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Burn Wound Infections Clinical Presentation

  • Author: Jairo A Fonseca, MD; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD  more...
 
Updated: May 25, 2016
 

History

The American Burn Association (ABA) has defined criteria for sepsis and wound infections.[18] Regular monitoring of burn wounds allows for early recognition of infection. Prolonged inpatient stay is one of the strongest risk factors for the development of colonization or infection, as longer hospitalizations increase the potential exposure to other colonized or infected patients and to environmental contamination. Large burn injuries are another strong risk factor, as open wounds are known to harbor bacteria.[19]

Local signs of burn wound infection include conversion of a partial-thickness injury to a full-thickness wound, worsening cellulitis of surrounding normal tissue, eschar separation, and tissue necrosis.

According to the ABA, the various types of burn wound infections include wound colonization, wound infection, invasive infection, cellulitis, and necrotizing infection/fasciitis.[18]

Wound colonization is characterized by the presence of low concentrations of bacteria on the surface without invasion or systemic signs or symptoms of infection. Tissue biopsies obtained from colonized but not infected skin usually reveal less than 105 bacteria per gram of tissue.

Wound infection is associated with higher concentration of bacteria (>105 bacteria per gram of tissue) within the wound or wound eschar but not a deeply invasive infection.

An invasive infection includes concentrations of bacteria (frequently >105 bacteria per gram of tissue) at an appropriate depth of the burn wound to cause suppurative separation of the eschar or graft loss with involvement of unburned tissue or the presence of a systemic response consistent with sepsis.

Cellulitis manifests as erythema, induration, warmth, and tenderness in the tissue surrounding the burn wound or wound eschar and, occasionally, the presence of sepsis. Erythema alone may not indicate cellulitis.

Necrotizing infection/fasciitis involves an aggressive invasive infection with involvement of structures below the skin.

Burn wound infections commonly occur in the first weeks of hospitalization. S aureus is the most common pathogen infecting burned patients, as it is an early colonizer. K pneumoniae wound infections occur around the same time as infections by S aureus and seem to be more prevalent in institutions that use systemic perioperative antimicrobial prophylaxis. As would be expected, infections by the nosocomial organisms P aeruginosa and A baumannii appear later in the course of the hospitalization, typically after 2 weeks of admission.[10]

Sepsis is an independent risk factor of mortality in the burned patient. This is a diagnostic challenge because the signs of sepsis (ie, elevated temperature, tachycardia, tachypnea, and leukocytosis) may be present in the burned patient without underlying infection.[20] Recognizing this difficulty, the ABA published burn-specific sepsis criteria with a total of 6 variables to consider. Meeting 3 of these criteria should prompt the clinician to consider the presence of a clinically significant infection and to initiate empirical antimicrobial therapy. A patient meets the definition of sepsis if these criteria are coupled with a documented infection (defined as a positive culture result, confirmatory histopathology finding, or a clinical response to antimicrobials).[18] Other studies have determined that a heart rate of more than 110 bpm, a systolic blood pressure of less than 100 mm Hg, and intubation are the best predictors of sepsis.[21]

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Causes

Risk factors for the development of a burn wound infection are as follows[3] :

  • Extremes of age
  • Comorbidities such as obesity and diabetes
  • Immunosuppression (eg, due to AIDS)
  • Invasive devices (eg, catheters)
  • Burns involving greater than 30% total body surface area (TBSA)
  • Full-thickness burns
  • Failure to cover burns or failed skin graft resulting in prolonged open burn wounds
  • Improper early burn care

Organisms frequently causing invasive burn wound infection are as follows:[10]

  • Gram-positive bacteria - S aureus, including MRSA; coagulase-negative Staphylococcus species; Enterococcus species, including vancomycin-resistant species
  • Gram-negative bacteria - P aeruginosa, Klebsiella species, Acinetobacter species, Escherichia coli, Serratia marcescens, Enterobacter species, Proteus species
  • Fungi (burn wounds complicated by fungal infections constitute an independent predictor for mortality in patients with a burned TBSA of 30-60% [6] ) - Candida species; Aspergillus species; Fusarium species; Phaeohyphomycetes (fungi with dark cell walls); Mucorales (eg, Rhizopus, Mucor, Absidia, and Apophysomyces species)
  • Viruses (Cutaneous disease typically occurs in healing partial-thickness burns and donor sites.) - Herpes simplex virus, varicella-zoster virus
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Physical Examination

