Assessment of Infection in Burn Injuries

Original Editor - Stacy Schiurring based on the course by Diane Merwarth

Top Contributors - Stacy Schiurring and Jess Bell

Introduction[edit | edit source]

Burn wound injuries place critical economic burden on healthcare infrastructures worldwide. They are also associated with high mortality rates due to severe complications. Infection is the most common complication in burn wound injuries. Thus, prompt and precise diagnosis is of critical importance for this patient population to prevent detrimental consequences and optimise healing outcomes.[1]

Burn wound injuries are at an increased infection risk for multiple reasons: (1) the body's physiological response to a burn injury presents with many of the same signs and symptoms of a developing infection, (2) the burn injury can impair many body systems which limits a patient's innate ability to fight off infection.[2]

Physiological Response to Burn Injuries[edit | edit source]

Burn wound injuries have both local and system consequences.[2] This requires the wound care professional to work closely with the interdisciplinary team to appropriately monitor and manage the patient in a holistic manner. Understanding the pathophysiological changes which occur after a burn wound injury will greatly improve the wound care professional's ability to prevent and/or manage infection.

Local response to burn wounds[edit | edit source]

The local response involves the area of the burn injury and the tissue directly surrounding it. This is best described using Jackson's Burn Model which divides the wound into three zones.[3]

  1. Jackson's Burn Model
    Zone of coagulation (also known as the zone of necrosis). This area sustains the most damage and suffers irreversible tissue loss.
  2. Zone of stasis. This area is found around the zone of coagulation. It demonstrates decreased tissue perfusion and is, therefore, potentially salvageable with proper care. This zone can also suffer complete tissue loss with prolonged hypotension, infection, or oedema.
  3. Zone of hyperaemia. This is the outermost zone of the injury. In this area, tissue perfusion is increased. This area will likely recover unless there is severe sepsis or prolonged hypoperfusion.

For more information, please review this page.

Systemic response to burn wounds[edit | edit source]

Burn wounds result in damage to multiple body systems, which can put the patient at higher risk for developing an infection.[2]

  1. Cardiovascular function[4] and burn shock[3]
    • Capillary permeability is increased, leading to the loss of intravascular proteins and fluids into the interstitial compartment, which leads to oedema[2][4]
    • Myocardial contractility is decreased,[4] there is a decrease in cardiac output immediately post-burn
    • These changes, when combined with fluid loss from the burn wound, result in systemic hypotension and end organ hypoperfusion[3]
    • Local vascular compromise occurs in deep, partial, and full-thickness injuries where the arterial supply is either damaged or destroyed as a result of the burn wound[2]
  2. Respiratory changes
    • Inflammatory mediators cause bronchoconstriction[4]
    • Acute respiratory distress syndrome (ARDS) can occur with severe burns[4]
    • Pulmonary function can be affected by oedema, regardless of if an inhalation injury occurred[3]
  3. Metabolic changes[2]
    • Basal metabolic rate can increase to three times its original rate post-burn[4]
    • A systematic immunoendocrine response will occur after a large burn injury and can continue for up to 3-years post-injury. This response can cause: (1) immune incompetence, (2) sepsis, (3) increased fracture risk, (4) slowing of growth rate, (5) reduced organ function, (6) decreased wound healing, and (7) death[3]
  4. Gastrointestinal changes
    • Absorption is affected due to gastrointestinal mucosal atrophy and decreased intestinal blood flow[3]
    • A patient post-burn is in a constant hypermetabolic state as a result of their burn injury. Initially, this will boost the energy response and help fight off infection and begin the healing process. However, as the hypermetabolic state becomes a prolonged response, it will be an energy drain and it becomes more difficult for the patient to mount defences and continue the healing process.[2]
    • Early enteral feeding is paramount to prevent malnutrition[3]
  5. Immunological changes
    • The immune response becomes globally depressed following a burn injury, the severity is dependent on the size of the burn wound
    • Burn wounds will cause both innate and adaptive immune responses[2]
    • Patient will have an excessive and prolonged inflammatory response[2]
    • Loss of the protective skin layer opens the body to the risk of infection[3][2]
    • Immune incompetence further depresses the body's ability to fight infection - sepsis is the leading cause of post-burn mortality[3]

