Infections of Skin, Muscle, and Soft Tissue

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135 Infections of Skin, Muscle, and Soft Tissue

Infections of skin, soft tissue, and muscle include a broad range of diseases from those originating in the skin (impetigo, ecthyma, erysipelas, pyoderma), superficial fascia (embolic ulcers, cellulitis), fascia cleft, and deep fascia (necrotizing fasciitis) to muscle (myonecrosis). In this chapter, we focus on infections of skin, soft tissue, and muscle that are commonly encountered in intensive care units (ICUs) and are often severe and potentially life threatening. These infections include necrotizing soft-tissue infections (NSTIs), soft-tissue infections of the neck and head, and infectious complications of bites, burns, and pressure ulcers.

Necrotizing Soft-Tissue Infections

NSTIs represent a spectrum of infectious processes that are extensive and rapidly progressive. Based on the depth of skin and soft-tissue involvement, NSTIs are divided into three categories: necrotizing cellulitis, necrotizing fasciitis, and myonecrosis. Table 135-1 shows the classification of NSTIs. The sine qua non of these infections is necrosis of subcutaneous tissue, fascia, and muscle, with widespread undermining of the skin. The lack of anatomic boundaries and the fact that the infection is deep to the skin helps account for the severity of the infection as well as the frequent delay in its recognition. The trunk, extremities, and perineum are the most common sites of NSTIs, but other anatomic sites may be involved. For example, intraabdominal abscess, bowel perforation, and pancreatitis can present as necrotizing infection of the abdominal wall or extend into the thigh along the psoas muscle.^1,² Similarly, cervical fasciitis due to dental or neck abscess can extend to the mediastinum.

TABLE 135-1 Classification of Necrotizing Skin, Soft-Tissue, and Muscle Infections

Disease	Bacteriology	Comments
Necrotizing Cellulitis
Clostridial cellulitis	Clostridium perfringens	Local trauma, recent surgery; fascial/deep muscle spared
Nonclostridial cellulitis	Mixed: Escherichia coli, Enterobacter, Peptostreptococcus spp., Bacteroides fragilis	Diabetes mellitus predisposes; produces foul odor
Meleney’s synergistic gangrene	Staphylococcus aureus, microaerophilic streptococci	Rare infection; postoperative; slowly expanding, indolent, ulceration in superficial fascia
Synergistic necrotizing cellulitis	Mixed aerobic and anaerobic, including B. fragilis, Peptostreptococcus spp.	Diabetes mellitus predisposes; variant of necrotizing fasciitis type I; involves skin, muscle, fat, and fascia
Necrotizing Fasciitis
Type I	Mixed aerobic and anaerobic; staphylococci, B. fragilis, E. coli, group A streptococci, Peptostreptococcus spp., Prevotella, Porphyromonas spp., Clostridium spp.	Usually requires a breach in the mucous membrane layer either through surgery or penetrating injuries or from chronic medical conditions such as diabetes, peripheral vascular disease, malignancy, and anal fissures
Type II	Group A streptococci	Increasing in frequency and severity since 1985; very high mortality; often begins at site of nonpenetrating minor trauma such as a bruise or muscle strain but often no identified precursor
		Predisposing factors: blunt/penetrating trauma, varicella (chickenpox), intravenous drug abuse, surgical procedures, childbirth, NSAID use
Myonecrosis
Clostridial myonecrosis	Clostridium spp.	Predisposing factors: deep/penetrating injury, bowel and biliary tract surgery, improperly performed abortion and retained placenta, prolonged rupture of the membranes, and intrauterine fetal demise or missed abortion in postpartum patients. Recurrent gas gangrene occurs at sites of previous gas gangrene.
Streptococcal myonecrosis	Streptococci
Special Type of Necrotizing Soft-Tissue Infection
Fournier’s gangrene	Polymicrobial, with E. coli the predominant aerobe and Bacteroides the predominant anaerobe. Other microflora: Proteus, Staphylococcus, Enterococcus, aerobic and anaerobic Streptococcus, Pseudomonas, Klebsiella, and Clostridium	Necrosis of the scrotum or perineum that starts with scrotal pain and erythema and rapidly spreads onto anterior abdominal wall and gluteal muscle. It is more often seen in diabetics and can be associated with trauma.

