INTRODUCTION — Pressure ulcers are localized areas of tissue necrosis that tend to develop when soft tissue is compressed between a bony prominence and an external surface for a prolonged period of time [1]. They are a significant problem in critically ill patients, older adults, and in persons with spinal cord injury.

Pressure ulcers cause pain, decrease quality of life, and lead to significant morbidity and prolonged hospital stays, in part due to complicating infection. Infected pressure ulcers are a common problem, occurring in 4 to 6 percent of nursing home patients in two series [1,2].

The infectious complications of pressure ulcers are reviewed in this topic. The epidemiology, pathogenesis, clinical manifestations, staging, prevention, and treatment of noninfected pressure skin and soft tissue injuries are discussed separately. (See "Epidemiology, pathogenesis, and risk assessment of pressure-induced skin and soft tissue injury" and "Prevention of pressure-induced skin and soft tissue injury" and "Clinical staging and management of pressure-induced skin and soft tissue injury".)

Pressure ulcers that occur in the feet of patients with severe neuropathy and/or vascular insufficiency, often due to diabetes mellitus, are discussed separately. (See "Clinical manifestations, diagnosis, and management of diabetic infections of the lower extremities".)

CLASSIFICATION AND TERMINOLOGY — The National Pressure Injury Advisory Panel made changes to its classification in April 2016 and suggested using the terminology "pressure injury" instead of "pressure ulcer" to describe these wounds. The details of the terminology are discussed elsewhere. (See "Clinical staging and management of pressure-induced skin and soft tissue injury", section on 'Terminology'.)

We use the term "pressure ulcer" for the specific circumstance where the integrity of the skin surface is disrupted.

PATHOGENESIS — Local factors that contribute to infection of pressure ulcers include breaks in the integrity of the skin barrier, pressure-induced changes, and contamination from contiguous dirty areas, such as from fecal incontinence. Among patients with spinal cord injury, the majority of pressure ulcers develop in areas adjacent to the ischium, sacrum, and greater trochanter. (See "Epidemiology, pathogenesis, and risk assessment of pressure-induced skin and soft tissue injury".)

Colonization — Pressure ulcer colonization by microorganisms precedes development of infection. The ulcer is first colonized with skin flora, which is rapidly replaced by bacteria from the local environment and the urogenital or gastrointestinal tracts, often from direct fecal contamination [3].

Pressure ulcers are generally associated with a bacteria count of <10² colony forming units (CFU) per gram of tissue if cared for and kept free of necrotic tissue [4]. Higher concentrations of bacteria in pressure ulcers may inhibit normal wound healing without inducing a host response, a state known as critical colonization [5]. In one study, delayed healing of pressure ulcers occurred when bacterial counts were >10⁵ CFU per gram of tissue [6]. Quantitative bacterial counts to identify critical colonization, however, are not widely used in clinical practice.

The presence of biofilm is also being increasingly recognized as a cause of delayed healing [7]. Biofilm enables bacteria to better resist antimicrobials and host defenses [8].

MICROBIOLOGY — The microbiology of pressure ulcers is polymicrobial and similar in superficial and deep ulcers. Nearly all infected pressure ulcer cultures yield multiple organisms.

A retrospective study of 168 surgical samples evaluated the microbiology of infected pressure ulcers in 101 spinal cord injury (SCI) patients [9]. The predominant organisms were Enterobacter (29 percent), staphylococci (28 percent), and Enterococcus faecalis (16 percent). In a separate study of pressure ulcer-related bacteremia in SCI patients, the major organisms were staphylococci (including methicillin-resistant Staphylococcus aureus, methicillin-susceptible S. aureus, and coagulase-negative staphylococci), streptococci, Proteus mirabilis, and anaerobes [10].

DETERMINING EXTENT OF INFECTION — Infection occurs when microorganisms invade normal tissues, replicating and overwhelming host immune defenses. The extent of local infection associated with a pressure ulcer ranges from an infection limited to the superficial ulcer base to one with surrounding cellulitis to more extensive involvement of deeper structures (including fascia, muscle, and bone).

A poorly healing superficial ulcer with increased drainage but no surrounding erythema is suggestive of a limited superficial infection of the ulcer base; spreading erythema around an ulcer is suggestive of cellulitis, and a deep ulcer with necrotic muscle, undermined tissue, or sinus tracts is suggestive of a deeper infection of the soft tissue or bone. Clinical assessment should focus on identifying these features. However, the full extent of local infection may not be apparent until surgical debridement when adequate visualization of underlying tissue is achieved.

