Burn Wound Infections 

Updated: Dec 17, 2019
Author: Jairo A Fonseca, MD; Chief Editor: Pranatharthi Haran Chandrasekar, MBBS, MD 



Approximately 500,000 people seek medical attention for burns every year in the United States, 40,000 of whom require hospitalization.[1] Unlike other types of injury, burn wounds induce metabolic and inflammatory alterations that predispose the patient to various complications. Infection is the most common cause of morbidity and mortality in this population, with almost 61% of deaths being caused by infection.[2] (See the image below.)

Second-degree burns often are red, wet, and very p 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.

See Thermal Injuries: A Matter of Degree, a Critical Images slideshow, to help identify and treat various degrees and types of burn injuries.

Also, see the 5 Body Modifications and Piercing: Dermatologic Risks and Adverse Reactions slideshow to help recognize various body modifications and the related potential complications.

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 synthesis). The skin also provides primary protection against infection by acting as a physical barrier. When this barrier is damaged, pathogens can directly infiltrate the body, resulting in infection.[3]

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 risk of invasive wound infection. The pathogens that infect the wound are primarily gram-positive bacteria such as methicillin-resistant Staphylococcus aureus (MRSA)[4] 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 antimicrobial agents.[5, 6]

Fungal pathogens can also infect burn wounds. These infections occur more frequently after the use of broad-spectrum antibiotics. Among the fungal pathogens, Candida albicans is the most common cause of infection.[7] More recently, a trend toward nosocomially acquired, intrinsically resistant fungal infections (eg, Candida krusei) has been reported.[8]

Factors associated with improved outcome and infection prevention include early burn eschar excision, topical antibiotic therapy, and aggressive infection-control measures.[9]


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.[3]

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 conformation, destroy cell membranes, denature proteins, and release oxygen-free radicals; all of these phenomena lead to 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.[3, 9]

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 T regulatory cells and a decrease in the number of helper cells. The levels of inflammatory cytokines and complement are also decreased. In addition, burns decrease the chemotactic, phagocytic, and bactericidal activity of neutrophils. One of the primary concerns associated with burn injuries is the avascularity of eschar, preventing immune cells and systemically administered antibiotics from being delivered to the infection site.[3]

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 next 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, transferred through contact with healthcare workers.[3]

In animal models, the progression of burn wound infections has been assessed and the following progression observed: burn wound colonization, invasion into subjacent tissue (within 5 days), destruction of granulation tissue, visceral hematogenous lesions, manifestations of septic shock, and death.[10]

Early surgical debridement and skin grafting, use of topical and systemic antimicrobials, and enhanced infection-control practices have led to the replacement of beta-hemolytic streptococci with S aureus and gram-negative bacteria such as P aeruginosa, Klebsiella pneumoniae, and A baumannii as major pathogens in burn wound infections.[11]

In burns older than 7 days, biofilm may be detected in the ulcerated areas of the wounds. As biofilm formation is associated with chronicity of the wound, bacterial colonization is easier to eradicate in the first few days after injury, supporting early excision and closure of the burn wound.[12]

Fungal infections often develop later, after broad-spectrum antibiotics have been administered or after wound care has been delayed.[7, 13] Infections with anaerobes are rare, except after electrical injuries.[14] Infections with viruses such as herpes simplex virus and varicella-zoster virus rarely complicate burn wounds.



United States

According to the National Fire Protection Agency, US fire departments responded to 1.64 million fires during 2006. The total economic impact was estimated at $11.3 billion.[1] The American Burn Association (ABA) National Burn Repository reports that, among burns requiring hospitalizations, the most common place of occurrence was the household (73% of cases). Occupational (8%) and traffic-related injuries (5%) were much less common. One civilian fire death occurs every 2 hours and 41 minutes. The likelihood of a US resident dying of exposure to fire, flames, or smoke is 1 in 1442.[15]


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.