Many different descriptive terms and eponyms have been used to describe NSTIs. The most common infections encountered in ICU patients are postoperative progressive bacterial synergistic gangrene, clostridial cellulitis, synergistic gangrene, necrotizing fasciitis, Fournier’s gangrene, gas gangrene, and Meleney’s synergistic gangrene. Although the terminology and depth of infection may be different, the severity and emergent need for surgical intervention are common to all varieties of these infections.

Pathogenesis

Pathophysiologic factors involved in the development and progression of NSTIs are host resistance, bacterial pathogens involved, and local barrier factors.

Host Resistance

As shown in Table 135-2, individuals who are immunocompromised or have chronic diseases are more likely to develop necrotizing skin and soft-tissue infections than those without such medical problems.

TABLE 135-2 Factors Predisposing to Necrotizing Soft-Tissue Infections

Bacterial Pathogens

There are specific bacteria that are more likely than others to cause NSTIs, as shown in Table 135-1. Although necrotizing cellulitis and fasciitis may be caused by a single bacterial pathogen such as group A Streptococcus, Vibrio spp., or zygomycetes, about 80% of necrotizing cellulitis or fasciitis results from polymicrobial infections with synergistic facultative aerobes and anaerobic gas-forming organisms. An average of 4.4 organisms are isolated from polymicrobial necrotizing infections.³ The former includes gram-positive and gram-negative aerobes such as Streptococcus pyogenes, Staphylococcus aureus, Enterococcus faecalis, Escherichia coli, or Pseudomonas aeruginosa, and the latter includes Clostridium perfringens, Bacteroides fragilis, and Peptostreptococcus.⁴ Certain predisposing conditions can be correlated with specific bacteria—for example, trauma with Clostridium spp., diabetes mellitus with Bacteroides spp., S. aureus, and Enterobacteriaceae, and immunosuppression with Pseudomonas spp. and Enterobacteriaceae.⁵

Traditionally, gas gangrene is synonymous with clostridial infection, and gas in the soft tissue is thought to be a grave finding. The majority of gas-producing infections do not involve Clostridium spp. but are instead necrotizing infections due to other bacterial pathogens. Many bacteria, especially facultative gram-negative bacilli (e.g., E. coli), produce insoluble gases such as hydrogen, nitrogen, and methane whenever they are forced to use anaerobic metabolism. Thus, the presence of crepitus in a soft-tissue infection on physical examination or radiographs implies anaerobic metabolism and existence of an NSTI.

Local Barrier Failure

Most serious soft-tissue infections require some degree of tissue injury and break in the skin to establish infection. The break in the skin may be due to a surgical incision or trauma; it may be related to large wounds or very small ones. The tissue injury may be due to either blunt or penetrating trauma of any kind. However, in a significant percentage of cases, it is difficult to find evidence of a break in the skin or soft-tissue trauma.

Clinical Manifestations and Diagnosis

The critical aspect of diagnosing NSTIs is maintaining a high index of suspicion, which allows for early recognition of the nonlocalized necrotizing nature of the infection and the need for surgical intervention. Although necrotizing cellulitis and fasciitis may occur after significant tissue trauma or a relatively trivial injury, up to 40% of NSTIs have no identifiable cause. NSTIs with identifiable barrier failure are more likely to be polymicrobial and are easier to diagnose than the more virulent infections caused by a single organism. In necrotizing cellulitis, gas is invariably found in the skin, but the fascia and deep muscle are spared. Early clinical findings are similar to those of common wound infections, including local edema (89%), erythema (30%), fever (71%), and local cutaneous anesthesia (27%) due to cutaneous nerve necrosis.⁶ These are followed by gangrenous skin changes with rapid extension beyond the borders of the original infection. Synergistic polymicrobial necrotizing fasciitis is characterized by “dishwater pus.” Patients usually have high fever, but no obvious source of clinical infection can be detected. Pain in the area of infection is usually out of proportion to the physical findings. As the infection progresses, patients develop shock and multiple organ failure. Mortality rates are high, with necrotizing fasciitis being fatal in 23.5% of cases.⁷

Clostridial myonecrosis typically develops within 12 to 24 hours after a traumatic event or closure of a deep contaminated wound. Recurrent gas gangrene caused by C. perfringens has been described in individuals with nonpenetrating injuries at sites of previous clostridial myonecrosis, where spores of C. perfringens remain quiescent in tissue and then germinate when minor trauma provides conditions suitable for growth. Patients present with the triad of severe pain, tachycardia out of proportion to fever, and crepitus in the soft tissue. Once overt gangrene with edema and bronze, purplish, or brown discoloration with bullae and watery discharge occur, the disease is at an advanced stage. Gram stain of the exudate shows gram-positive rods occasionally accompanied by other flora. In contrast, streptococcal myonecrosis usually develops over 2 to 4 days after trauma or closure of a wound. The onset is not as rapid, patients do not appear as sick, pain is not as severe, and gas formation is not as obvious as in those with clostridial myonecrosis.