Determining extent of infection is important since the approach to evaluation and management varies depending on whether infection is superficial or deep (involving either soft tissue or bone). These are outlined below. (See 'Superficial infection' below and 'Soft tissue infection' below and 'Osteomyelitis' below.)

SUPERFICIAL INFECTION — A limited superficial infection of a pressure ulcer typically presents as a poorly healing ulcer, often with increased exudate or wound drainage without associated soft tissue erythema. Systemic manifestations, including fever, chills, and malaise, are not typically seen; if present, they suggest either a deeper local infection or an unrelated infection. The diagnosis of a limited superficial infection in typical practice is based on these clinical features alone.

Management consists of initial local wound care followed by a one- to two-week trial of topical antiseptics to reduce bacterial concentrations in clean pressure ulcers that have failed to heal after two to four weeks of optimal wound care (algorithm 1) [11]. Other fundamental components of local wound care include debridement of necrotic tissue, use of a moist wound dressing, nutritional support, and pressure relief. (See "Clinical staging and management of pressure-induced skin and soft tissue injury".)

Several topical antiseptic agents reduce bacterial counts without damaging the wound, including silver sulfadiazine 1% cream and other silver compounds [12,13]. We typically use silver sulfadiazine. Dressings impregnated with silver, honey, or cadexomer iodine are reasonable alternatives to topical antiseptics. Some other antiseptic agents, including peroxide and chlorhexidine gluconate, are cytotoxic to human fibroblasts, can delay healing, and should not be used [3]. Povidone-iodine or other iodine-containing products are often used, although reports on their potential harm are mixed [14,15]. (See "Basic principles of wound management", section on 'Antiseptics and antimicrobial agents'.)

This approach is consistent with guidelines from the National Pressure Injury Advisory Panel, which emphasize the importance of managing microbial burden [16]. However, evidence supporting the benefit of topical antiseptics is inconclusive, as reflected in a systematic review of 12 trials [14]. Furthermore, a subsequent meta-analysis of 39 studies was unable to determine specific dressings or topical agents that were most likely to heal pressure ulcers, and it was not clear that any were more effective than saline gauze [17].

In some centers, bacterial concentrations in tissue are monitored following debridement and topical antiseptic treatment to confirm the reduction in bacterial burden (eg, tissue concentration of bacteria reduced to <10⁵ colony forming units per gram of tissue).

If there is no clinical improvement with optimal wound care and topical antiseptics, then the wound should be carefully examined, consideration given to other diagnoses, and further workup pursued. This could include a soft tissue biopsy for culture and evaluation for underlying osteomyelitis. (See 'Diagnosis' below.)

Topical antibiotics are generally no longer recommended due to concerns of adverse drug reactions and development of antimicrobial resistance [16].

SOFT TISSUE INFECTION

Clinical features — Soft tissue infection of pressure ulcers often presents with local signs of soft tissue involvement, such as warmth, erythema, induration, local tenderness, purulent discharge, and a foul odor [18]. Findings may vary depending on the depth of infection:

●Cellulitis (ie, infection limited to the epidermis, dermis, and subcutaneous fat) associated with pressure ulcers typically presents as a limited area of erythema, warmth, induration, or tenderness of the surrounding skin or superficial subcutaneous tissue; in some patients, only some of these signs are present. Systemic signs of infection are seen in some cases and include fever, chills, and malaise; in older individuals, mental status changes may be noted. Leukocytosis may also be present.

●Involvement of deeper tissue, such as fascia and muscle, may cause tissue discoloration or frank necrosis. In some cases, there may be extensive necrosis of deep tissue down to bony surfaces with significant exudate. Often there are systemic signs of infection with complicating sepsis in patients with deeper soft tissue infections. Occasionally, changes in the surrounding soft tissue are subtle, but the patient presents with systemic manifestations of infection.

Bloodstream infection is common in patients with sepsis associated with pressure ulcer-related soft tissue infections; in one study, the bloodstream infection rate was as high as 79 percent [19].