"Burn shock results from the interplay of direct tissue injury, hypovolemia, and the release of multiple mediators of inflammation, with effects on both the microcirculation and the function of the heart and lungs."[5]

Additional Risk Factors for Burn Injury Infection[edit | edit source]

Additional risk factors of burn wound injuries for infection:[2]

  1. An increased length of stay in the ICU
  2. Increased wait time for test results (ie wound cultures or biopsies) to identify the source of infection delays the use of targeted antibiotics or antimicrobial agents to most effectively treat infection
  3. Possibly a delay due to transportation time to a burn centre for skilled aggressive care
  4. A delay for surgery due to patient medical instability or lack of surgical facility
  5. Any burn greater than 20% total body surface area of deep partial and/or full thickness injury is a high risk for infection, regardless of the patient's underlying conditions
  6. Infection risk increases more when the patient is less than four years old or more than 55 years old
  7. Infection risk is increased for patients who are immunocompromised or who have pre-existing comorbidities that put them at risk for developing an infection
  8. The presence of eschar in the wound increases the risk of infection

Signs and Symptoms of Sepsis in a Burn Wound[edit | edit source]

The detection of a burn wound infection has multiple layers of complexity. The normal response to a burn injury mimics many of the signs and symptoms of infection. Therefore, the ability to identify an infection is masked by the patient's response to the burn injury.[2] To review covert and overt signs and symptoms of infection, please see this article.

While infections are one of the most common complications following a burn wound injury, sepsis is the leading cause of death in both adult and paediatric burn patients. The diagnosis and management of sepsis in burns also has multiple layers of complexity. The diagnosis of sepsis in patients with severe burns (>20% total body surface area) is complicated by the overlap of clinical signs of the typical post-burn hypermetabolic response with those of sepsis.[6]

For a burn wound to be diagnosed as septic, the patient must exhibit at least three of the following:

Table is modified from: Norbury W, et. al.  Infection in burns.  Surg Infect, 2016; 17(2): 250-255.
Not age specific Adults Children
Temperature >39°C or <36.5°C

(>102.2°F or <97.7°F)

Progressive tachycardia >110 beats/min (bpm) >2 SD [standard deviations] above age-specific norm (85% age-adjusted maximum heart rate)
Progressive tachypnea
  • Not ventilated: >25 bpm
  • Minute ventilation >12 L/min when ventilated
>2 SD above age-specific norm (85% age-adjusted maximum respiratory rate)

(will not apply until 3 days after initial resuscitation)

<100,000/mcL <2 SD below age-specific norm

(in the absence of pre-existing diabetes mellitus)

  • Untreated plasma glucose >200 mg/dL or equivalent mM/L
  • Insulin resistance. Examples include:
    • >7 units of insulin/hour intravenous drip (adults)
    • Resistance to insulin (>25% increase in insulin requirements over 24 hours)
Inability to continue enteral feedings >24 hours Examples include:
  • Abdominal distension
  • Enteral feeding intolerance (residual >150 mL/h in children or 2× feeding rate in adults)
  • Uncontrollable diarrhea (>2,500 mL/d for adults or >400 mL/d in children)
Have a documented infection Documented one of the following:
  • Culture-positive infection OR
  • Pathologic tissue source identified OR
  • Clinical response to antimicrobials

Sources of Infection[edit | edit source]

Research shows that burn wounds are sterile for the first 6-12 hours after initial injury. However, contamination occurs soon there after and the proliferation of bacteria increases rapidly.[2]

Sources of contamination in a burn wound:[2]

  1. Normal skin flora
  2. Endogenous sources, such as the lungs or the gut, or any mucosal membranes where bacteria thrive in a normal system
  3. Exogenous sources, such as the environment or cross-contamination

Bacterial infections[edit | edit source]

For more in-depth information on bacterial infections, please read this article.

