key: cord-0035298-4acm5yg0 authors: Shahrokhi, Shahriar title: Infections in Burns date: 2013-02-09 journal: Burn Care and Treatment DOI: 10.1007/978-3-7091-1133-8_4 sha: 472b33a93c9d9c6ba47da83b75a7d58794178fe7 doc_id: 35298 cord_uid: 4acm5yg0 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 Can result in impaired wound healing and graft failure - 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 ] . In general the organisms causing burn wound infection/invasion have a chronological appearance. Initially, Gram-positive organisms are commonplace, while Gramnegative organisms become predominant after 5 days post-burn injury. Yeast and fungal colonization/infection follow, and fi nally 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 con fi rm 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 4 .1 ). In order to provide the thermally injured patient with adequate treatment, it is important to have knowledge of each institution's bacterial fl ora 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-speci fi c fungal infections [ 12 ] . The diagnosis of fungal infection is complicated by delay in their identi fi cation 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. 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 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 un-excised burns) • Aggressive excision of necrotic/infected tissue • Topical agents (Table • 4.2 ) 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 substitute for aggressive surgical management of wound infections. Use of antibiotics and antifungals should be reserved for patients demonstrating • systemic signs of sepsis (see ABA criteria for de fi nition 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 speci fi cally to the organism (Table 4. 3 ), i.e., narrow the coverage as soon as sensitivities become available. The most common pathogens (from any source) in the late phase of a patient's admission are: Gram-positive Staphylococcus aureus (only ~60 % susceptible to cloxacillin) Gram-negative (generally more predominant in the late phase) Pseudomonas aeruginosa (>80 % susceptible to piperacillin/tazobactam) Based on this data, septic patients admitted 5 days or more should be started on an empiric regimen of: Piperacillin/tazobactam 4.5 g IV q6 h (renal dosing required) + Vancomycin 1 g IV q12 h (with pre-and post-levels around the third dose) Or Meropenem 500 mg IV q6 h (renal dosing required) Includes at least three of the following: Temperature >39° or <36.5 °C Progressive tachycardia Adults >110 bpm • Children >2 SD above age-speci fi c norms (85 % age-adjusted max heart • rate) 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 speci fi c organisms associated with the site of infection [ 17 ] 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 Ventilator-associated pneumonia (VAP) as de fi ned 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 in fl uenza ) 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 bene fi cial in the overall outcome of the patients [25] [26] [27] [28] [29] [30] . These broad-spectrum antimicrobials would need to be de-escalated as culture and sensitivities become available [31] [32] [33] . As VAP is an increasing common complication with signi fi cant consequences, VAP prevention strategies need to be implemented and ABA guidelines (Box 4.2 ) utilized to improve overall patient outcome. Mechanically ventilated burn patients are at high risk for developing VAP, • with the presence of inhalation injury as a unique risk factor in this patient group. VAP prevention strategies should be used in mechanically ventilated burn • patients. Clinical diagnosis of VAP can be challenging in mechanically ventilated • burn patients where systemic in fl ammation and acute lung injury are prevalent. Therefore, a quantitative strategy, when available, is the preferable method to con fi rm the diagnosis of VAP. An 8-day course of targeted antibiotic therapy is generally suf fi cient to • treat VAP; however, resistant Staphylococcus aureus and Gram-negative bacilli may require longer treatment duration. 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 ] 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 ] . 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 identi fi cation 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 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 de fi nition 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 de fi cit < −6 mEq/L, temperature <36 °C, use of vasoactive medications, and glucose >150 mg/dL) is capable of outperforming the ABA model [ 48 ] . 