Diagnostic evaluation

Clinical suspicion and presumptive diagnosis — Diagnosis of soft tissue infection of a pressure ulcer is based on clinical features and is straightforward in patients with obvious changes (erythema, warmth, induration, fluctuance, tenderness, drainage, or tissue necrosis) in surrounding skin and underlying soft tissue (see 'Clinical features' above). A higher index of suspicion may be necessary in cases where the ulcer and surrounding tissue have not significantly worsened but the patient has symptoms of systemic infection (eg, fever, chills, malaise, mental status changes, leukocytosis) or sepsis. In such cases, the possibility of a pressure ulcer-related infection should be suspected if evaluation does not identify an alternate source of infection. Additional workup involves microbiologic evaluation, as discussed below. (See 'Microbiologic evaluation' below.)

Conversely, exudate alone without additional signs or symptoms of soft tissue or systemic involvement should prompt consideration of a limited, superficial infection that is amenable to local debridement and wound care. (See 'Superficial infection' above.)

Microbiologic evaluation — Identification of causal pathogen(s) with in vitro antimicrobial susceptibility testing are essential to define targeted antibiotic therapy. A limitation of microbiologic evaluation is that it does not distinguish between bacterial invasion and colonization, since all pressure ulcers are colonized with microorganisms. The most useful specimen for culture is a biopsy of the deepest tissue involved, which is usually obtained during debridement of an ulcer. Aspiration of material below the ulcer margin is an alternative specimen source. Once obtained, the specimen should be rapidly transported to the laboratory in appropriate specimen containers for aerobic and anaerobic cultures. Swab cultures should be avoided for clinical management. Blood cultures should be obtained in the initial evaluation of patients who have systemic manifestations of infection.

Deep tissue specimens from a surgically cleaned and debrided ulcer remain the gold standard for wound culture. Although swab culture is frequently used, the results reflect surface colonization rather than infection. In one study, for example, the microbiology of 72 pressure ulcers was assessed by superficial swab, needle aspiration, and deep tissue culture [20]. More swab cultures were positive for microorganisms (96 percent) than either needle aspiration (43 percent) or deep tissue biopsies (63 percent). Microorganisms identified on swab culture most likely represented colonization whereas those from deep tissue biopsies were more likely to be responsible for infection. Additionally, organisms identified on swab culture may not include all infecting pathogens that would warrant appropriate antibiotic coverage. In a retrospective study that included patients who underwent both surgical biopsy and surface swab for culture, almost two-thirds of surgical specimens grew more bacterial species than surface swabs [9].

Other studies have supported the use of needle aspiration as an alternative to deep tissue biopsy. In one study, there was near complete concordance between microorganisms recovered by needle aspiration from below the ulcer margin to those recovered by tissue biopsy from 12 decubitus ulcers from nursing home residents; sensitivity and specificity of aspirate cultures were 93 and 99 percent, respectively [21]. If needle aspiration is performed, local anesthesia should not be used because of its potential antibacterial activity.

Although we do not recommend them, swab cultures are often performed. If swab cultures demonstrate colonization with resistant bacteria, then these results are used to define an optimal empiric antimicrobial treatment regimen (see 'Antibiotic therapy' below). Identification of antimicrobial resistance among swab culture isolates may also be useful in determining whether additional infection prevention and control interventions are needed.

Select radiological imaging — Imaging is not necessary for evaluation of all patients with pressure-ulcer related soft tissue infections. However, in patients with systemic manifestations of infection, positive blood cultures, or indwelling medical devices (eg, cardiac valves, cardiac implantable electronic devices, vascular grafts, prosthetic joints), magnetic resonance imaging (MRI) (or computed tomography, if MRI is not feasible) may be useful in identifying underlying necrotic tissue or abscess requiring debridement that may represent an unrecognized focus of infection [20,21].

Imaging is also warranted when there is suspicion for underlying osteomyelitis. (See 'Clinical suspicion and initial evaluation' below.)

Management — Ulcers complicated by soft tissue infection require systemic antimicrobial therapy in addition to debridement of necrotic tissue.

Debridement — Full debridement of all necrotic tissue is essential to achieve control of associated soft tissue infection. For patients who present with sepsis, surgical debridement should be performed urgently. (See "Basic principles of wound management", section on 'Surgical'.)

Antibiotic therapy — Systemic antimicrobial therapy is warranted in patients with soft tissue infections (beyond a limited, superficial infection) associated with pressure ulcers. When possible, regimen selection should be based upon culture results, ideally cultures of deep tissue obtained at the time of debridement (see 'Microbiologic evaluation' above). Since culture results from debrided tissue are often not immediately available, initial antibiotic therapy is often empiric, with tailoring of antibiotics when results of culture and susceptibility testing become available.