Management

Initial management of NSTIs involves aggressive fluid resuscitation, appropriate broad-spectrum parenteral antibiotics, and most importantly, expedient and radical surgical débridement. Other adjunctive therapies such as hyperbaric oxygen and immunoglobulin have been used, but their efficacy has not been as well established.

Antibiotics

For type I necrotizing fasciitis (mixed aerobic and anaerobic), antibiotic treatment should be guided initially on results of the Gram stain. Early empirical treatment should be initiated with extended-spectrum penicillins (e.g., ampicillin-sulbactam, piperacillin-tazobactam, ticarcillin-clavulanic acid) or carbapenem antibiotics (e.g., imipenem-cilastatin). If there is a suspicion that resistant coliforms might be participating, such as in patients who have been hospitalized or who have been treated with antibiotics recently or where there is suspicion of rectal or intestinal involvement, a third-generation cephalosporin, aminoglycoside, or aztreonam combined with either clindamycin or metronidazole may be used. For those patients with severe cases or in whom clostridia are suspected, clindamycin in addition to penicillin is useful for inhibiting toxin production. The incidence of both community- and hospital-acquired methicillin-resistant S. aureus (MRSA) is increasing, and consideration of anti-MRSA treatment should be based on patient history and local resistance patterns. Nosocomial infections should be empirically treated.

Although there are no data from clinical trials establishing the benefit of combined therapy in type II necrotizing fasciitis (group A streptococci), penicillin G combined with clindamycin is the antibiotic therapy of choice. Clindamycin, but not metronidazole, is recommended not for its antianaerobic properties but because of its additional activity against gram-positive organisms, including specific inhibition of toxin production.⁸ Cefotaxime and ceftriaxone are acceptable alternatives. For patients allergic to penicillin, vancomycin is the recommended treatment.

Surgical Intervention

Early surgical débridement is critical in the management of NSTIs. Aggressive surgical excision of all involved tissue with a margin of normal-appearing tissue is mandatory. All necrotic tissue should be excised back to healthy bleeding margins. Additional incisions parallel to cutaneous nerves and blood vessels may be used to assess fascial viability without elevating the skin. The wound should be frequently reexamined for viability of tissue and repeat operative débridement is frequently required. Aggressive fascial débridement of abdominal surgical wounds may necessitate the use of prosthetic material to replace an abdominal wall defect, as depicted in Figure 135-1. In Fournier’s gangrene and perineal/perirectal NSTI, a colostomy for fecal diversion may be necessary to keep the wound clean. The testes generally survive because their blood supply is usually spared, but they may need to be temporarily implanted in the soft tissue of the medial thighs if the scrotum must be débrided. On rare occasion, NSTI of the extremities may require amputation.

Figure 135-1 Necrotizing fasciitis of the abdominal wall after extensive débridement and application of porcine dermal collagen implant for temporary abdominal closure (left) and after healing of anterolateral thigh flaps to reconstruct the abdominal wall (right).

Myonecrosis or gas gangrene requires radical débridement to viable muscle. When this process involves the extremities, control of the infection is more easily achieved, although as mentioned previously, amputation may be necessary. In contrast, clostridial myonecrosis involving the trunk may present some very difficult therapeutic decisions because the removal of nonviable tissue may leave the peritoneal or thoracic cavities open and their contents exposed. Temporary coverage with prosthetic materials may be necessary. Trunk infections are therefore associated with a grim prognosis.