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. The causes of death were reported in 3,463 cases; 27% died of multiple organ failure, 14% died of withheld treatment, 12% died of trauma wounds, 12% died of burn shock, 11% died of pulmonary failure/sepsis, 11% died of cardiovascular failure, 5% died of other causes, and 4% died of burn wound sepsis. 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.[1]

Among the 19,655 reported 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 complications. Septicemia (1,672) and other infections (1,250) accounted for 15% of complications.[1]

Socioeconomic Status

The rates of admissions to burn units increase in proportion with diminishing socioeconomic status, with 95% of burn-related deaths occurring in low- and middle-income countries (LMICs). Additionally, there is an association between burn mortality and gross domestic product (GDP).[16] This can be explained as those with the least available resources are exposed to burn hazards such as poor housing quality (eg, a household with no separated kitchen), lack of smoke detectors, cigarette smoking, heavy drinking, solo parenthood, household overcrowding, and low educational level.[17]


According to the American Burn Association, among burn wounds requiring admission, 59% occurred in whites, 20% in blacks, 14% in Hispanics, and 7% in other ethnicities.[15]


Both the National Burn Registry and the American Burn Association report a higher incidence of burn wounds in males than in females, with approximately 69.7% of cases being in males.[1, 15]


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.[18]


The overall prognosis depends on numerous factors, including the patient’s age, percentage of TBSA burned, comorbidities, initial management strategies, and the support necessary for long-term rehabilitative care.

Patient Education

For patient education resources, see the First Aid and Injuries Center and the Thermal Heat or Fire) Burns article.




The American Burn Association (ABA) has defined criteria for sepsis and wound infections.[19] 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.[20]

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.[19]

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.[11]

Sepsis is an independent risk factor of mortality in the burned patient.[21] 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.[22] 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).[19] 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.[23]


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:[11]

  • 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% [7] ) - 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

Physical Examination

Signs of wound infection are as follows:[19]

  • 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:[19]

  • 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:[22]

  • 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


Burn wound infections are often the source of bacteria responsible for other systemic infections including bloodstream infections and pneumonia. This can lead to multisystem organ failure and death.[22]

Sepsis can contribute to multisystem organ failure and death.[22]

Early wound excision is associated with bleeding complications that require transfusions. Given the evidence that increased blood transfusion is associated with higher infection rates in the general trauma population, further data is needed to evaluate the overall utility of early excision especially as the overall data supporting this technique is limited although it is considered standard of care in most burn facilities.[24]





Laboratory Studies

Diagnosis of wound infection should focus on a careful physical examination that is performed frequently by personnel trained in the management of burns.

Laboratory tests or changes in laboratory values such as white blood cell (WBC) count, neutrophil percentage, erythrocyte sedimentation rate (ESR), and C-reactive protein (CRP) level are of low yield in detecting or predicting burn infections because of the inflammatory response associated with the burn itself.[25]

Laboratory examinations are useful for the initial risk assessment. Low prealbumin levels (100-150 mg/L) in burned patients are associated with a higher incidence of sepsis and organ dysfunction, lengthier stays, decreased ability of wound healing, and a higher mortality rate.[9, 26, 27]

In patients with suspected wound infections, procalcitonin (PCT) levels of 0.56 ng/mL have a reported sensitivity of 75% and a specificity of 80% when compared with quantitative swab culture.[28] Although these levels cannot be considered diagnostic, they should prompt the physician to start searching for an infectious source. In the only study that has compared PCT to American Burn Association (ABA) criteria for diagnosing sepsis, PCT was found to have potential utility in diagnosing sepsis in the burned patient. A threshold of 1.5 ng/mL had a sensitivity of 88% and specificity of 92% to diagnose septic complications in burned patients, with high levels found to be an independent predictor of mortality.[29] Without strong evidence to support a PCT threshold in burned patients, one recommendation is that PCT be obtained at admission and then monitored routinely to detect acute changes to guide the start of empirical antibiotic therapy.[28] PCT may also have a role in monitoring response to antimicrobial therapy, as appropriate antimicrobial therapy is associated with a reduction in PCT levels by the third day of treatment. In contrast, patients who died of multiple organ failure secondary to sepsis had PCT levels that remained elevated despite treatment.[28]

Diagnosis of a burn wound infection relies on clinical examination as outlined above (see Clinical) and culture data, including the following:[30]

  • Quantitative biopsy can be used to confirm infection but is not reliable. This procedure is useful in identifying the infecting pathogen.
  • Quantitative swab is of limited value but may aid in identifying the infecting pathogen.
  • Tissue histopathology allows for quantification and evaluation of infection depth and involvement of non-burned skin.