In mild cases of cellulitis (eg, limited erythema of surrounding skin and no systemic signs of infection), a trial of empiric oral antibiotics is a reasonable initial step. Examples of empiric oral regimens include the following (other regimens that have similar spectra of activity are also appropriate):

●Trimethoprim-sulfamethoxazole (2 double-strength tablets every 12 hours) plus

Amoxicillin-clavulanate (875/125 mg every 12 hours)

OR

●Clindamycin (300 to 450 mg every 6 to 8 hours) plus

Ciprofloxacin (500 mg every 12 hours), levofloxacin (500 to 750 mg every 24 hours), or moxifloxacin (400 mg every 24 hours)

In patients with more severe cellulitis and deeper soft tissue infection (eg, involving fascia and muscle) or systemic manifestations of sepsis, we suggest initial empiric therapy with parenteral antibiotics. Examples of empiric parenteral regimens include the following (other regimens that have similar spectra of activity are also appropriate):

●Vancomycin (15 to 20 mg/kg every 8 to 12 hours) or other methicillin-resistant S. aureus (MRSA) active agent (table 1)

PLUS one of the following

●Piperacillin-tazobactam (3.375 g every 6 hours or 4.5 g every 6 to 8 hours) or

●Imipenem (500 mg every 6 hours) or

●Ceftazidime (2 g every 8 hours) plus metronidazole (500 mg every 8 hours)

Since many patients with pressure ulcers live in a hospital, nursing home, or institutional setting, antibiotic-resistant microorganisms are often responsible for their infections. Knowledge of antimicrobial resistance patterns in an institution is important in selecting therapy. Additionally, empiric anti-pseudomonal coverage should be included in patients who have had prior cultures from the ulcer that grew Pseudomonas species. Of the above regimens, those that contain ciprofloxacin (dosed at 750 mg every 12 hours), levofloxacin (dosed at 750 mg every 24 hours), piperacillin-tazobactam (dosed at 4.5 g every 6 hours), imipenem, and ceftazidime provide pseudomonal coverage.

Transition to oral therapy is appropriate when the patient has clinically responded with resolution of systemic signs of infection, regression of surrounding erythema, and improvement in the appearance of soft tissue. In some cases of limited deeper tissue involvement, initial antibiotics may be administered orally in conjunction with tissue debridement. Oral therapy options are outlined above. A lack of timely response to therapy should prompt consideration of requiring debridement and/or a need to alter antibiotics to appropriately target the infecting pathogen(s).

Antibiotics should be tailored when culture and susceptibility results from tissue debridement are available. Data on optimal duration of treatment are limited. It should be based on rate of response, area affected, and whether there was associated bloodstream infection, and is typically 5 to 14 days.

We generally treat skin and soft tissue infections associated with pressure ulcers with broader spectrum antibiotic regimens than routine cellulitis given the polymicrobial nature of these infections. There are no trials evaluating the optimal systemic antibiotic regimen for pressure ulcer-related infection. Based on the microbiology, we typically include empiric coverage for MRSA, streptococci, enteric gram-negative organisms, and anaerobes. For patients with severe infection, we aim to empirically cover more resistant enteric gram-negative organisms because of risk of resistance associated with the health care exposures that most patients with pressure ulcers have. (See 'Microbiology' above.)

OSTEOMYELITIS — Osteomyelitis is a frequent complication of infected pressure ulcers and has been reported in 17 to 32 percent of patients [22,23].

Clinical features — Clinical features of osteomyelitis in the setting of a pressure ulcer are variable and often present with a poorly healing wound. There may be visible bone that may be soft on palpation, with or without associated soft tissue infection. Some patients may present with signs or symptoms of systemic infection (eg, fever, sepsis). However, delayed wound healing is occasionally the only sign of underlying osteomyelitis. The erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) may be elevated, but a low value does not rule out osteomyelitis. Although rare in developed nations where early diagnosis and initiation of antimicrobial therapy in patients with osteomyelitis typically occurs, pathologic fracture can complicate osteomyelitis [24].