Adjunctive Therapy

Hyperbaric Oxygen

The use of hyperbaric oxygen (HBO) in NSTIs is controversial. Although there are no randomized prospective studies of HBO in these infections, in vitro data and reviews of clinical series seem to show beneficial effects of HBO when combined with antibiotics and surgical débridement in the management of clostridial infection.^9,¹⁰ Hyperbaric oxygen is toxic to clostridia and inhibits bacterial growth, blocks production of alpha toxin, and preserves marginally perfused tissue. Debate also exists about the use of HBO for nonclostridial necrotizing skin and soft-tissue infection. In one report, the addition of HBO to the surgical and antimicrobial treatment of nonclostridial necrotizing fasciitis significantly reduced mortality and the need for débridement.⁹

Intravenous Immunoglobulin

Intravenous immunoglobulin (IVIG) has been administered to patients with streptococcal and staphylococcal toxic shock syndrome and may be efficacious in the treatment of this toxin-mediated disorder. Some studies have demonstrated IVIG has some beneficial effect in the treatment of NSTIs, theoretically owing to its neutralization of circulating clostridial toxins and streptococcal superantigens.¹¹ However, a large multicenter retrospective cohort study of children with streptococcal toxic shock syndrome showed no improvement in outcomes with administration of IVIG.¹² There is no clear consensus at this time regarding the efficacy of IVIG.

Important Soft-Tissue Infections of the Head and Neck

Ludwig’s Angina

In 1836, German physician Wilhelm Frederick von Ludwig described five patients with gangrenous induration of the connective tissues of the neck that progressed rapidly to involve the tissues covering the muscles between the larynx and the floor of the mouth.¹³ Ludwig’s angina is a potentially life-threatening, rapidly progressive, diffuse “woody” or brawny cellulitis of the submandibular and sublingual spaces that occurs most often in young adults with dental infections.

Pathogenesis

In adults, 50% to 80% of cases of Ludwig’s angina are caused by dental caries, and the disease has a mortality rate of 5% to 10%.¹⁴ Submandibular and sublingual spaces freely communicate, and with involvement of the deep cervical fascia, infection may spread rapidly, with grave consequences. Extension along the carotid sheath or the retropharyngeal space can cause mediastinitis.¹⁵ Infection is commonly caused by oral cavity anaerobes such as Fusobacterium, anaerobic streptococci, Bacteroides, spirochetes, and hemolytic Streptococcus organisms, although the infection may be mixed with Staphylococcus and Streptococcus, Klebsiella, or a combination of aerobic or anaerobic organisms.¹⁶ The presence of anaerobes commonly accounts for the occurrence of gas in the tissues.

Clinical Manifestations

The patient is febrile and complains of severe neck pain and swelling, odynophagia, dysphagia, drooling, and leaning forward to maximize the airway diameter. Patients usually have a recent history of dental work, obviously poor dental hygiene, or deep neck abscess.

Examination may reveal a tender, symmetrical, and indurated swelling, sometimes with palpable crepitus in the submandibular area. The tongue may be swollen or displaced upward and backward, and the mouth is held open because of the lingual swelling. The presence of stridor, dyspnea, decreased air movement, or cyanosis suggests airway compromise. The appearance of significant asymmetry of the submandibular area is an ominous sign because it may represent an extension of the inflammation to the parapharyngeal space.

Radiographic views of the teeth may indicate the source of infection, and lateral views of the neck will demonstrate soft-tissue swelling around the airway and possibly submandibular gas. Computed tomography (CT) of the neck may be recommended to determine the extent of inflammation.

The diagnosis of Ludwig’s angina is usually made clinically according to three criteria: (1) presence of cellulitis with little or no pus in both submandibular and sublingual spaces; (2) presence of gangrene with serosanguineous putrid fluid; and (3) rapidly spreading cellulitis in connective tissue, fascia, and muscles, without glandular tissue and lymphatic involvement.¹⁷

Management

Acute Epiglottitis

Acute epiglottitis is a rare, potentially life-threatening bacterial infection causing inflammation and edema of the epiglottis, aryepiglottic folds, and surrounding tissues. Before the era of Haemophilus influenzae vaccine, epiglottitis used to be a primarily pediatric infection. However, in recent years, the infection has become primarily an adult disease.

Pathogenesis

Invading bacteria cause inflammation and edema of the epiglottis, aryepiglottic fold, and surrounding tissues. These structures then may protrude downward and over the glottic opening, causing airway obstruction. In the past, most of the cases (50%-70%) were caused by H. influenzae B (HIB).²² However, at the present time, other bacteria including group A β-hemolytic Streptococcus, S. aureus, and Streptococcus pneumoniae have become more common, and more patients present with epiglottic abscess.

