eMedicine Specialties > Infectious Diseases > Skin and Soft-Tissue Infections

Burn Wound Infections

Author: Clinton Murray, MD, Program Director, Infectious Disease Fellowship, San Antonio Uniformed Services Health Education Consortium
Coauthor(s): Duane R Hospenthal, MD, PhD, Chief, Infectious Disease Service, Brooke Army Medical Center and Associate Professor, Department of Medicine, Uniformed Service University of Health Sciences
Contributor Information and Disclosures

Updated: Apr 16, 2008

Introduction

Background

Approximately 500,000 persons seek medical treatment for burns every year in the United States. Of these, approximately 40,000 are hospitalized for burn injuries, including 25,000 admissions to the approximately 125 medical centers that specialize in burn care. Typically, 4,000 people die from fire and burns every year; of these, approximately 3,500 deaths are due to residential fires, and 500 are due to motor vehicle and aircraft accidents, electrical injuries, chemical exposures, or hot-liquid and substance spills. Among fatalities, nearly 75% die at the scene of the incident or during initial transport. Of those who reach medical care, infection is a major cause of morbidity and mortality.  
 
The skin, one of the largest organs in the body, performs numerous vital functions, including fluid homeostasis, thermoregulation, immunologic functions, neurosensory functions, and metabolic functions (eg, vitamin D). The skin also provides primary protection against infection by acting as a physical barrier. When this barrier is damaged, pathogens have a direct route to infiltrate the body, possibly resulting in infection.
 
In addition to the nature and extent of the thermal injury influencing infections, the type and quantity of microorganisms that colonize the burn wound appear to influence the future risk of invasive wound infection. The pathogens that infect the wound are primarily gram-positive bacteria such as methicillin-resistant Staphylococcus aureus (MRSA) and gram-negative bacteria such as Acinetobacter baumannii-calcoaceticus complex , Pseudomonas aeruginosa, and Klebsiella species. These latter pathogens are notable for their increasing resistance to a broad array of different antimicrobial agents. In addition, burn wounds are commonly infected with fungal pathogens.

Factors that are associated with improved outcome and prevention of infection likely include early burn-eschar excision, topical and prophylactic antibiotics, and aggressive infection-control measures.

Pathophysiology

The burn wound typically has 3 characteristic areas of involvement. The first is the zone of coagulation, which is nearest the heat source and includes dead tissue that forms the burn eschar. The second is the zone of stasis, which is adjacent to the area of necrosis; this area is viable but is at a substantial risk for ongoing necrosis and ischemic damage due to perfusion defects. The third is the zone of hyperemia, which includes relatively healthy skin with increased blood flow and vasodilation in response to the injury; the cellular injury in this area is minimal.

Wounds reflect the mechanism of the burn. In thermal burns, the degree of cellular damage varies based on the duration and temperature of exposure. Increasing temperatures alter molecular confirmation, destroy cell membranes, denature protein, and release oxygen-free radicals, all resulting in cell death and burn eschar. Types of chemical burns differ and include those due to reducing agents (eg, hydrochloric acid), oxidizing agents (eg, sodium hypochlorite), and corrosive agents (eg, phenol); each causes burn injuries with varying modes of action.
 
Burns alter not only the innate immune character of the skin but also other arms of the immune system. Overall, T-cell activity is reduced through an increase in the number of suppressor cells and a decrease in the number of helper cells. The levels of inflammatory cytokines and complement are also decreased. In addition, burn decrease the chemotaxis and phagocytic and bactericidal activity of neutrophils. One of the primary concerns associated with burn injuries is that the eschar is avascular, preventing immune cells and systemically administered antibiotics from being delivered to the site of infection.
 
Immediately following a thermal burn, the surface of the burn wound is free of microorganisms. However, deep cutaneous structures that survive the initial burn injury (eg, sweat glands, hair follicles) often contain staphylococci, which colonize the wound surface during the subsequent 48 hours. Over the following 5-7 days, other microbes, including gram-negative and gram-positive bacteria, colonize the wound. These potential pathogens typically come from the patients’ gastrointestinal tract, upper respiratory tract, or the hospital environment, transferring through contact with health care workers.

Fungal infections often develop later, after broad-spectrum antibiotics have been administered or after wound care has been delayed. Infections with anaerobes are rare, except after electrical injuries. Infections with viruses such as herpes simplex virus and varicella-zoster virus rarely complicate burn wounds.