The use of routine wound cultures as part of surveillance procedures has been proposed to provide early identification of organisms colonizing the wound, to monitor response to therapy, to guide empiric therapy, and to evaluate for nosocomial transmission. However, this has not been shown to improve patient outcomes, and routine application has been brought into question.

Ono et al (2015) demonstrated that, among cases of local infection with Staphylococcus species, the burn wound exudate pH rises prior to the onset of clinical signs of local infection.[31]

Imaging Studies

No imaging studies have been identified as useful for detecting wound infections.


Multiple biopsy samples from several areas of the burn wound should be obtained and sent for histopathology and microbiological workup of the pathogens and their resistance profiles.

After cleaning the wound with isopropyl alcohol, 2 parallel incisions 1-2 cm in length and 1.5 cm apart with a depth to obtain a portion of the underlying fat are made in the skin. Alternatively, biopsy samples typically weighing 0.02-0.5 g may be obtained with a 3-mm punch-biopsy technique.

Biopsy is a commonly bypassed procedure because of technical difficulty within the microbiology section working up these types of samples or a lack of local histopathological expertise.

Histologic Findings

Bacteria are most commonly detected using Gram or hematoxylin and eosin (H&E) stains.

Fungi may be visualized on periodic acid-Schiff (PAS) or Gomori methenamine silver (GMS) staining, but recovery in culture is required for definitive identification.[13] Note the following:

  • Aspergillus-like morphology - Presence of parallel-walled, branching, septate hyphae may indicate Aspergillus species, Fusarium species, phaeohyphomycetes, or other molds
  • Mucor-like morphology (mucormycosis) - Presence of wide, ribbonlike, rarely septate hyphae most commonly denotes Mucorales (eg, Rhizopus, Mucor, Rhizomucor, Absidia)
  • Yeast-like morphology - Presence of budding yeasts or rounded yeast-like structures; many yeasts, including most Candida species, also produce hyphae and pseudohyphae in tissue

Herpes simplex virus can be isolated via identification of inclusions on light or electron microscopy or other viral particles on biopsy specimen or lesion scraping.


Various stages are used to diagnose burn wound infections.[3]

Stage I is colonization and includes the following substages:

  • Superficial - Microorganisms present only on burn wound surface

  • Penetrating - Variable depth of microbial penetration of eschar

  • Proliferating - Variable level of microbial proliferation at nonviable–viable tissue interface (subeschar space)

Stage II is invasion and includes the following substages:

  • Microinvasion - Microorganisms present in viable tissue immediately subjacent to subeschar space

  • Deep invasion - Penetration of microorganisms to variable depth and expanse within viable subcutaneous tissue

  • Microvascular involvement - Microorganisms within small blood vessels and lymphatics (thrombosis of vessels is common)



Medical Care

The goal of medical care is to prevent infection. Early excision and grafting is the current standard of care and the primary surgical method for reducing infection risk and length of hospital stay and increasing graft take.[10] A 2015 meta-analysis of all available randomized controlled studies found that early excision reduced mortality rates in all burned patients who did not have an inhalation injury.[32] A fast and permanent closure of full-thickness burns can be obtained with autografts (a split-thickness skin graft from an uninjured donor site on the same patient).[10] Nonetheless, donor sites are painful and impose their own wound-healing burden on the patient.[10] If donor sites are insufficient owing to an extensive burn area, allografts, xenografts, skin substitutes, or a dermal analog should be considered.[10]

Wound care should be directed at thoroughly removing devitalized tissue, debris, and previously placed topical antimicrobials. A broad-spectrum surgical antimicrobial topical scrub such as chlorhexidine gluconate should be used along with adequate analgesia and preemptive anxiolytic in order to permit adequate wound care.

For analgesia, the use of opiates is debated, as these medications induce tolerance and addiction and may promote pain, a phenomenon known as opioid-induced hyperalgesia.[33] Multimodal pain management should therefore be considered. Opioid-sparing agents include acetaminophen, ketamine, and alpha-adrenergic agonists such as clonidine and dexmedetomidine.[33] Nonsteroidal anti-inflammatory agents should be avoided, as they impair wound healing[10] and increase the risk of acute kidney injury and bleeding.

