Burns and Soft Tissue Infections

Carla M. Carvalho and Paul Maggio

BURNS

Background

Each year in the United States, 450,000 people require medical treatment for burns, with 40,000 requiring hospitalization and 30,000 requiring specialty care in a Burn Center. 2012 data estimated the number of deaths from thermal injuries at 3,400 per year.¹ The three most common causes of residential fire deaths are believed to be careless smoking, arson, and defective or improperly used heating devices.^2,3 Factors affecting mortality include patient age >60 years, total body surface area (TBSA%) burned >40%, and the presence of inhalation injury (IHI).⁴

Diagnostic Evaluation

The size and depth of a thermal injury are often challenging to accurately determine, but these parameters are important in guiding in the resuscitation and triage of the injured patient. The depth of injury is typically heterogeneous, and the extent of tissue injury may not be visually apparent, particularly in the acute setting. In addition, the extent of a burn injury may deepen over time in a process known as burn wound progression.

Traditionally, burns were classified as first, second, third, and fourth degree. While this nomenclature still exists, a clinically more meaningful classification consists of superficial (or epidermal), superficial partial thickness, deep partial thickness, and full thickness (Table 35.1). Both classifications are based on the depth of skin penetration of the burn. Superficial, or first-degree burns, involve only the epidermis. Second-degree burns include superficial partial thickness and deep partial-thickness burns, which extend, respectively, into the superficial and deep layers of the hypodermis. Full-thickness, or third-degree, burns involve the epidermis, hypodermis, and the subcutaneous fat beneath the skin.

Calculating the TBSA involved in a burn injury helps to identify patients who require a higher level of care. This can be done using the “rule of nines” for adults and the Lund-Browder chart for children and infants.⁵ For smaller or patchy burns, the patient’s palmar surface can be used. The patient’s palmar surface, including fingers, represents approximately 1% TBSA. Table 35.2 outlines the American Burn Association criteria for burn center referral.⁶

IHI—which has a reported incidence of 1.5% to 19.6% among all burn patients—is an independent predictor of mortality and a leading cause of death in burn patients.^7–9 IHI should be suspected in burn patients presenting with persistent cough, stridor, facial burns, or singed nasal hair, particularly if the patient was injured in an enclosed space. Injury to the upper airway from direct thermal exposure or chemical irritation results in upper airway edema and may lead to early airway obstruction. This differs from the parenchymal lung injury seen in patients with IHI, which is the result of chemical by-products of combustion transported to the lower airways on particles of soot. Airway injury varies from mild desquamation to complete disruption of the epithelial lining, cast formation, and airway obstruction. Fiberoptic laryngoscopy and bronchoscopy are the standard for diagnosing injury to the upper airway, and findings include soot, erythema, edema, and inflammation.

Management Guidelines

The management of burns is complex and involves integrated and prolonged care from teams, including physicians, nurses, therapists, and nutritionists. In the acute setting, treatment strategies must incorporate a high suspicion for an IHI, maintenance of normal hemodynamics, and appropriate volume resuscitation.

IHI may result in the rapid compromise of a patient’s airway. Early endotracheal intubation is indicated in the following situations: if upper airway patency is threatened; if gas exchange or compliance is impaired; if there are significant signs of worsening airway edema (e.g., new hoarseness); if there is clinical expectation of worsening edema (e.g., circumferential neck burns); or if the patient’s mental status precludes airway protection. There is no indication in inhalational injury for prophylactic steroids or antibiotics.