Clinical Manifestations and Management

Early signs of epiglottitis include hoarseness, dysphagia, odynophagia, and a sore throat (present in 94% of patients).²³ Some authors advocate direct or indirect laryngoscopy on adult patients without respiratory distress; it is safe to perform such procedures in the operating room or ICU, where both the equipment and personnel required for emergency intubation are at hand. The most common misdiagnosis is streptococcal pharyngitis. Patients who can maintain their airway and adequate oxygenation should be closely observed in an ICU where definitive airway management can be achieved in a controlled fashion. Corticosteroids, racemic epinephrine, and heliox can be considered for initial management, but their role is unresolved. Dyspnea and stridor indicate impending airway obstruction, and emergency airway control should be established. Flexible fiberoptic laryngoscopy is usually used during intubation because it provides direct visualization of the airway while serving as a guide for intubation.

The third-generation cephalosporins, cefotaxime and ceftriaxone, are the antibiotics of choice for acute epiglottitis. These antibiotics are usually effective against H. influenzae, streptococci, and staphylococci. A number of other antibiotics including cefuroxime, ampicillin-sulbactam, piperacillin-tazobactam, ticarcillin-clavulanic acid, and levofloxacin are also effective in epiglottitis.

Infections of Bite Wounds

It is estimated that 4.7 million dog bites, 400,000 cat bites, and 250,000 human bites occur in the United States annually. In addition to bites, exposure to mouth flora can also occur in clenched-fist injuries and finger or thumb sucking, The incidence of infection after cat bites can be more than 50%, and infection after dog or human bite wounds can be 15% to 20%. Wild animal bites also are a potential source of serious infection. Although the majority of patients with bite wounds do not seek medical attention, some bite wounds can become disasters, leading to severe infections and sepsis that result in loss of limb function or even require amputation. Although many of these wounds may look innocuous initially, they may lead to serious infections (i.e., NSTIs) and sepsis. Complications also include lymphangitis, septic arthritis, tenosynovitis, and osteomyelitis.

Pathogenesis

The microbiology of bite wounds generally is polymicrobial, reflecting the aerobic and anaerobic microbiology of the oral flora of the biter and the skin of the victim, as well as the environment.

Soft-tissue infections caused by human mouth flora are usually due to a mixture of pathogens.²⁴ It has been reported that the human mouth hosts 42 different species of bacterial flora, of which aerobes (Eikenella corrodens, Staphylococcus, Streptococcus, and Corynebacterium spp.) are the most common isolates from infected bite wounds.²⁵ E. corrodens is a slow-growing, gram-negative bacillus frequently associated with chronic infection and abscess formation in human bites. Commonly isolated anaerobes include Bacteroides and Peptostreptococcus spp.

As in human bites, polymicrobial infections are frequently encountered in animal bites. Whereas almost any oral flora isolate is a potential pathogen, Pasteurella multocida is the most prevalent organism found in 50% of dog bite wounds and 70% of cat bite wound infections.^26,²⁷ S. aureus, α-, β-, and δ-hemolytic streptococci, gram-negative organisms, and anaerobic microorganisms that are usually part of the normal mouth flora of animals also have all been isolated.

Management

Management goals for bite wounds are to prevent or appropriately treat infection and minimize soft-tissue deformity. For domestic animal bites, unless the animal is suspected of having rabies, rabies prophylaxis is not necessary. Many wild animals including skunks, raccoons, foxes, and bats should be considered rabid unless proved otherwise, and a bite by such an animal should result in rabies prophylaxis. Tetanus immunization status must also be determined, and if not up to date, tetanus toxoid should be administered. Tetanus immune globulin should also be considered for those victims whose last tetanus booster was more than 10 years before the bite injury. Radiography is indicated if there are any concerns that deep structures are at risk. These include hand wounds, deep punctures, and crushing bites, especially those over joints.

Meticulous wound care is the cornerstone of human or animal bite wound management. Copious irrigation of the wound decreases the incidence of wound infection. Careful débridement of devitalized tissue, particulate matter, and clot is also necessary to reduce the infection risk and improve the cosmetic result. Puncture wounds and dog bite injuries of the hand should not be closely primarily. Other wounds with extensive crush injuries or those requiring extensive débridement can be approximated and be closed by delayed primary or secondary intention.

