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4.1 Burn Wound Infections

4.1.1 Diagnosis and Treatment of Burn Wound Infections

4.1.1.1 Introduction

Infections remain a leading cause of death in burn patients. This is as a result of loss of the environmental barrier function of the skin predisposing these patients to microbial colonization leading to invasion. Therefore, reconstitution of the environmental barrier by debriding the devitalized tissue and wound closure with application of allograft versus autograft is of optimal importance.

Given that infections are a common complication of the thermally injured patient, early diagnosis and treatment are of paramount importance. The pathophysiological progression of burn wound infection runs the spectrum from bacterial wound colonization to infection to invasive wound infection. The characteristics of each are as follows:

  • Bacterial colonization

    • Bacterial levels <105

    • Does not necessarily prevent wound healing

  • Bacterial infection

    • Bacterial levels >105

    • Can result in impaired wound healing and graft failure

    • Can lead to systemic infection

  • Invasive wound infection

    • Clinically can have separation of the eschar from wound bed

    • Appearance of focal dark brown, black, or violaceous discoloration of the wound [1]

    • Presence of pyocyanin (green pigment) in subcutaneous fat

    • Erythema, edema, pain, and warmth of the surrounding skin

    • Associated with signs of systemic infection/sepsis and positive blood cultures

Of note there are particular clinical signs unique to fungal and viral infections. An unexpected and rapid separation of the eschar is characteristic of fungal infection [2], while vesicular lesions caused by HSV-1 can be found in healed or healing burn wounds [3].

4.1.1.2 Common Pathogens and Diagnosis

In general the organisms causing burn wound infection/invasion have a chronological appearance. Initially, Gram-positive organisms are commonplace, while Gram-negative organisms become predominant after 5 days post-burn injury. Yeast and fungal colonization/infection follow, and finally multiresistant organisms appear typically as result of broad-spectrum antibiotics or inadequate burn excision or patient response to therapy [4].

As part of infection surveillance of burn patients, clinicians need to pay close attention to clinical signs of wound infection and rapidly confirm their diagnosis. There is some controversy as to the exact method of diagnosis, with some advocating for quantitative cultures—with >105 organisms per gram tissue being diagnostic of invasive infection [5]—and others arguing for histological examination as the only reliable method of determining invasive infection [6–9] since quantitative cultures are only positive in 50 % of histological invasive wound infections [9]. The most common pathogens of burn wound invasion are MSSA, MRSA, and Pseudomonas aeruginosa species (Table 4.1).

Table 4.1 Common pathogens of burn wound infection
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In order to provide the thermally injured patient with adequate treatment, it is important to have knowledge of each institution’s bacterial flora as they vary with geography and over time [10, 11].

Fungal infections have increased in frequency with the use of topical agents, and the incidence of mycotic invasions has doubled. Even though the burn wound is the most commonly infected site, there is an increasing trend toward systemic and organ-specific fungal infections [12].

The diagnosis of fungal infection is complicated by delay in their identification as cultures typically require 7–14 days [13], and their clinical presentation is similar to low-grade bacterial infections. Diagnosis can be aided by arterial blood samples as well retinal examination.

4.1.1.3 Clinical Management

Early excision and wound coverage is the mainstay of modern burn care and best method of minimizing burn wound infection. Any delay in the surgical treatment of burn wounds leads to increased bacterial loads, and any wound with bacterial counts exceeding 105 organisms per gram of tissue can develop burn wound sepsis even after burn wound excision [9].

The treatment of burn wound infections involves both local and systemic therapy.

4.1.1.3.1 Local

  • Early excision of burn eschar (for un-excised burns)

  • Aggressive excision of necrotic/infected tissue

  • Topical agents (Table 4.2) to minimize bacterial colonization [14]

    Table 4.2 Topical agents and the antimicrobial activity
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The use of any particular topical agent should be based on suspected organism in the wound but is at times guided by the availability of the agent on hospital formulary. These are not substitute for aggressive surgical management of wound infections.

4.1.1.3.2 Systemic

  • Use of antibiotics and antifungals should be reserved for patients demonstrating systemic signs of sepsis (see ABA criteria for definition of sepsis (Box 4.1)).

  • Use of systemic prophylaxis can reduce the rate of surgical wound infections but can increase bacterial antimicrobial resistance [15].

  • The choice of antimicrobials needs to be based on each institution’s antibiogram and tailored specifically to the organism (Table 4.3), i.e., narrow the coverage as soon as sensitivities become available.

    Table 4.3 Ross Tilley Burn Centre guidelines for empiric antibiotic therapy
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  • Yeast species (Candida) are typically sensitive to fluconazole, while fungal infections would most likely require treatment with amphotericin or caspofungin (the use is for systemic infection, as wound infections require surgical debridement).

  • Viral infections (typically HSV) require treatment with acyclovir.