Signs of wound infection are as follows:[18]

  • Suppurative separation of the eschar
  • Graft loss with involvement of unburned tissue or the presence of a systemic response consistent with sepsis
  • Change in wound color (eg, focal areas of red, brown, or black)
  • Green discoloration of the subcutaneous fat

Signs of cellulitis are as follows:[18]

  • Erythema (erythema alone may not require treatment)
  • Induration
  • Warmth
  • Tenderness
  • Sepsis (occasionally)

Signs of necrotizing infection/fasciitis signs include aggressive invasive infection with involvement of structures below the skin (eg, muscle, bone, organs).

Signs of sepsis are as follows:[20]

  • Temperature greater than 39°C or less than 36.5°C
  • Progressive tachycardia (>110 beats per minute)
  • Progressive tachypnea - More than 25 breaths per minute without assisted ventilation; minute ventilation greater than 12 L/min if intubated and mechanically ventilated
  • Thrombocytopenia (< 100,000/μL; does not apply immediately after initial resuscitation)
  • Hyperglycemia (in the absence of pre-existing diabetes mellitus) - Plasma glucose levels greater than 200 mg/dL in the absence of treatment; significant resistance to insulin (>25% increase in insulin requirement) [2]
  • Inability to continue enteral feedings for more than 24 hours - Abdominal distension, high gastric residuals, uncontrollable diarrhea
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Contributor Information and Disclosures
Author

Jairo A Fonseca, MD Postdoctoral Fellow, Emory Vaccine Center, Yerkes National Primate Research Center, Emory University School of Medicine

Jairo A Fonseca, MD is a member of the following medical societies: American College of Physicians, American Society of Tropical Medicine and Hygiene

Disclosure: Nothing to disclose.

Coauthor(s)

Duane R Hospenthal, MD, PhD, FACP, FIDSA, FASTMH Adjunct Professor of Medicine, Department of Medicine, University of Texas Health Science Center at San Antonio

Duane R Hospenthal, MD, PhD, FACP, FIDSA, FASTMH is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, American Society of Tropical Medicine and Hygiene, Infectious Diseases Society of America, International Society for Infectious Diseases, International Society of Travel Medicine, Medical Mycological Society of the Americas, Armed Forces Infectious Diseases Society, International Society for Human and Animal Mycology, American College of Physicians, American Society for Microbiology, Society for Healthcare Epidemiology of America

Disclosure: Nothing to disclose.

Specialty Editor Board

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

Disclosure: Received salary from Medscape for employment. for: Medscape.

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: American College of Physicians, Alliance for the Prudent Use of Antibiotics, The Foundation for AIDS Research, Southern Society for Clinical Investigation, Southwestern Association of Clinical Microbiology, Association of Professors of Medicine, Association for Professionals in Infection Control and Epidemiology, American Clinical and Climatological Association, Infectious Disease Society for Obstetrics and Gynecology, Orleans Parish Medical Society, Southeastern Clinical Club, American Association for the Advancement of Science, Alpha Omega Alpha, American Association of University Professors, American Association for Physician Leadership, American Federation for Medical Research, American Geriatrics Society, American Lung Association, American Medical Association, American Society for Microbiology, American Thoracic Society, American Venereal Disease Association, Association of American Medical Colleges, Association of American Physicians, Infectious Diseases Society of America, Louisiana State Medical Society, Royal Society of Medicine, Sigma Xi, Society of General Internal Medicine, Southern Medical Association

Disclosure: Received royalty from Baxter International for other.

Chief Editor

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.

Additional Contributors

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, Louisiana State Medical Society

Disclosure: Nothing to disclose.

Acknowledgements

Clinton Murray, MD Program Director, Infectious Disease Fellowship, San Antonio Uniformed Services Health Education Consortium

Clinton Murray, MD is a member of the following medical societies: American College of Physicians-American Society of Internal Medicine, American Medical Association, American Society for Microbiology, American Society of Tropical Medicine and Hygiene, Association of Military Surgeons of the US, and Infectious Diseases Society of America

Disclosure: Nothing to disclose.

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Second-degree burns often are red, wet, and very painful. Their depth, ability to heal, and tendency to result in hypertrophic scar formation vary enormously.
 
 
 
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