Topical antimicrobials for the prevention and treatment of burn wound infection include mafenide acetate, silver sulfadiazine, silver nitrate solution, and silver-impregnated dressings. These various therapies differ in their ability to penetrate eschars, antimicrobial activities, and adverse-event profiles.[34, 35]

The method of antimicrobial delivery may also affect results. A clinical trial comparing silver sulfadiazine as a cream or as a powdered spray showed the latter formulation achieved higher rates of infection prevention and sterilization.[36] Silver formulations may be associated with drug pressure, resulting in infections with resistant bacteria or fungus. A 2013 meta-analysis showed a statistically significant increase in burn wound infections and a longer length of stay in patients treated with silver sulfadiazine than in patients receiving wound dressing or skin substitutes. Of note, the included trials were at a high or unclear risk of bias.[37]

In the event of a localized MRSA burn wound infection, fusidic acid and gentamycin sulfate can be used as topical treatment. Topical vancomycin is also available and has been demonstrated to be more effective than the systemic formulation with a lower adverse effect rate.[36]

Antibiotic prophylaxis at the time of wound manipulation has also been studied in patients with burns. Only a few studies have supported this use of systemic antibiotics during acute burn surgery. Antibiotics appear to be of no value in the preoperative setting;[37] however, surgical prophylaxis in patients with burns of more than 40% TBSA appears to reduce the rate of burn wound infections, although it does not affect mortality.[32] In nonsurgical patients, systemic antibiotic prophylaxis does not affect the incidence of burn wound infection or sepsis.[37]

Treatment of airway colonization is not recommended, as local airway antibiotic prophylaxis does not influence sepsis or mortality rates.[37] Furthermore, selective decontamination of the digestive tract with nonabsorbable antibiotics plus cefotaxime significantly increases the risk of MRSA infection.[37]

When an infection is identified, antimicrobial therapy should be directed at the pathogen recovered on culture. In the setting of invasive infection or evidence of sepsis, empiric therapy should be initiated. The incidence of bacteremia in critically ill adult patients with burn wounds is reported to be 4%. The most frequent pathogens in North American burn centers include S aureus and P aeruginosa;[33] therefore, these microorganisms should be considered when choosing empiric therapy. It is important to remember that gram-negative pathogens isolated from burn centers (ie, P aeruginosa, A baumannii, Enterobacter species, K pneumoniae, E coli,Proteus species) do not differ significantly among burn centers worldwide.[38] A local burn facility's antibiogram should also be established to help direct empirical therapy.

Antimicrobial-resistant bacterial infection among burn patients is associated with prolonged stays in the hospital. Isolates recovered after 7, 14, and 21 days of hospitalization are considerably more likely to be resistant to the antibiotics tested compared with admission-day isolates. Changing resistance patterns throughout hospitalization can significantly affect empirical therapy choices for patients who develop infection weeks after arriving in the hospital. Inadequate initial antimicrobial therapy to treat multidrug-resistant (MDR) infections results in higher mortality rates.[11]

If an multidrug-resistant pathogen is isolated, colistin should be considered.[39] An evaluation of the antimicrobial activities of colistin against gram-negative bacteria isolates worldwide demonstrated that this medication is still effective with constant resistance levels. It is necessary to remember that this medication has a narrow therapeutic window, with nephrotoxicity and neurotoxicity being the most common adverse effects. Therefore, evaluation of the patient by an expert multidisciplinary group while the antibiotic therapy is underway is required.[40]

If fungi are observed on histopathology, culture samples to detect the infecting genus and species are necessary, as the available antifungals have varying activity against different fungi. Amphotericin B was once the agent of choice because of its broad spectrum, but some facilities have seen increased rates of infections with Fusarium species and Aspergillus terreus, which are innately resistant to amphotericin B. In these cases, voriconazole is often used. A newer agent, posaconazole, may have broader antifungal activity.[8, 13]

In addition to maintaining a hospital antibiogram, many centers monitor individual patient colonization using admission and scheduled (often weekly) cultures of wounds (or other sites). This can be informative despite the low yield, as samples that are positive for resistant pathogens can help tailor the choice of empirical antibiotic therapy if patients subsequently become septic.[41]

Hyperglycemia is associated with an increase in inflammatory response and occurs in burned patients because of the increased rate of glucose production and impaired tissue glucose extraction. Tight glucose control has been suggested to improve survival and to reduce the sepsis risk.[9, 42]