Frequency

United States

According to the National Fire Protection Agency, US fire departments responded to 1.64 million fires during 2006. There were a total of 3,245 civilian fire-related deaths and 16,400 civilian fire-related injuries, resulting in one fire death every 162 minutes and one injury every 32 minutes. The total economic impact was estimated at $11.3 billion.

International

At the beginning of the 21st century, the Centre of Fire Statistics estimated that the average number of fires worldwide was 7-8 million, resulting in 70,000-80,000 fire deaths and 500,000-800,000 fire injuries. In Europe, 2-2.5 million fires were reported, resulting in 20,000-25,000 fire deaths and 250,000-500,000 fire injuries. The World Fire Statistics from the Geneva Association reported that, by country, the highest number of fire deaths in 2004 occurred in the United States (4,250), followed by Japan at 2,050 and the United Kingdom at 530. When adjusted for deaths per 100,000 persons between 2002 and 2004, of the 25 countries that reported data, the highest rate was in Hungary (2.1); Japan reported 1.79, the United States reported 1.39, the United Kingdom reported 0.97, Spain reported 0.61, and Singapore reported 0.08.

Mortality/Morbidity

According to the National Burn Repository’s 10-year rolling data collection from January 1, 1996, through June 30, 2006, the mortality rate associated with burns was 5.3% overall, with older age and higher-percentage total body surface area (TBSA) burned correlating with higher mortality rates.¹ The causes of death were reported in 3,463 cases; 27% died of multiple organ failure, 14% died from withheld treatment, 12% died from trauma wounds, 12% died from burn shock, 11% died from pulmonary failure/sepsis, 11% died from cardiovascular failure, 5% died from other causes, and 4% died from sepsis burn wound. Burns covering 1-10% of the TBSA carried the lowest risk of mortality (0.7%), increasing as the percentage of TBSA burned increased. The mortality rate was 78% in patients with 90% of their TBSA burned.
 
Among the 19,655 reported cases of complications included in the analysis, pulmonary complications including pneumonia (3,361), acute respiratory distress syndrome (885), and respiratory failure (1,944) constituted the greatest percentage of cases (31%). Cellulitis (1,988) and wound infections (1,950) were responsible for 17% of the complications. Septicemia (1,672) and other infections (1,250) were the other categories that included infectious complications (15%).

Race

Among 142,318 patients with burns reported in the National Burn Registry, 58% were white, 17.4% were African American, 12.8% were Hispanic, 2% were Asian, 0.6% were Native American, 1.8% were classified as other, and data were missing for 7.3%.

Sex

Among 142,318 burn patients reported in the National Burn Registry, 69.7% were male and 30.3% were female.

Age

Most burns occur in persons aged 5-30 years, with only 8% occurring in persons older than 70 years. Younger individuals are more likely to have scald burns, while older individuals are more likely to be burned by fire. With the same percentage of TBSA burned, older patients have a higher mortality rate.

Clinical

History

The American Burn Association (ABA) recently published criteria for sepsis and wound infections. Regular monitoring of burn wounds allows for the early recognition of infection. Local signs of burn wound infection include conversion of a partial-thickness injury to 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.

• 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.

Physical

• Wound infection 
  • 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 (focal areas of red, brown, or black)
  • Green discoloration of the subcutaneous fat
• Cellulitis  
  • Erythema (Erythema alone may not require treatment.)
  • Induration
  • Warmth
  • Tenderness
  • Sepsis (occasionally)
• Necrotizing infection/fasciitis - Aggressive invasive infection with involvement of structures below the skin (eg, muscle, bone, organs)
• Signs of sepsis  
  • Temperature greater than 39^o C or less than 36.5^o C
  • Progressive tachycardia (>110 beats per minute)
  • Progressive tachypnea
    • More than 25 breaths per minute without assisted ventilation
    • Minute ventilation greater than 12 L per minute 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

Causes

• Risk factors for the development of a burn wound infection  
  • Extremes of age
  • Comorbidities such as obesity and diabetes
  • Immunosuppression (eg, due to AIDS)
  • Invasive devices (eg, catheters)
  • Burns involving greater than 30% 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  
  • Gram-positive bacteria  
    • S aureus, including MRSA
    • Coagulase-negative S taphylococcus 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%.³ )  
    • Candida species
    • Aspergillus species
    • Fusarium species
    • Phaeohyphomycetes(dark molds)
    • Zygomycetes (eg, Rhizopus, Mucor, Absidia)
  • Viruses (Cutaneous disease typically occurs in healing partial-thickness burns and donor sites.)  
    • Herpes simplex virus
    • Varicella-zoster virus

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