Surgical site infections
Surgical site infections (SSIs) are the most common healthcare-associated infections among surgical patients. It is obviously important to improve patient safety by reducing the occurrence of SSIs. Preventing SSIs is a global priority. Bacteria are becoming increasingly resistant to antibiotics, making SSI prevention even more important nowadays.
SSIs are a major clinical problem in terms of morbidity, mortality, length of hospital stay, and overall direct and not-direct costs worldwide. Despite progress in prevention knowledge, SSIs remain one of the most common adverse events in hospitals. SSI prevention is complex and requires the integration of a range of measures before, during, and after surgery.
Both the World Health Organization (WHO) and the Centers for Disease Control and Prevention (CDC) have recently published guidelines for the prevention of SSIs. The 2016 WHO Global guidelines for the prevention of surgical site infection are evidence-based including systematic reviews presenting additional information in support of actions to improve practice.
The guidelines include 13 recommendations for the pre-operative period, and 16 for preventing infections during and after surgery. They range from simple precautions such as ensuring that patients bathe or shower before surgery, appropriate way for surgical teams to clean their hands, guidance on when to use prophylactic antibiotics, which disinfectants to use before incision, and which sutures to use.
The proposed recommendations are as follows:
“Strong” – Expert panel was confident that benefits outweighed risks, considered to be adaptable for implementation in most (if not all) situations, and patients should receive intervention as course of action.
“Conditional” – Expert panel considered that benefits of intervention probably outweighed the risks; a more structured decision-making process should be undertaken, based on stakeholder consultation and involvement of patients and healthcare professionals.
Importantly, the guidelines recommend that antibiotic prophylaxis should be used to prevent infections before and during surgery only. Antibiotics should not be used after surgery, as is often done. Antibiotic prophylaxis should be administered for operative procedures that have a high rate of postoperative surgical site infection, or when foreign materials are implanted. Antibiotic prophylaxis should be administered within 120 min prior to the incision. However, administration of the first dose of antibiotics is dependent on its pharmacological characteristics. Underlying patient factors may also affect drug disposition (e.g., malnourishment, obesity, cachexia, and renal disease with protein loss may result in suboptimal antibiotic exposure through increased antibiotic clearance in the presence of normal or augmented renal function). Additional antibiotic doses should be administered intraoperatively for procedures > 2–4 h (typically where duration exceeds two half-lives of the antibiotic). There is no evidence to support the use of postoperative antibiotic prophylaxis. The key evidence-based recommendations outlined in these guidelines should be adopted by all healthcare staff that care for surgical patients throughout all stages of that patient’s surgical care.
SSIs are generally classified according to CDC criteria. SSIs are classified as superficial incisional infection, deep incisional infection, and organ space infection. Superficial incisional infections are the most common type of SSIs. Deep incisional and organ/space are the types of SSIs that cause the most morbidity. Organ space infections are not genuine soft-tissue infections.
Incisional SSIs are the results of several factors. All surgical wounds are contaminated by bacteria, but only a minority actually develops clinical infection. Colonization occurs when the bacteria begin to replicate and adhere to the wound site. If the host’s immune response is not sufficient to eliminate or overcome the effects of the bacteria, infection occurs. In most patients, infection does not develop because host defenses are efficient to eliminate colonizers at the surgical site; however, in some patients, host defenses fail to protect them from SSIs. It is well known that surgical trauma increases inflammatory response and counter-regulatory mechanisms. Such regulatory mechanism can decrease postoperative immune response, promoting SSIs.
The pathogens isolated from infections differ, primarily depending on the type of surgical procedure. In clean-contaminated or contaminated surgical procedures, the aerobic and anaerobic pathogens of the normal endogenous microflora of the surgically resected organ are the most frequently isolated pathogens. In clean surgical procedures, in which the gastrointestinal, gynecologic, and respiratory tracts have not been entered, Staphylococcus aureus from the exogenous environment or the patient’s skin flora is the usual cause of infection. Nevertheless, in some specific body areas such as the groin skin could also be colonized by enteric flora. Moreover, it is possible that procedures such as hip prosthesis or vascular bypass, performed on this anatomical region, might eventually be infected by Gram-negative bacteria.
An important determinant of SSI is the integrity of host defenses. Important host factors include the following: age, malnutrition status, diabetes, smoking, obesity, colonization with microorganisms, length of hospital stay or previous hospitalization, shock and hypoxemia, and hypothermia.
It is a common practice to cover surgical wounds with a dressing. The dressing acts as a physical barrier to protect the wound from contamination from the external environment until the wound becomes impermeable to microorganisms.
Postoperative care bundles recommend that surgical dressings be kept undisturbed for a minimum of 48 h after surgery unless leakage occurs. However, there are currently no specific recommendations or guidelines regarding the type of surgical dressing.
The diagnosis of incisional surgical site infection is clinical. Symptoms may include localized erythema, induration, warmth, and pain at the incision site. Purulent wound drainage and separation of the wound may occur. Most patients have systemic signs of infection such as fever and leukocytosis. Information on the microbiological species present in the wound is useful for determining antibiotic choice and predicting response to treatment.