Rough timeline of bacterial concentrations in a burn wound:[2]

  • Early phase of infection: gram-positive usually the first identified
    • Staphyloccus aureus is typically the first pathogen found in burn wound infection, this includes Methicillin-resistant Staphylococcus aureus (MRSA)
    • Staphylococcus aureus is also typically the first microbe identified in sepsis and in arterial bacterial dissemination from the wound
  • At five days from the time of injury: gram-negative bacteria become predominant, and
    • Pseudomonas aeruginosa is the primary bacteria identified. It is the most common pathogen found in burn wounds and is very common in the development of biofilms.
  • Later stages: development of fungal or yeast infection independent or in combination with an already existing bacterial infection

Fungal infections[edit | edit source]

For more in-depth information on fungal infections, please read this article.

Fungal infections are also a major concern for patients with burn wound injuries. It can often be difficult to distinguish a fungal infection from a bacterial infection in a burn wound by appearance alone.[2]

Risk factors for developing a fungal infection in a burn wound:[2]

  1. Total body surface area involvement >30%
  2. Long hospital length of stay
  3. Multiple comorbidities

Clinical observations for a fungal infection in a burn wound:[2]

  1. Changes in the wound appearance
    • An unanticipated separation of eschar is a key sign of fungal infection
  2. Rapid conversion from a partial thickness burn to a deep partial or a full thickness burn wound
  3. A blackening of the burn wound tissue
  4. A persistent ongoing fever which remains unchanged with antibiotic therapy

Candida albicans and Aspergillus are the most common fungal pathogens. Aspergillus can be a very serious fungal infection and requires urgent assessment and potential surgical debridement.

Sample collection[edit | edit source]

Biopsy[edit | edit source]

Wound biopsies are an important diagnostic component in the management of chronic wounds to monitor for potential malignancy or infection.[7] The tissue biopsy, especially in burn wounds, has long been recognised as the gold standard. It is the most quantitative method of collecting tissue and identifying the level of bacterial contamination or infection in a wound.[2]

Taking a wound biopsy requires sampling at the wound edge and in the wound bed. The procedure is invasive and requires skill on the part of the caregiver to collect the sample. Biopsies require extra time for results to become available but allow for accurate targeted antibiotics or antimicrobials to be used against the infection. It has been found that bacteria are not homogeneously present in the wound bed, but they are in pocketed in different areas. Therefore, multiple biopsies should be collected from a single burn wound.[2]

It is also recommended to take wound biopsies for wounds that have not responded to treatment after 2–6 weeks.[7]

Semiquantitative swab culture[edit | edit source]

There is controversy over the effectiveness of performing a swab culture and if the results will represent the infection. However, there is research which shows a correlation between bacteria identified in a swab culture and the bacteria identified from a tissue sample, specifically a biopsy. A swab culture will not give the level of quantitative results as a biopsy, but if done appropriately, the results will identify the microbes that need to be targeted with antimicrobial interventions.[2]

Benefits of performing a swab culture:[2]

  • Less invasive than a biopsy
  • Can be easily performed by the bedside clinician
  • Provides quicker results which allow more timely targeted antimicrobial interventions

General Guidelines for the Treatment of Burn Wound Infections[edit | edit source]

Unfortunately, there are no standardised protocols for treatment of a burn wound infection.[2]

Topical antimicrobial agents[2][edit | edit source]

  • These treatments need to be individualised
  • Once a local infection has been identified, begin a topical antimicrobial agents
  • For spreading or systemic infection, begin systemic antimicrobial agents
  • More than one broad-spectrum antibiotic may be initiated while awaiting tissue sample results
  • Fungal infections will require topical and antifungal agents, with the potential for surgical debridement
  • Due to the nature of rapidly forming biofilms, treatment may include biofilm-based wound management

Surgical interventions[2][edit | edit source]

  • Will be needed to to remove biofilm population. The wound usually requires frequent surgical debridement. It has been found that a biofilm will start to reform within 24 hours of being disrupted, and it becomes mature in three days. Therefore, it is important to follow up with appropriate biofilm-based wound management.
  • Fungal infections may require surgical debridement
  • Early excision of eschar, which provides a good environment for bacterial proliferation
  • Skin grafts to close a wound immediately and decrease exposure to new sources of infection

Infection Prevention[2][edit | edit source]