Cultures of clinically uninfected wounds are not indicated. However, it is recommended that cultures be performed in infected wounds that are not improving despite apparently adequate antibiotic treatment. In bite victims, prophylactic broad-spectrum antibiotics are recommended for patients with high-risk bites but are only of proven benefit in human bites.²⁸ The high-risk factors for infection include human bites, wounds of the hand, foot, face, scalp, and perineum, puncture wounds, crush wounds that cannot be débrided, bites over vital structures (artery, nerve, or joint), patient age older than 50 years, or patients who are immunosuppressed.²⁹ In most patients, amoxicillin-clavulanic acid is the preferred antibiotic. Alternatives include moxifloxacin, amoxicillin, doxycycline, and cefuroxime. In human bites, amoxicillin-clavulanic acid will cover E. corrodens as well as most other oral flora and is the recommended antibiotic. Other options include second- or third-generation cephalosporins, quinolones, or doxycycline. In patients who are allergic to penicillin, trimethoprim-sulfamethoxazole is an alternative for both dog and cat bites, whereas quinolones or erythromycin may be used for human bites.

Patients who require inpatient care for complex wounds, systemic toxicity, established infection, or suspicion of musculoskeletal, neurologic, or vascular involvement, or patients who are at very high risk of invasive infection (e.g., immunosuppression), should be treated with parenteral antibiotics, irrigation, and débridement with cultures.³⁰ Consultation with a hand surgeon should be considered in those with hand wounds, because the risk of severe infection of bite wounds on a hand is higher than other sites.

Infections of Burn Wounds

Burn wound infection/sepsis is one of the most common causes of death in burn patients. It is estimated that more than 100,000 of the 2.5 million burned patients in the United States require hospital admission, and 12,000 patients die per year.³¹ The highest risk of bacterial invasion from skin flora into the eschar occurs 5 to 7 days after burn. Mechanisms of burn wound infection include breakdown of the natural cutaneous barrier, compromised host defenses, and exposure to pathogenic and opportunistic bacteria. The surface of a burn contains a large amount of necrotic tissue and protein-rich wound exudate, so it provides an excellent growth medium for surface bacteria, leading to bacterial colonization and invasion. Burns are also associated with an immunocompromised status. The percentage of total body surface area (TBSA) burned and the duration of hospitalization correlate well with the incidence of wound infections.³² The predisposing factors for development of burn wound infection are listed in Table 135-3.

TABLE 135-3 Predisposing Factors for Burn Wound Infections

Burn wound greater than 30% total body surface area

Full-thickness burn

Extremes in patient age

Preexisting diseases: immunosuppression, diabetes mellitus, vascular insufficiency

Virulence and antibiotic resistance of colonizing pathogens

Failure of skin graft

Prolonged open burn wound

Improper initial burn wound care

Pathogenesis

After thermal injury, all burn wounds become contaminated with microorganisms, either from the patient’s endogenous flora or from resident microorganisms in the burn unit. This colonization is initially without clinical significance. However, surface-colonizing bacteria can penetrate the avascular eschar and proliferate beneath the eschar at the viable/nonviable tissue interface. When host defense mechanisms are compromised, bacteria can break this barrier and spread systemically, resulting in bacteremia and sepsis.

The most common organisms found in burn wound infections are bacteria, and 70% to 90% are endogenous to the patient. Bacterial organisms can also be acquired by cross-infection, principally from the hands of healthcare professionals. Before the era of penicillin, streptococci and staphylococci were the predominant pathogens. Since the 1950s, P. aeruginosa has become the most important species.³³ Other important bacterial species include S. aureus, group A Streptococcus, Enterobacter cloacae, E. faecalis, Klebsiella spp., and Acinetobacter spp.³⁴ Fungi, especially Candida albicans and Aspergillus spp., and viruses (herpesvirus) are also pathogens that can be isolated from infected burn wounds.³⁵

Clinical Manifestations and Diagnosis

Successful treatment of burn wound infections largely depends on early detection of infection. Burn wound infection is difficult to diagnose on the basis of clinical signs and symptoms, because burn-induced inflammatory responses (e.g., fever, leukocytosis) are indistinguishable from those of infection. The local signs of infection may be absent, minimal, or late. Diagnosis is generally based on a combination of clinical signs that indicate sepsis (e.g., fever, leukocytosis, organ dysfunction, hyperdynamic state) and the results of surveillance cultures. Any of the findings listed in Table 135-4 should raise suspicion of burn wound infection.³⁶ The practice of culturing the burn wound surface does not accurately predict progressive bacterial colonization or incipient burn wound sepsis. Qualitative and quantitative correlations are poor between flora on the surface of the burn wound and bacterial colonization and invasion of the deep layers of the eschar. It has been reported that biopsy of the wound with quantitative cultures of greater than 10⁵ CFU per gram of tissue is an accurate indicator of invasive burn would infection.³⁷ When bacterial invasion to viable tissue is detected, excision of the infected wound is important, and systemic antibiotics are indicated.