Diagnosis

Clinical suspicion and initial evaluation — Osteomyelitis in the setting of pressure ulcers should be suspected when a chronic ulcer fails to heal, has exposed bone, or the patient experiences recurrent soft tissue infections associated with a chronic ulcer. Complications of unrecognized osteomyelitis include flap reconstruction failure, sepsis, and bloodstream infection. As a result, the diagnosis should also be considered in these settings [25]. A complete blood count, ESR, CRP, and blood cultures should be obtained; these results, however, can be normal in patients with biopsy proven osteomyelitis. Positive blood cultures should heighten suspicion of an underlying infection at the ulcer site and can provide microbiologic information to help guide therapy. Abnormal inflammatory markers can support the diagnosis. Nevertheless, patients with clinically suspected osteomyelitis should generally undergo further evaluation with magnetic resonance imaging (MRI). Radiologic findings consistent with osteomyelitis should generally prompt bone biopsy to confirm the diagnosis. (See 'Radiologic imaging' below and 'Bone biopsy' below.)

Although suggestive, exposed bone does not confirm a diagnosis of osteomyelitis in pressure ulcers. Several reports have found that Stage 4 ulcers with exposed bone were consistent with histology-confirmed osteomyelitis in fewer than half of cases, with the rate in one report being as low as 17 percent [22,23,26]. Duration of the ulcer may also not be a reliable indication of an underlying diagnosis of osteomyelitis [22].

A diagnosis of osteomyelitis cannot reliably be made on the basis of clinical findings alone in patients with pressure ulcers. This issue was addressed in a study of 36 patients with pressure ulcers who were evaluated for osteomyelitis [23]. The clinical judgment of clinicians was accurate in diagnosing biopsy-proven osteomyelitis in only 56 percent of patients. There were no clinical signs or symptoms that correlated with a final diagnosis of osteomyelitis, including the presence of fever, bone exposure, duration of the ulcer, purulent drainage, leukocytosis, or elevated ESR.

Radiologic imaging — In patients with suspected osteomyelitis associated with pressure ulcers, we obtain MRI to assess for evidence of bony involvement; imaging can also provide useful anatomic detail in planning for surgical debridement, since it may show abscesses that need drainage. Findings consistent with osteomyelitis on radiographic imaging should generally prompt bone biopsy for histology to confirm the diagnosis and cultures to identify the infecting organism(s) and antibiotic susceptibilities. This is largely the same as the approach to osteomyelitis in general. (See "Nonvertebral osteomyelitis in adults: Clinical manifestations and diagnosis", section on 'Clinical approach'.)

If an MRI is performed and is negative for osteomyelitis, then pursuit of bone biopsy is not necessary; the patient should be evaluated for other factors that could be responsible for a nonhealing ulcer, such as need for alternative wound care management and/or additional debridement.

Use and selection of radiologic imaging studies in the diagnosis of osteomyelitis and radiographic findings indicative of osteomyelitis are discussed separately (see "Approach to imaging modalities in the setting of suspected nonvertebral osteomyelitis"). However, there are specific considerations in making decisions on imaging studies in patients with suspected osteomyelitis related to pressure ulcer:

●Although MRI is the radiologic test of choice for evaluating potential osteomyelitis, and thus is our preferred modality for patients with suspected pressure ulcer-associated osteomyelitis, reports on its accuracy in this setting are varied. One study with 44 paralyzed patients revealed a high sensitivity and specificity of 98 percent and 89 percent, respectively, as compared with bone biopsy [27]; however, another study with 34 patients with 44 pressure ulcers showed a specificity of only 22 percent despite a high sensitivity of 94 percent [28]. This highlights the importance of histologic examination from a bone biopsy to definitively diagnosis pressure ulcer-associated osteomyelitis.

●Plain radiography has a limited role in the diagnosis of pressure ulcer-associated osteomyelitis, since bone changes due to osteomyelitis may not be distinguishable from those due to pressure alone.

Bone biopsy — When osteomyelitis is suspected in patients with pressure ulcers, every effort should be made to obtain a bone biopsy, with histopathologic and microbial analysis in order to confirm the diagnosis of osteomyelitis and guide the selection of antibiotic therapy. No other modality (eg, radiographic study) or clinical feature (eg, exposed bone) can definitively make the diagnosis of osteomyelitis. However, biopsy is not feasible in all patients, and an individualized approach to medical therapy is necessary. In cases where biopsy is not practical or feasible and a preponderance of the clinical and radiologic data is consistent with osteomyelitis, particularly in patients who are frail, treatment based on a presumptive diagnosis of osteomyelitis is appropriate.