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) Obtain appropriate cultures before starting antibiotics provided this does not signi fi cantly delay antimicrobial administration Obtain two or more BCs One or more BCs should be percutaneous One BC from each vascular access device in place >48 h Culture other sites as clinically indicated Perform imaging studies promptly to con fi rm and sample any source of infection, if safe to do so Antibiotic therapy Begin intravenous antibiotics as early as possible and always within the fi rst hour of recognizing severe sepsis and septic shock Broad-spectrum: one or more agents active against likely bacterial/fungal pathogens and with good penetration into presumed source Reassess antimicrobial regimen daily to optimize ef fi cacy, prevent resistance, avoid toxicity, and minimize costs Consider combination therapy in Pseudomonas infections Consider combination empiric therapy in neutropenic patients Combination therapy £ 3-5 days and de-escalation following susceptibilities Duration of therapy typically limited to 7-10 days; longer if response is slow or there are undrainable foci of infection or immunologic de fi ciencies Stop antimicrobial therapy if cause is found to be noninfectious Source identi fi cation and control A speci fi c anatomic site of infection should be established as rapidly as possible and within fi rst 6 h of presentation Formally evaluate patient for a focus of infection amenable to source control measures (e.g., abscess drainage, tissue debridement) Implement source control measures as soon as possible following successful initial resuscitation (exception: infected pancreatic necrosis, where surgical intervention is best delayed) Choose source control measure with maximum ef fi cacy and minimal physiologic upset. Remove intravascular access devices if potentially infected (continued) Give red blood cells when hemoglobin decreases to <7.0 g/dL (<70 g/L) to target hemoglobin of 7.0-9.0 g/dL in adults. A higher hemoglobin level may be required in special circumstances (e.g., myocardial ischemia, severe hypoxemia, acute hemorrhage, cyanotic heart disease, or lactic acidosis) Do not use antithrombin therapy Mechanical ventilation of sepsis-induced ALI/ARDS Target a tidal volume of 6 mL/kg (predicted) body weight in patients with ALI/ARDS Target an initial upper limit plateau pressure £ 30 cm H 2 O. Consider chest wall compliance when assessing plateau pressure Allow PaCO 2 to increase above normal, if needed, to minimize plateau pressures and tidal volumes Set PEEP to avoid extensive lung collapse at end expiration Maintain mechanically ventilated patients in a semi-recumbent position (head of the bed raised to 45°) unless contraindicated Use a weaning protocol and an SBT regularly to evaluate the potential for discontinuing mechanical ventilation SBT options include a low level of pressure support with continuous positive airway pressure 5 cm H 2 O or a T piece Do not use a pulmonary artery catheter for the routine monitoring of patients with ALI/ARDS Use a conservative fl uid strategy for patients with established ALI who do not have evidence of tissue hypoperfusion Sedation, analgesia, and neuromuscular blockade in sepsis Use sedation protocols with a sedation goal for critically ill mechanically ventilated patients Use either intermittent bolus sedation or continuous infusion sedation to predetermined end points (sedation scales), with daily interruption/lightening to produce awakening Avoid neuromuscular blockers where possible. Monitor depth of block with train-of-four when using continuous infusions Glucose control Use intravenous insulin to control hyperglycemia in patients with severe sepsis following stabilization in the ICU Aim to keep blood glucose <150 mg/dL (8.3 mmol/L) using a validated protocol for insulin dose adjustment Provide a glucose calorie source and monitor blood glucose values every 1-2 h (4 h when stable) in patients receiving intravenous insulin Interpret with caution low glucose levels obtained with point of care testing, as these techniques may overestimate arterial blood or plasma glucose values Bicarbonate therapy Do not use bicarbonate therapy for the purpose of improving hemodynamics or reducing vasopressor requirements when treating hypoperfusion-induced lactic acidemia with pH ³ 7.15 DVT prophylaxis Use a mechanical prophylactic device, such as compression stockings or an intermittent compression device, when heparin is contraindicated Use either low-dose UFH or LMWH, unless contraindicated Stress ulcer prophylaxis Provide stress ulcer prophylaxis using H2 blocker or proton pump inhibitor Consideration for limitation of support Discuss advance care planning with patients and families. Describe likely outcomes and set realistic expectations a Adapted from Dellinger et al. [ 47 ] Current approach to prevention and treatment of Pseudomonas aeruginosa infections in burned patients The diagnosis and treatment of infection in the burn patient Herpesvirus infection in burned patients Burn wound infections Quantitative bacteriology: its role in the armamentarium of the surgeon Comparison of quantitative microbiology and histopathology in divided burn-wound biopsy specimens The changing epidemiology of infections in burn patients Burn wound infections: current status Effects of burn wound excision on bacterial colonization and invasion Changes in bacterial isolates from burn wounds and their antibiograms: a 20-year study Common pathogens in burn wound and changes in their drug sensitivity Sepsis in pediatric burn patients Fungal burn wound infection. 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