Propranolol has been studied for its potential benefits in burns. It is suggested that this drug may restore glycemic control, reduce peripheral lipolysis, and enhance the immune response to sepsis by modulation of the catecholamine release during severe burn injury. In a prospective, randomized trial of propranolol following injury, decreased healing time and hospital length of stay was noted.[9]

A meta-analysis in the use of recombinant growth hormone (rhGH) in burn patients could not find any study reporting burn wound infection as an outcome. It was observed that, among both children and adults with burns larger than 40% TBSA, rhGH hastened burn wound healing and reduced length of hospital stay. An increased risk for hyperglycemia was observed; nonetheless, rhGH treatment did not affect mortality.[43]

Patients with burns are also at risk for tetanus. Tetanus vaccination plus anti-tetanus immunoglobulin should be administered to patients who have no history of vaccination with booster tetanus toxoid vaccination given at 4 weeks and 6 months.

Surgical Care

This is fundamental to the care of the patient. Systemic and local antibiotics have limited effect in improving morbidity and mortality unless they are used in combination with adequate surgical care.


Consultation with an infectious disease specialist is suggested if multidrug-resistant bacteria are present.[44]


After a severe burn injury, a prolonged and persistent hypermetabolic response has been noted (believed to be secondary to elevation of catecholamines, cortisol, and inflammatory mediators). This response augments the metabolic rate, leading to muscle catabolism and immunosuppression.[45, 26]

The loss of body mass associated with severe burns has been associated with higher infection rates, delayed wound healing, and longer hospital stays; therefore, the initiation of early and aggressive nutritional support is required.[45, 10] Nutrition assessment should include a complete history and physical examination, evaluating features that may affect nutrition management.[26]

To manage the postburn hypermetabolic state and its complications, enteral nutrition is a safe, widely available, and effective measure that should be started within the first 24 hours of admission. Early enteral nutrition has been shown to deliver caloric requirements and diminish the hypermetabolic response, thus reducing complications. Delays in enteral nutrition initiation are associated with gut mucosal damage, decreased absorption, and bacterial translocation, leading to poorer outcomes.[9, 45] Early enteral nutrition should be started in patients with burns larger than 20% TBSA, even in patients who can be fed orally, as orally fed patients have higher complications and infection rates.[46]

Carbohydrate and fat intake must be closely monitored in burn patients, as their excesses can increase the risk of infection and sepsis.[10] Carbohydrates should be delivered at a rate of 7 g/kg/day, and fat should comprise less than 25% of the calories obtained from nonprotein sources.[47]

Although low albumin levels have been related with poor outcomes (see Laboratory Studies), albumin supplementation to maintain levels higher than 2 g/dL do not affect the length of stay, time to wound healing, or in-hospital mortality rate.[48]

A 2013 meta-analysis evaluated the use of glutamine supplementation in severely burned patients, showing a reduction in gram-negative infections and mortality with this intervention.[49]


Patients may be as active as they can tolerate. Aggressive physical and occupational therapy of extremity injuries is necessary to prevent long-term morbidity.[50]


Burn wound infections are often the source of bacteria responsible for other systemic infections, including bloodstream infections and pneumonia. This can lead to sepsis, multisystem organ failure, and death.[22]

Early wound excision is associated with bleeding complications that require transfusions. Given the evidence that increased blood transfusion is associated with higher infection rates in the general trauma population, further data are needed to evaluate the overall utility of early excision, especially since the overall data supporting this technique are limited, although it is considered the standard of care in most burn facilities.[24]


The prevention of burn wound infection is a team approach that includes the support of surgeons, nurses, infection-control providers, and infectious disease physicians. Emphasis on early wound care, infection-control practices, and long-term rehabilitative care is necessary to improve the morbidity and mortality associated with burns.

Early removal of full-thickness burned tissue, as well as early definitive wound closure and strict enforcement of infection-control procedures, is necessary to mitigate poor outcomes.