Patients who suffer IHI are at higher risk of pneumonia, which is a major cause of morbidity and mortality in the ICU. Correctly diagnosing pneumonia in a patient with IHI can be challenging; chest radiographs can be hard to interpret, and carbonaceous sputum can mask purulent secretions, so careful consideration of white blood cell count (WBC), patient temperature, chest radiograph findings, and sputum culture results is required. Antibiotics are likely overprescribed in IHI. In one study, a 20% false-positive rate for pneumonia was observed in IHI patients whose pneumonia diagnosis was established using the Clinical Pulmonary Infection Score.¹⁰ Patients with IHI who develop ventilator-associated pneumonia are at higher risk of acquiring multidrug-resistant (MDR) pathogens. Routine surveillance cultures from endotracheal aspirates have been shown to predict MDR etiology in IHI-associated ventilator-associated pneumonia (VAP) with a sensitivity and specificity of 83% and 96.2%, respectively.¹¹

In patients suffering significant thermal injury, total body water typically remains constant, although fluid shifts result in greater intracellular and interstitial volumes and decreased circulating plasma volume. Initial volume resuscitation of burn patients with >20% TBSA should be guided by one of several well-known formulas that address the need to replace sequestered fluid. The commonly used Parkland formula calls for 4 mL of crystalloid per kilogram per percent TBSA burned, with half of the required 24-hour volume given in the first 8 hours, and the remaining half is given in the second 16 hours.¹²

Although formulas help to establish initial goals for resuscitation in the acute setting, administered fluids should ultimately be titrated based on organ perfusion. Military guidelines for burn resuscitation that incorporate hourly fluid input and output significantly improve the combined outcome of mortality and abdominal compartment syndrome.¹³ Use of the electronic medical record to guide resuscitation has been shown to decrease total IV crystalloid volumes infused and better maintain targeted urine output.¹⁴

Recent studies have looked at the role of B-type natriuretic peptide (BNP) in guiding volume resuscitation. A recent prospective study studied 38 burn patients prospectively and followed BNP levels.¹⁵ Those patients with higher BNP levels at day 3 received less fluid resuscitation and had significantly lower Sequential Organ Failure Assessment (SOFA) scores. The study suggested this finding could be explained by lower capillary leakage in these patients, resulting in greater intravascular fluid retention and consequently higher levels of BNP. These findings suggest a potential role for markers such as BNP to help adjust volume infused during resuscitation.

Burn patients epitomize the physiologic stress response because burn injury is often of longer duration and of greater severity than other critical illness. Alterations in immunologic and endocrinologic function characterize the intense stress response in burn injury, and glucose control has emerged as an important early management strategy in this setting.^15–18 Recently, preliminary results from a prospective study of 40 burn patients (24 diabetic and 16 nondiabetic) showed delayed closure of index burn wounds, despite grafting, in diabetic patients.¹⁹ The NICE-SUGAR study, which showed an increase in 90-day mortality for those patients receiving insulin therapy to maintain a target blood glucose level of 81 to 108 mg/dL compared to those with a goal blood glucose level of <180 mg/dL, provides a useful guide for glucose management in burn patients.²⁰

A patient with chemical burns presents unique challenges for the treating physician. In addition to skin damage or loss, there is potential for systemic toxicity. For most acids, copious fluid irrigation, often hours in duration, is indicated. Evaluation of skin pH at onset and periodically during irrigation treatment may or may not be useful. In the case of hydrofluoric acid, fluoride ions may be absorbed systemically and bind with positive ions such as calcium, causing potentially lethal effects. Treatment depends on clinical scenario; for patients with signs of locally isolated symptoms, a calcium gluconate slurry applied topically may suffice. In patients with signs of systemic toxicity, intra-arterial injection of calcium gluconate is necessary (see Chapter 49).

SKIN AND SOFT TISSUE INJURY

Background

Skin and soft tissue infections (SSTIs) account for more than 14 million outpatient visits and 869,000 hospital admissions in the United States each year. The number of hospital admissions related to SSTIs increased by 29% between 2000 and 2004, a fact likely explained by the emergence of community-acquired methicillin-resistant Staphylococcus aureus (MRSA).²¹ Surveillance of MRSA is carried out by the U.S. Centers for Disease Control and Prevention, and this information is accessible online.²²