Infections of burn wounds are typically found in patients with burns exceeding 20 % TBSA and most commonly in the lower extremities [17]. However, there are no specific organisms associated with the site of infection [17]. Moreover, these infections can have dire consequences:

  • Conversion of superficial to deeper burn wounds

  • Systemic infection and sepsis

  • Graft loss requiring further surgery for regrafting

  • Increased hospital length of stay

  • Conversion of donor sites requiring surgical debridement and grafting

  • Increased mortality, more so with yeast and fungal infection

4.1.1.4 Conclusion

Burn wound infection is an all too common complication of the thermally injured patient. These infections tend to have a chronological appearance and depend on burn size, depth, length of hospital stay, and geographical location. The common organisms remain Staphylococcus and Pseudomonas; however, more resistant strains are becoming prevalent. The clinician needs to be vigilant with surveillance of burn wounds and institute aggressive treatment of wound infection once clinical signs appear before systemic illness sets in. It is of utmost importance to have ongoing assessment of the unique flora of each institution in order to better utilize systemic therapy.

4.2 Ventilator-Associated Pneumonia

Ventilator-associated pneumonia (VAP) as defined by CDC (Center for Diseases Control) is an infection that occurs in a mechanically ventilated patient with an endotracheal or tracheostomy tube (traditionally >48 h after hospital admission) [18, 19]. The diagnosis of VAP in the thermally injured patient can be challenging, as fever, leukocytosis, tachycardia, and tachypnea can be present in these patients without infection. The sources of bacteria are typically the oropharynx and upper gastrointestinal tract [20–24]. The organisms also have a temporal pattern, community-acquired organisms (Streptococcus pneumoniae and Haemophilus influenza) are dominant in the early-phase VAP and Gram-negative and multiresistant organisms (i.e., MRSA) are the common pathogens in late-stage VAP.

Regardless of the organisms, early antimicrobial treatment guided toward the likely organism based on the onset of VAP (early vs. late) is beneficial in the overall outcome of the patients [25–30]. These broad-spectrum antimicrobials would need to be de-escalated as culture and sensitivities become available [31–33].

As VAP is an increasing common complication with significant consequences, VAP prevention strategies need to be implemented and ABA guidelines (Box 4.2) utilized to improve overall patient outcome.

4.3 Central Line-Associated Infections

Central catheters inserted into veins and arteries are common practice in the management of the critically ill thermally injured patient and can be associated with infection rates from 1.5 to 20 % [35–37]. The introduction of central line insertion bundles by CDC has dramatically reduced these infections [38, 39]. These measures include:

  • Hand washing

  • Full-barrier precautions during line insertion

  • Cleaning the skin with chlorhexidine

  • Avoiding the femoral site if possible

  • Removing unnecessary catheters

In burn patients some unique features complicate the use of the central catheters. Typically there are associated burn wounds in close proximity, and it has been shown that catheters within 25 cm2 of an open wound are at an increased risk of colonization and infection [40]. Other risk factors associated with increased rate of infection are [41]:

  • Age (extremes of age have more infection)

  • Sex (female)

  • %TBSA burned

  • % full-thickness burns

  • Presence of smoke inhalation

  • Type of burn (flame)

  • Number of surgical procedures performed

  • Larger number of CVCs

  • Longer insertion of the catheter

  • Wound burn infection or colonization

  • Insertion of the venous catheter in emergency situation

  • Longer stay in hospital

  • More operations

  • Insertion site near the burns wound

The diagnosis of catheter-related infection (CRI) is based on clinical and microbiological criteria (see Table 4.4). Following the diagnosis of CRI prompt treatment is essential as delay in catheter removal or in the start of appropriate antimicrobial therapy can result in increased morbidity and mortality [43].

Table 4.4 Catheter-related infection [42]
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Currently there is no clear evidence that routine exchange of lines decreases the rate of catheter-related blood stream infections (CRBSI) [44]; however, all catheters need to be removed once a CRBSI is diagnosed or once they are no longer needed.

As with all severe infections empiric antimicrobial treatment should be initiated immediately and should take into account the severity of the illness, the site of catheter insertion, and the institutions’ antibiogram [45]. These broad-spectrum antimicrobials need to be de-escalated after identification and susceptibility testing of the microorganism.

4.4 Guidelines for Sepsis Resuscitation

As described in the previous segments of this chapter, infections in the thermally injured patient have dire consequences. Sepsis occurs at a rate of 8–42.5 % in burn patients with a mortality of 28–65 % [46]. Much research has been conducted in the optimal management of the septic patient. The following Table 4.5 summarizes the guidelines as recommended by the surviving sepsis campaign committee [47]. Only the strong recommendations with high level of evidence are included. This is to be used as a tool to guide the delivery of optimal clinical care for patients with sepsis and septic shock. The ABA criteria for definition of sepsis (see Box 4.1) in the burn patients have been established. However, Mann-Salinas and colleagues have challenged the predictive ability of ABA criteria demonstrating that their multivariable model (heart rate >130, MAP <60 mmHg, base deficit <  −6 mEq/L, temperature <36 °C, use of vasoactive medications, and glucose >150 mg/dL) is capable of outperforming the ABA model [48].

Table 4.5 Guidelines for management of sepsis and septic shock [47]a
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