TABLE 135-4 Clinical Signs Suggestive of Burn Wound Infection

Progression of second-degree to third-degree burn injury

Increased pain, erythema, color changes

Unexpected change in appearance or depth of wound

Unexpected rapid eschar separation

Metastatic septic lesion in unburned tissue

Systemic signs of sepsis

Management

Prevention of Burn Wound Infections

Systemic antibiotic prophylaxis is not routinely administered to burn patients admitted to the hospital, because the unexcised burn wound does not lead to significant bacteremia.³⁸ Frequent wound dressing changes with evaluation of the burn wound and surrounding tissue allow for early detection and therapy of cellulitis. In many burn units in the United States, early excision and grafting of burn wounds has become the standard of care. Early excision is defined as the staged excision of all deep partial- and full-thickness burns by the third to seventh postburn day. The philosophy of early burn wound excision has resulted in improved survival in patients with TBSA burns greater than 30% to 40%, shorter hospital length of stay, lower costs of hospital care, and fewer painful dressing changes. If for some reason such as hemodynamic instability or severe respiratory failure, the patient cannot undergo early excision and coverage, surveillance wound cultures should be performed several times per week to diagnose burn wound infection early. In addition, strict antiseptic measures such as handwashing, barrier isolation, and equipment and room cleaning decrease the incidence of wound infection.

Topical antimicrobials are commonly used in burn patients. Their use has substantially decreased the incidence of conversion of partial-thickness to full-thickness wounds by local infection, and thereby has reduced mortality associated with burn wound infection. In addition, these agents may prolong the sterility of the full-thickness burn wound. However, they have not eliminated the need for aggressive removal of necrotic tissue and closure of the wound with autografts. The commonly used topical agents are listed in Table 135-5. According to an international survey, silver sulfadiazine is the topical agent of choice for partial- to full-thickness burn wounds.³⁹ Nanocrystalline silver mesh dressings that adhere for a week have reduced the discomfort of dressing changes and allow more outpatient care of partial-thickness burn wounds.⁴⁰

TABLE 135-5 Commonly Used Topical Agents in Burn Wounds

Treatment of Burn Wound Infections

Antibiotics

Systemic antibiotics are not used prophylactically in patients with burn wounds.⁴¹ Instead, they should be reserved for use in cases of known or suspected invasive infection. As long as bacterial culture results are available, antibiotics with the narrowest spectrum of activity should be used to minimize the development of resistant organisms. Recommendations for empirical therapy are based on the length of time since the burn was sustained, previous administration of antibiotics to the patient, and knowledge of likely pathogens and the local antibiogram. Combination of multiple antibiotics for a single infection is only used when bacteremia persists in the face of therapeutic doses of a single antibiotic. Inappropriate use of multiple antibiotics does not decrease mortality. Instead, it promotes overgrowth of resistant pathogens such as Candida spp., enterococci, and multiple antibiotic-resistant species.

Surgical Intervention

Invasive bacterial or fungal burn wound infections are treated with surgical excision to the level of viable tissue. Early burn wound excision significantly reduces bacterial colonization and reduces the risk of invasive burn wound infection. Patients who undergo topical treatment and delayed burn wound excision exhibit greater bacterial colonization and increased rates of infection.⁴² Wounds that can be excised completely should be covered with an allograft or autograft. If complete débridement is not possible, topical antimicrobials should be applied and the wound reexamined within 24 hours for possible repeat débridement.

Infections of Pressure Ulcers

Pressure ulcers are caused by localized tissue necrosis and infection due to prolonged compression between a bony prominence and an external surface. Pressure ulcers in ICU patients occur primarily in patients with impaired mobility due to injury, weakness, sedation, or use of paralytic agents. Pressure ulcers result in significant morbidity in critically ill patients. Although infection of decubitus ulcers is high in the nursing home setting and in spinal cord injury patients, it is an uncommon cause of infection or sepsis in ICU patients.⁴³ Pressure ulcers may pose a risk to other hospitalized patients by serving as a reservoir for resistant organisms such as MRSA, vancomycin-resistant enterococci, and multiply-resistant gram-negative bacilli.