  1. Vigilance
    • Close observation for overt and covert signs and symptoms of infection
    • Closely monitoring vital signs and lab values for signs of infection
    • Accurate and thorough documentation of wound appearance and features
  2. Frequently reassess and update care plan based on the patient's response to current interventions
  3. Manage patient's comorbidies
  4. Maintain optional nutrition and water intake
    • Oral intake is the most valuable and the most effective method
    • A nasogastric tube is the second most effective method
    • Enteral nutrition is the least favourable because it doesn't utilise the gut
  5. Manage oedema
    • Minimising oedema by elevating the extremities
    • Applying compression bandages to the extremities if tolerated
  6. Provide psychosocial support and education
    • A positive mental attitude can aide in wound healing and infection prevention
    • Include the patient in care plans
  7. Temperature control
    • Prevent the patient from being too hot or too cold, so adjust the temperature in the patient's room or in the operating room (OR). Often hospitals are set a minimum of 29-31°C (85-88 °F) room temperature to prevent patients with a burn wound from becoming too cold.
    • Dressing considerations: Wounds can cool down when dressings become saturated with drainage or when left exposed to air too long during a dressing change.
  8. Recommended strategies for minimising the onset of infection in medical facilities
    • Universal precautions, proper use of personal protective equipment (PPE), and hand hygiene
    • Patients at high risk for developing an infection should be placed in a negative pressure room with strict isolation precautions.
    • Wound care should be done with aseptic (sterile) technique when possible, otherwise clean (non-sterile) techniques should be used.
    • Strict aseptic technique should be used when inserting any kind of device (intravenous line, intra-arterial line, foley catheter). It is also recommended for these devices to be removed as soon as they are no longer necessary to support the patient's recovery from their burn injury.
    • Environmental control to include: (1) a complete cleaning of the patient's room twice/day with wipe down of all high-touch surfaces, (2) terminally cleaning the room anytime the patient is not present, (3) after the patient has been discharged from the room, it is recommended to complete three days of terminal clean prior to use by another person.
  9. Surveillance cultures are recommended by many burn centres
    • This includes nasal cultures, cultures of the wound, possibly anal cultures with the onset of vancomycin-resistant enterococcus (VRE)
    • It is recommended that cultures be collected on admission and weekly throughout the hospital stay

Resources[edit | edit source]

Optional Additional Recommended Reading:

Optional Video:

Please view this optional video for an overview of burn wound anatomy and classification, as well as a detailed description of burn wound pathophysiology.


References[edit | edit source]

  1. Farhan N, Jeffery S.  Diagnosing burn wounds infections: the practice gap and advances with Moleculight bacterial imaging.  Diagnostics, 2021; 11: 268-286
  2. 2.00 2.01 2.02 2.03 2.04 2.05 2.06 2.07 2.08 2.09 2.10 2.11 2.12 2.13 2.14 2.15 2.16 2.17 2.18 2.19 2.20 2.21 2.22 2.23 2.24 2.25 Merwarth, D. Management of Burn Wounds. Assessment of Infection in Burn Injuries. Plus. 2022.
  3. 3.0 3.1 3.2 3.3 3.4 3.5 3.6 3.7 3.8 Whitaker I, Shokrollahi K, Dickson W. Burns. OUP Oxford, 2019.
  4. 4.0 4.1 4.2 4.3 4.4 4.5 Hettiaratchy S, Dziewulski P. Pathophysiology and types of burns. Bmj. 2004 Jun 10;328(7453):1427-9.
  5. Wurzer P, Culnan D, Cancio LC, Kramer GC. Pathophysiology of burn shock and burn edema. InTotal burn care 2018 Jan 1 (pp. 66-76). Elsevier.
  6. Nunez Lopez O, et. al. Predicting and managing sepsis in burn patients: current perspectives.  Therap. Clin. Risk Mngmt, 2017; 17: 1107-1117
  7. 7.0 7.1 Ponnarasu S, Schmieder GJ. Excisional Biopsy. InStatPearls [Internet] 2021 Sep 2. StatPearls Publishing.
  8. YouTube. Burns (DETAILED) Overview - Types, Pathophysiology, TBSA | Armando Hasudungan. Available from: [last accessed 01/12/2022]