The approach to bone biopsy and the histologic findings of osteomyelitis are discussed elsewhere. (See "Nonvertebral osteomyelitis in adults: Clinical manifestations and diagnosis", section on 'Bone biopsy'.)

Management — For pressure ulcers complicated by osteomyelitis, full debridement of all necrotic bone and tissue, treatment with antibiotics targeting the pathogen(s) recovered from bone biopsy (or empiric antibiotic therapy based on likely pathogens), and associated flap coverage, when feasible, are essential components of management.

Debridement and flap coverage of pressure ulcers are discussed elsewhere. (See "Clinical staging and management of pressure-induced skin and soft tissue injury".)

Empiric antibiotic therapy of osteomyelitis associated with pressure ulcer should target similar pathogens as those associated with soft tissue infections of pressure ulcers, specifically methicillin-resistant S. aureus, streptococci, enteric gram-negative organisms, and anaerobes. Antibiotic therapy is typically parenteral; regimens are the same as those outlined above for deep soft tissue infections (see 'Antibiotic therapy' above). Once cultures and sensitivities are available, antibiotics should be tailored to target recovered pathogens. Specific regimens for culture-directed therapy of osteomyelitis associated with pressure ulcers follows the same principles as treatment of chronic osteomyelitis and is discussed in detail elsewhere. (See "Nonvertebral osteomyelitis in adults: Treatment", section on 'Antibiotic therapy'.)

We typically administer at least six weeks of antibiotics therapy for biopsy-proven pressure ulcer-related osteomyelitis; however, some have suggested shorter durations of treatment may be appropriate for osteomyelitis restricted to the superficial bony cortex [29]. If the baseline ESR or CRP is elevated, they may be useful for monitoring the response to therapy. No clinical trial data are available to define the optimal duration of therapy. Although one observational study did not find an association between duration of antibiotics and biopsy proven recurrent infection, the low number of events reduce confidence in the findings [30].

Case series have suggested that long-term cure can be achieved with a combined medical and surgical approach, often with flap coverage of the ulcer. In a retrospective cohort study of 220 patients with sacral osteomyelitis, 39 percent received antibiotics alone, 25 percent were treated with antibiotics and surgical debridement, and 13 percent received a mucocutaneous flap; those patients treated with a combined approach were less likely to be readmitted to the hospital in the following 12 months [31].

Several adjunctive therapies to treat pressure ulcers include negative pressure wound therapy and electrical stimulation and are discussed in detail elsewhere. (See "Clinical staging and management of pressure-induced skin and soft tissue injury", section on 'Adjunctive therapies'.)

OTHER COMPLICATIONS — Patients with pressure ulcers may develop bloodstream infection with or without clinical signs of sepsis (eg, unexplained fever, tachycardia, hypotension, and/or deterioration in mental status). The frequency of bloodstream infection and/or sepsis in patients with pressure ulcers is illustrated by the following retrospective studies in different patient populations:

●In 21 patients with a sepsis syndrome associated with infected pressure ulcers, 16 had documented bloodstream infection [32].

●In 123 episodes of bloodstream infection in a chronic spinal cord injury population, the source was the decubitus ulcer in 21 (17 percent) [10].

●In 44 HIV-infected patients with pressure ulcers, 12 had bloodstream infection; in 6, the source was the pressure ulcer [33].

High mortality rates (29 to 50 percent) have been reported in patients with pressure ulcers and complicating bloodstream infection [10,32,34].

Other infectious complications of pressure ulcers include septic arthritis, endocarditis, and meningitis [27,35].

INFECTION CONTROL — Most pressure ulcers occur in institutionalized patients with spinal cord injuries or nursing home residents. Infection control is important in limiting the spread of resistant microorganisms by cross-contamination, and in reducing colonization and infection rates of pressure ulcers. Recommendations include:

●Follow universal precautions that are appropriate for the health care setting and the patient's condition.

●Use clean gloves for each patient. When treating multiple ulcers on the same patient, attend to the most contaminated ulcer last (eg, in the perianal region). Remove gloves and wash hands between patients.

●Use sterile instruments to debride pressure ulcers.

●Use clean dressings, rather than sterile ones, to treat pressure ulcers, as long as dressing procedures comply with institutional infection control guidelines.