SSTIs include a spectrum of diseases, ranging from superficial cellulitis to life-threatening necrotizing soft tissue infection (NSTI). A classification scheme developed in 1998 by the U.S. Food and Drug Administration (FDA) divided SSTIs into two broad categories: uncomplicated skin and soft tissue infections and complicated skin and soft tissue infections.²³ In general, uncomplicated infections could be treated with antibiotics or surgical drainage alone. Complicated infections were those that penetrated tissues more deeply and required more extensive surgery. Although the terms uncomplicated and complicated continue to be used, the FDA revised its classification in 2010. These infections are now known as, respectively, milder skin infections and acute bacterial skin and skin structure infections (ABSSSI). Milder skin infections include superficial cutaneous abscesses and impetigo; ABSSSIs include cellulitis, major cutaneous abscesses, wound infections, and burn infections and are defined by a minimum of 75 cm² of redness, induration, or erythema.

Another important classification for SSTIs differentiates non-NSTIs from NSTIs. NSTIs include necrotizing fasciitis, synergistic necrotizing cellulitis, clostridial myonecrosis, and Fournier gangrene. A diagnosis of NSTI need not be preceded by a diagnosis of SSTI, as patients sometimes present to emergency departments with infections that have progressed beyond the superficial tissue. NSTIs progress rapidly and can lead to severe sepsis, multiorgan failure, and death, and carry mortality rates of 20% to 60%.^24,25 Although the factors that lead to higher mortality rates remain incompletely defined, WBC > 30 and patient transfer from an outside institution (e.g., skilled nursing facility) prior to delivery of definitive therapy have been shown to be independent predictors of mortality by multivariable analysis.²⁶

Diagnostic Evaluation

ABSSSIs and milder skin infections are often identified in emergency departments. Cellulitis is a common mild skin infection characterized by spreading erythema localized to the skin or superficial soft tissues. It is typically the result of a break in the skin or superficial wound, and patients are usually afebrile. Common pathogens include beta-hemolytic streptococci and, less commonly, Staphylococcus aureus. Treatment consists of antibiotics alone. Cutaneous or deep abscesses are pockets of pus within the dermis or soft tissues, which may or may not have associated cellulitis or erythema. Abscesses may develop spontaneously, particularly in the immunocompromised patient, or they may represent the progression of a superficial bite wound, skin injury, or surgical incision. Abscesses are typically polymicrobial, with S. aureus occurring as a single pathogen in only 25% of cases. Treatment consists of incision and drainage and antibiotics. Inadequate drainage places the patient at risk of developing NSTI.

The diagnosis of NSTIs can be difficult, and clinical suspicion should be high in a patient with risk factors such as IV drug use, obesity, diabetes, immunosuppression, malignancy, and cirrhosis.²⁷ Clinical findings may be subtle and nonspecific, and the classic symptoms of crepitus, epidermolysis, and erythema may not occur in the first 24 to 48 hours of the disease. In subacute forms of NSTIs, symptoms may be mild and limited to drainage from the wound’s edge. Pain, edema, fever, and an elevated WBC often manifest as the disease progresses and are the findings commonly reported in large series. Pain may be out of proportion to examination, or it may be blunted in patients with diabetic or other associated neuropathies.

NSTIs require immediate and aggressive surgical intervention, making rapid diagnosis essential to optimize outcomes. Because “hard signs” of NSTI (bullae, crepitus, skin necrosis, gas on radiograph) may be absent in over 50% of patients, several laboratory adjuncts are useful in establishing the diagnosis. One study comparing patients with non-NSTIs and NSTIs found a WBC > 15,400 and a serum sodium <135 mmol/L to be associated with NSTIs.²⁶ In this study, these values were highly sensitive, with a negative predictive value (NPV) of 99%, but poorly specific, with a positive predictive value (PPV) of only 26%. In 2004, the Laboratory Risk Indicator for Necrotizing Fasciitis (LRINEC) score was developed as an adjunct to clinical evaluation for establishing a diagnosis of NSTI.²⁷ The LRINEC score is based on independent laboratory variables associated with NSTI: C-reactive protein, WBC, hemoglobin, sodium, glucose, and serum creatinine. A LRINEC score of ≥6 had a PPV of 92% and a NPV of 96% for NTSI. These results have been subsequently validated in other studies, including a multicenter study of 209 patients that showed a higher rate of mortality and amputation in patients with LRINEC scores of ≥6.^28,29

