key: cord-0060706-67xkusho authors: Shahrokhi, Shahriar title: Infections in Burns date: 2020-12-22 journal: Burn Care and Treatment DOI: 10.1007/978-3-030-39193-5_5 sha: 739c7dee4cd6ff65cc43ac82403193ee7800e202 doc_id: 60706 cord_uid: 67xkusho 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. 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 <10 5 . -Does not necessarily prevent wound healing. • Bacterial infection. -Bacterial levels >10 5 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] . In general, the organisms causing burn wound infection/invasion have a chronological appearance. Initially, Gram-positive organisms are com-S. Shahrokhi (*) Division of Plastic and Reconstructive Surgery, Sunnybrook Health Sciences Centre, Toronto, ON, Canada e-mail: shar.shahrokhi@sunnybrook.ca monplace, while Gram-negative organisms become predominant after 5 days post-burn injury. Yeast and fungal colonization/infection follow, and finally multi-resistant organisms appear typically as a 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 >10 5 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] [7] [8] [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 1) . 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 change 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 towards 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 and duration of treatment can be aided by arterial blood samples as well as retinal examination. Early excision and wound coverage is the mainstay of modern burn care and the 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 10 5 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. • Early excision of burn eschar (for unexcised burns). • Aggressive excision of necrotic/infected tissue. • Use of topical agents (Table 2) to minimize bacterial colonization [14] . 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 a substitute for aggressive surgical management of wound infections. • Use of systemic antibiotics and antifungals should be reserved for patients demonstrating systemic signs of sepsis (see ABA criteria for definition of sepsis (Box 1)). • Use of systemic prophylaxis can reduce the rate of surgical wound infections but can increase bacterial antimicrobial resistance [15] . [16] Includes at least three of the following: Temperature > 39° or < 36.5 °C. Progressive tachycardia • Adults >110 bpm. • Children >2 SD above age-specific norms (85% age-adjusted max heart rate). Progressive tachypnea • Adults >25 bpm not ventilated. Minute ventilation >12 L/min ventilated. • Children >2 SD above age-specific norms (85% age-adjusted max respiratory rate). Thrombocytopenia (will not apply until 3 days after initial resuscitation) • Adults <100,000/mcl. • Children >2 SD below age-specific norms. Hyperglycemia (in the absence of preexisting diabetes mellitus) In addition, it is required that a documented infection (defined below) is identified: • Culture-positive infection. • Pathologic tissue source identified. • Clinical response to antimicrobials. 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. • The choice of antimicrobials needs to be based on each institution's antibiogram and tailored specifically to the organism (Table 3) , i.e., narrow the coverage as soon as sensitivities become available. 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. 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] [21] [22] [23] [24] . The organisms also have a temporal pattern, community-acquired organisms (Streptococcus pneumoniae and Haemophilus influenza) are dominant in the early-phase VAP and Gramnegative and multi-resistant organisms (i.e., MRSA) are the common pathogens in late-stage VAP. Regardless of the organisms, early antimicrobial treatment, guided towards 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 cultures 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 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] [36] [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 25cm 2 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] : The diagnosis of catheter-related infection (CRI) is based on clinical and microbiological criteria (see Table 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] . 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. 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 5 summarizes the guidelines as recommended by the surviving sepsis campaign committee originally published in 2008 [47] and later revised in 2016 [48] . 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. Requires one of the following with no other recognized cause: Fever (>38 °C), hypotension (SBP <90 mmHg), oliguria, paired quantitative blood cultures with a > 5:1 ratio catheter versus peripheral, differential time to positivity (blood culture obtained from a CVC is positive at least 2 h earlier than a peripheral blood culture) The ABA criteria for definition of sepsis (see Box 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 [49] . In addition, the new Sepsis-3 clinical criteria for identification of sepsis and septic shock [50] [51] [52] have been developed, which defines sepsis and septic shock as follows: • Sepsis-Suspected or documented infection and an acute increase of >2 SOFA points. • Septic Shock-Sepsis and vasopressor therapy needed to elevate MAP >65 mmHg and lactate >2 mmol/L (18 mg/dL) despite adequate fluid resuscitation. More recently, the publication by Stanojcic and colleagues as well as Yan and colleagues demonstrated that the Sepsis-3 had superior sensitivity in predicting sepsis in comparison to Mann-Salinas and ABA criteria for sepsis; however, none of the aforementioned had the accuracy to be a stand-alone diagnostic tool within the burn population [53, 54] . 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