Pathogenesis and Classification

Risk factors for pressure ulcers in patients in ICUs are essentially the same as for those on a general hospital floor. They include limited physical activity, impaired sensory perception, poor nutritional status, chronic disorders (e.g., diabetes mellitus, cardiovascular disease, and cerebrovascular accident), impaired circulation, low serum hemoglobin concentration, and increased blood urea nitrogen and serum creatinine concentrations.⁴⁴ Also, a number of infectious complications have been implicated in the development of pressure ulcers. In order of frequency, these are local infection, cellulitis of surrounding tissue, contiguous osteomyelitis, and bacteremia.⁴⁵

Several different classification systems have been developed to describe the extent of pressure ulcers. Table 135-6 shows the most commonly used system promulgated by the National Pressure Ulcer Advisory Panel.⁴⁶

TABLE 135-6 National Pressure Ulcer Advisory Panel Classification of Pressure Ulcers

Staging	Description
I	Intact skin with non-blanchable redness of a localized area usually over a bony prominence. Darkly pigmented skin may not have visible blanching; its color may differ from the surrounding area. The area may be painful, firm, soft, warmer or cooler as compared to adjacent tissue.
II	Partial-thickness loss of dermis presenting as a shallow open ulcer with a red pink wound bed, without slough. May also present as an intact or open/ruptured serum-filled blister.
III	Full-thickness skin loss. Subcutaneous fat may be visible, but bone, tendon, or muscle are not exposed. Slough may be present but does not obscure the depth of tissue loss. May include undermining and tunneling.
IV	Full-thickness tissue loss with exposed bone, tendon, or muscle. Slough or eschar may be present on some parts of the wound bed. Often include undermining and tunneling.

Infections of pressure ulcers are usually polymicrobial. Aerobes commonly recovered include staphylococci (including MRSA), enterococci, Proteus mirabilis, E. coli, and Pseudomonas spp. Anaerobic Peptostreptococcus, Bacteroides fragilis, and Clostridium spp. are also found in these infections. Pressure ulcers are a major reservoir of MRSA. Making an accurate microbiological diagnosis is usually impractical and difficult because all pressure ulcers are colonized with microorganisms, and a superficial culture will not distinguish between colonizing and infecting organisms. If it is necessary to determine the microbiology accurately, it is more appropriate to perform deep-tissue biopsy or direct a needle through intact skin and aspirate a specimen for bacterial culture from the margin of the ulcer.

Management

There are many different approaches to the treatment of pressure ulcers; however, none has been shown to be more effective than any other. Prevention of decubitus ulcers, including pressure relief with support surfaces and repositioning, appropriate nutrition, and skin moisturizers, is the best prophylactic treatment.⁴⁷ Once the ulcer has been established and infection is present, débridement of necrotic and marginally viable tissue is absolutely necessary to obtain healing. Topical agents such as povidone-iodine, hydrogen peroxide, and others have been widely used, but there is no difference in terms of outcome among these agents. Proper use of occlusive dressings such as balsam Peru/trypsin/castor oil preparations increases patient comfort, enhances healing, decreases the possibility of infection, saves time, and reduces costs.⁴⁸ Topical antimicrobial agents have not been shown to be effective. Systemic antibiotic therapy should be reserved for infected ulcers. Skin grafting of clean wounds, if the underlying cause of the pressure ulcer has been removed, is an accepted method of treatment and has been shown to be effective. However, adequate treatment frequently requires much more complex therapies, including tissue flaps and sometimes even amputation to effect wound closure. Treatment of recalcitrant wounds can be difficult and costly. Several newer therapeutic strategies include alginates, a variety of wound dressings, and growth factor therapies (e.g. platelet-derived growth factor). Cultured and tissue-engineered skin substitutes have emerged and are in varying degrees of clinical evaluation.⁴⁹

A variety of empirical antibiotic regimens have been suggested for patients with pressure ulcer–associated cellulitis, osteomyelitis, or bacteremia. In general, any regimen active against the majority of organisms likely to be causal is appropriate. Although advanced inanition is the most common cause of failure of these lesions to heal, osteomyelitis has to be ruled out by physical examination and radiograph. If osteomyelitis is present, a more extended course of therapy is required and, frequently, amputation.

Mechanical therapies aimed at healing decubitus ulcers include removal of all necrotic and undermined tissues and some strategy to relieve the pressure that caused the ulcer.⁵⁰ Once dead tissue has been débrided, the ulcer may be covered with a negative-pressure wound therapy sponge, a moist dressing, or an engineered skin substitute. Studies have shown that these dressings are cost-effective in treating chronic wounds.⁵¹ However, before such local therapy is chosen, it is very important that infection be controlled and that the patient is in good nutritional balance.