Imaging may be helpful in diagnosing NSTI and in delineating the extent of infection, particularly in the stable patient with subtle findings. Plain radiographs uncommonly show subcutaneous gas, and these studies must be interpreted with caution. Computed tomography may also be helpful, but magnetic resonance imaging remains the most sensitive imaging modality.³⁰ Importantly, since a diagnosis of NSTI can often be made by clinical exam and laboratory data, imaging should not delay operative intervention.

Management Guidelines

The successful treatment of patients with SSTIs relies on four management principles: (a) prompt diagnosis with differentiation between nonnecrotizing and necrotizing SSTI; (b) early initiation of empiric broad-spectrum antibiotics, with coverage for specific pathogens based on risk and coverage for MRSA for all patients; (c) early debridement of NSTIs and surgical drainage for abscesses; and (d) definition of pathogen (by culture) and subsequent de-escalation of antimicrobial therapy.³¹

MRSA has emerged as the most common identifiable cause of severe SSTIs.³² A multi-institutional study across the United States recently reported MRSA in 320 out of 422 enrolled patients who arrived in emergency departments with skin infections. Community-acquired MRSA (CA-MRSA) is now commonly responsible for SSTIs and NSTIs seen in emergency departments. In one study, SSTIs accounted for 74% of all CA-MRSA infections.³³ Timely treatment with empiric anti-MRSA antimicrobials such as vancomycin, linezolid, or daptomycin is warranted in all cases of severe SSTIs and improves outcomes.³⁴ Several other SSTI and NSTI pathogens have been associated with rapid clinical deterioration. These include Streptococcus pyogenes, Clostridium spp., and Vibrio spp.³⁵ SSTIs and NSTIs can also be polymicrobial. Specific antibiotic regimens for non-MRSA organisms have not been studied rigorously, but treatment should cover gram-positive, gram-negative, and anaerobic organisms. Typical antibiotics for these cases (combined with an anti-MRSA agent) include imipenem, meropenem, and piperacillin–tazobactam. Finally, streptococcal and staphylococcal infections are associated with toxin production, and the addition of antitoxin antimicrobials such as linezolid or clindamycin should be incorporated in all patients with severe SSTIs or NSTIs.

The mainstay of treatment for NSTIs has been surgical debridement. Multiple studies support early aggressive debridement as predictive of better outcome.^36,37 A recent retrospective study showed a median 8.6-hour time to operation when NSTI patients were treated by the emergency general surgery service, and an overall mortality of 9.6% in 52 patients.³⁸ Both the time to operation and mortality rate were lower than in other studies, which may suggest that early identification and surgical intervention of NSTI could reduce mortality. Surgical debridement includes excision of all nonviable tissue to achieve adequate source control; however, no prospective data exist to guide specific surgical therapy as pertains to number or size of incisions. The fundamental principles that guide surgical therapy include (a) the extent of the resection, which is usually determined intraoperatively upon gross inspection of the tissues; (b) full-thickness soft tissue or fascial excision for necrotizing fasciitis; (c) serial wound inspections and debridements; and (d) fecal diversion (e.g., colostomy) if there is involvement of the perineum and scrotum. Several authors advocate for return to the operating room within 24 hours for further debridement, if necessary, of devitalized tissue.³⁹ In patients with NSTIs, serial operations are not uncommon.

For patients with NSTIs, critical care management is an important component in treatment. Patients often present with accompanying severe sepsis or septic shock. In addition to antibiotic and surgical therapy, early goal-directed therapy, including aggressive resuscitation, appropriate hemodynamic monitoring, and glucose control, is recommended.^40,41

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