Further Outpatient Care

Patients require prolonged occupational and physical therapy support based on the site of the burn.[30]

Further Inpatient Care

A primary goal during hospitalization is to prevent nosocomial transmission of multidrug-resistant pathogens, especially in patients with a greater percentage of total body surface area (TBSA) burn (approximately 30%) or who are known to be colonized with multidrug-resistant bacteria such as MRSA, vancomycin-resistant Enterococcus species, or gram-negative bacteria known to develop resistance (eg, Pseudomonas, Klebsiella, Acinetobacter species).[6, 11]

Hand hygiene should be aggressively implemented. Standard precautions should be used in the care of all patients with burn injuries. Patients should be managed in single rooms, if possible, with use of contact precautions. Gowns and gloves should be used when contact with infected material or open wounds is expected. Masks and caps should be implemented based on the presence of multidrug-resistant bacteria. The use of individual-patient equipment should be considered.[20]

For catheter insertion, locations distal from the wound are necessary since catheters inserted near or through burn wounds are more frequently associated with infection development and earlier bacterial contamination with higher numbers of colony-forming units than catheters inserted distant from the wound. If a central venous catheter is required, femoral insertion sites are associated with higher infection rates.[51]

Routine surveillance cultures may be used in conjunction with isolation precautions for all or those patients with multidrug-resistant bacterial colonization or previous infection. Surveillance cultures, isolation, and hand hygiene, used in conjunction with regular feedback and education and environment control measures, have been shown to control the transmission of resistant pathogens.[9]


Aggressive infection-control procedures should be undertaken when transferring patients between facilities because of the risk of transferring multidrug-resistant bacteria.



Medication Summary

The goals of antimicrobial therapy are to treat an underlying infection, to reduce morbidity, and to prevent mortality. Topical therapy is often applied to prevent infection and to treat ongoing infections or used as an adjunct to surgical treatment and systemic antibiotics. Systemic antimicrobial agents should be directed at the underlying pathogen recovered from culture or determined empirically from the local burn unit’s antibiogram while culture results are pending. If carbapenem resistance is confirmed for an isolated gram-negative bacteria, colistin should be considered.[40]

Antifungal agents may also be used; however, pathogen identification is necessary to determine the ideal antifungal agent, as amphotericin B is not active against all fungal infections.

Antibacterial, Topical

Class Summary

Topical therapy is typically applied to prevent infection and to treat infection when adequate surgical management is not possible.

Chlorhexidine gluconate (Hibiclens, Hibistat, Tegaderm CHG Dressing)

Effective, safe, and reliable topical wash. Polybiguanide with bactericidal activity; usually supplied as a gluconate salt. At physiologic pH, the salt dissociates to a cation that binds to negatively charged bacterial cell walls and extramicrobial complex, causing bacteriostatic and bactericidal effects. Active against gram-positive and gram-negative organisms, facultative anaerobes, aerobes, and yeast.

Commercially available central venous catheters impregnated with chlorhexidine and silver sulfadiazine are available.

Silver sulfadiazine (Silvadene, SSD, Thermazene)

Silver sulfadiazine is useful in the prevention of infections from second- or third-degree burns. It has bactericidal activity against many gram-positive and gram-negative bacteria, including yeast. It has poor eschar penetration.

Silver nitrate

Silver nitrate coagulates cellular protein and removes granulation tissue. It exhibits activity against gram-positive bacteria, gram-negative bacteria, and candidal species. The major drawbacks are that it has poor penetration of eschar, requires the use of occlusive dressings, and turns black upon contact with tissues.

Mafenide (Sulfamylon)

Mafenide is a topical sulfonamide. Through competitive inhibition of para-aminobenzoic acid, interferes with bacterial folic acid synthesis. It diffuses freely into the eschar and is highly effective against gram-negative organisms, including pseudomonal species.

Vaccine, Inactivated (Bacterial)

Class Summary

These agents are used for tetanus immunization. A booster injection against tetanus in previously immunized individuals is recommended to prevent this potentially lethal syndrome.

Tetanus toxoid

Tetanus immune globulin (TIG) is used for passive immunization of any person with a wound that may be contaminated with tetanus spores. Tetanus toxoid is used to induce active immunity against tetanus in selected patients. Burns are extremely tetanus-prone wounds. All burn patients with an incomplete immunization history should receive a dosage of tetanus toxoid (Td for adults or children >7 y, DTP or TD for children < 7 y). Children with up-to-date primary immunization series are considered to be up-to-date for tetanus immunization status. If the patient has a history of complete immunization and the last immunization with absorbed tetanus toxoid is within the last 5 years, further immunization is not required. If the history of tetanus immunization is unknown, both Td and TIG should be administered.

Tetanus immune globulin (HyperTET S/D)

Used for passive immunization of any person with a wound that may be contaminated with tetanus spores.