●Clean dressings may also be used in the home setting.

●Special isolation precautions for patients infected or colonized with methicillin-resistant S. aureus, vancomycin-resistant enterococci, or extended spectrum beta-lactamase-producing gram-negative bacilli.

General issues of infection control are discussed in detail elsewhere. (See "Infection prevention: Precautions for preventing transmission of infection" and "Infection prevention: General principles" and "Infection prevention: General principles", section on 'General principles'.)

PREVENTION — The best strategy for preventing infections of pressure ulcers is to prevent formation of the pressure ulcer. This is one of the most important aspects of care of the poorly mobile or immobile patient. Efforts to minimize the extrinsic risk factors of pressure, friction, shear stress, and moisture are pivotal. Health care workers and family members who provide care should be educated on ways to reduce these extrinsic factors [18]. (See "Prevention of pressure-induced skin and soft tissue injury".)

SUMMARY AND RECOMMENDATIONS

●Infections of pressure ulcers are a common problem among debilitated and poorly mobile patients and lead to significant morbidity and prolonged hospital stays. (See 'Introduction' above.)

●Infections of pressure ulcers are typically polymicrobial, and the microbiology is similar in superficial and deep ulcers. The most commonly isolated organisms include staphylococci and streptococci, as well as enterococci, Enterobacter, Proteus, and anaerobes. (See 'Microbiology' above.)

●The extent of local infection associated with a pressure ulcer ranges from an infection limited to the superficial ulcer base to one with surrounding cellulitis to more extensive involvement of deeper structures (including the fascia, muscle, and bone). (See 'Determining extent of infection' above.)

●A limited superficial infection associated with a pressure ulcer typically presents as a poorly healing ulcer and is often associated with increased exudate or wound drainage without associated soft tissue erythema. Management of superficial infection consists of local wound care and a trial of topical antiseptics to reduce bacterial concentrations. (See 'Superficial infection' above.)

●The diagnosis of soft tissue infection (cellulitis or deeper soft tissue infection) of a pressure ulcer is based on clinical features including erythema, warmth, induration, fluctuance, tenderness, drainage, or tissue necrosis. Often, there are systemic signs of infection with complicating sepsis in patients with deeper soft tissue infections. (See 'Clinical suspicion and presumptive diagnosis' above.)

●Systemic antimicrobial therapy is warranted for patients with soft tissue infections (beyond a limited, superficial infection) associated with pressure ulcers in addition to debridement of necrotic tissue. Ideally, culture of deep tissue specimens should be performed at the time of debridement. Initial therapy is typically empiric and tailored when results of culture and susceptibility testing become available. (See 'Management' above.)

●Osteomyelitis in the setting of pressure ulcers should be suspected when a chronic ulcer fails to heal, has exposed bone, or is associated with recurrent soft tissue infections. Occasionally delayed wound healing is the only sign of infection. When osteomyelitis is suspected, we often obtain magnetic resonance imaging to assess for bony involvement and favor bone biopsy, with histopathologic and microbial analysis, to confirm the diagnosis and guide the selection of antibiotic therapy. (See 'Diagnosis' above.)

●Full debridement of necrotic bone and tissue, antibiotic therapy, and associated flap coverage, when feasible, are essential components of management of osteomyelitis complicating pressure ulcers. (See 'Management' above.)

●For empiric antibiotic therapy of cellulitis, deeper soft tissue infection, and osteomyelitis associated with pressure ulcers, we suggest a regimen that is active against methicillin-resistant Staphylococcus aureus, streptococci, enteric gram-negative organisms, and anaerobes (Grade 2C). The patient’s disease severity and individual risk of resistance should also inform the breadth of gram-negative antibiotic coverage. The antibiotic regimen should be tailored to results of culture and susceptibility testing. Duration of treatment depends on the extent of infection, with 5 to 14 days for soft tissue infection and at least 6 weeks for osteomyelitis. (See 'Antibiotic therapy' above.)

●As most pressure ulcers occur in institutionalized patients or nursing home residents, infections with resistant microorganisms is common. Infection control is important in limiting their spread by cross-contamination. Additionally, prevention of the development of pressure ulcers will decrease infection rates and is thus critical to the care of poorly mobile patients. (See 'Infection control' above and 'Prevention' above and "Prevention of pressure-induced skin and soft tissue injury".)