web cultures may be useful in establishing probable pathogen) Dicloxacillin or cephalexin.



Add trimethoprim/ sulfamethoxazole or tetracycline or clindamycin if concern for methicillin-resistant S aureus



  First-generation cephalosporin (cefazolin); clindamycin; vancomycin
Breast/arm - - (not mastitis)



Complicating breast cancer surgery/lymph node dissection



No pathogen identifiable in most infections



Group A or Non-group A beta-hemolytic streptococci most likely organisms



    Dicloxacillin, cephalexin. Add trimethoprim/ sulfamethoxazole or tetracycline or clindamycin if concern for methicillin-resistant S aureus Fever, recent chemotherapy, neutropenia Multiple regimens, none clearly superior –Piperacillin/tazobactam or ceftazidime plus aminoglycoside;



or



ciprofloxacin plus beta-lactam



or



monotherapy with piperacillin/tazobactam or cefepime



Aquatic environment --



Fresh water/ salt water/ brackish water/ swimming pools/ aquarium



Puncture/ laceration



Aeromonas hydrophila, Pseudomonas and Plesiomonas species, Vibrio species, Erysipelothrix rhusiopathiae, Mycobacterium marinum, and others   A hydrophila and Vibrio vulnificus may produce rapidly progressive soft-tissue infection and sepsis Fluoroquinolone (eg, ciprofloxacin or levofloxacin)



Note: For M marinum infection, use clarithromycin plus either ethambutol or rifampin



  Third- or fourth-generation cephalosporin (eg, ceftazidime or cefepime) or fluoroquinolone (eg, ciprofloxacin or levofloxacin)
Clenched-fist injury E corrodens (gram-negative anaerobe, 29 % of wounds); aerobic gram-positive cocci, anaerobes   Lacerations over metacarpophalangeal joints should be considered human bites; anesthetize wounds and irrigate; reevaluate within 24-48 h



Lacerations of extensor tendon



Amoxicillin/ clavulanate; penicillin allergic:



Moxifloxacin



or



(clindamycin or metronidazole) plus (doxycycline or cefuroxime or trimethoprim/ sulfamethoxazole)



Failure to respond to oral therapy marked by increasing pain and swelling or purulent drainage Beta-lactam/beta-lactamase inhibitor (eg, ampicillin/sulbactam)
Odontogenic facial cellulitis Aerobic and facultative organisms: group A beta-hemolytic streptococci, Neisseria and Eikenella species



Anaerobes: Prevotella and Peptostreptococcus species



  Require extraction or root canal Amoxicillin-clavulanate



or



clindamycin



  Beta-lactam/beta-lactamase inhibitor (eg, ampicillin/sulbactam) or



clindamycin



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