An incisional SSI should be sampled if there is a clinical suspicion of infection. Lack of standardized criteria for diagnostic microbiology of SSIs present a challenge to monitor the global epidemiology of surgical site infection. Emergence of antibiotic resistance has made the management of SSIs difficult. Moreover, rapidly emerging nosocomial pathogens and the problem of multidrug resistance necessitates periodic review of isolation patterns and their sensitivity.
Adequate treatment of incisional SSIs should always include:
- Surgical incision and drainage of abscess.
- Debridement of necrotic tissue, if present.
- Appropriate wound care.
- Resuscitation to improve perfusion when sepsis is present.
- Adequate empiric antibiotic therapy when indicated.
- De-escalation when antibiogram is available.
Incisional SSIs should always be drained, irrigated, and if needed, opened and debrided. If fascial disruption is suspected, drainage should always be performed. Percutaneous drainage, wound irrigation, and negative pressure-assisted wound management are new and effective options that reduce the need for open management of wound infections. In cases where open management is needed, once the infection has cleared, the wound can be closed.
Superficial incisional SSIs that have been opened can usually be managed without antibiotics.
In patients with incisional SSIs with the presence of any systemic inflammatory response criteria or signs of organ failure such as hypotension, oliguria, decreased mental alertness, or in immunocompromised patients, empiric broad-spectrum antibiotic treatment should be started with coverage for Gram-positive cocci and/or the expected flora at the site of operation. Definitive antibiotic treatment is guided by the clinical response of the patient and, when available, results of gram stain, wound culture, and antibiogram
Catheter-acquired urinary infections
Urinary tract infections (UTIs) are the most common hospital-acquired infections. Most UTIs are attributable to use of an indwelling urethral catheter. Catheter-acquired urinary infections (CA-UTIs) have received significantly less attention than other hospital–acquired infections, such as surgical site infections, hospital-acquired/ventilator-associated pneumonia, and bacteremia probably because CA-UTIs present apparent lower morbidity and mortality compared with the other infections, as well as limited financial impact. However, because they are common, their cumulative impact is large.
The indwelling urethral catheter is an essential tool for many hospitalized patients. It is placed for a number of reasons, including output monitoring of unstable patients, voiding management for patients with urethral obstruction, and perioperative use for selected surgical procedures. However it may carry predictable and unavoidable risk of UTI perturbing host defense mechanisms and providing easier access of uropathogens to the bladder. Fortunately, most CA-UTIs are asymptomatic and do not require antimicrobial treatment.
Asymptomatic bacteriuria is defined as culture growth of ≥105 cfu/mL of uropathogenic bacteria in the absence of symptoms compatible with UTI in a patient with indwelling urethral, indwelling suprapubic, or intermittent catheterization.
Symptomatic bacteriuria (urinary tract infection) is defined as culture growth of ≥103colony forming units (cfu)/mL of uropathogenic bacteria in the presence of symptoms or signs compatible with UTI without other identifiable source in a patient with indwelling urethral, indwelling suprapubic, or intermittent catheterization. Compatible symptoms include fever, suprapubic or costovertebral angle tenderness, and otherwise unexplained systemic symptoms such as altered mental status, hypotension, or evidence of a systemic inflammatory response syndrome.
CA-UTI may be extraluminal or intraluminal. Extraluminal infection occurs via entry of bacteria into the bladder along the biofilm that forms around the catheter in the urethra. Intraluminal infection occurs due to urinary stasis because of drainage failure, or due to contamination of the urine collection bag with subsequent ascending infection. Extraluminal is more common than intraluminal infection
The diagnosis of CA-UTI is made by the finding of bacteriuria in a catheterized patient who has signs and symptoms of UTI or systemic infection that are otherwise unexplained.
CA-UTIs are often polymicrobial and may be caused by multi-drug resistant uropathogens. Urine cultures are recommended prior to treatment to confirm that an empirical regimen provides appropriate coverage and to allow tailoring of the regimen on the basis of antimicrobial susceptibility data. Gram-negative organisms predominate in hospital-acquired urinary tract infections, almost all of which are associated with urethral catheterization. After the second day of catheterization, it is estimated that the risk of bacteriuria increases by 5 to 10% per day.
The treatment of CA-UTIs includes antibiotic therapy and catheter management.
Bacteriuria in the absence of symptoms is very common among catheterized patients. Treatment of asymptomatic bacteriuria does not affect patient outcomes and increases the likelihood of emergence of resistant bacteria. Thus, with few exceptions such as immunosuppressed patients, antibiotic treatment for asymptomatic bacteriuria in catheterized patients is not indicated. Removal of the catheter allows resolution of bacteriuria in one third to one half of cases,
Empiric antibiotic therapy for patients with CA- UTI depends on patients’clinical conditions and whether the infection has proceeded beyond the bladder (which we use to distinguish acute complicated UTI from acute uncomplicated cystitis)
Antibiotic selection for both acute complicated UTI and acute uncomplicated cystitis should take into account risk factors for resistant infection (past urine cultures, previous antibiotic therapy, health care exposures and helthcare setting resistance patterns).
Once culture and susceptibility results are available, the antimicrobial regimen should be tailored to the specific organism isolated.
The optimal duration of therapy is uncertain. Seven days is the recommended duration of antimicrobial treatment for patients with CA-UTI who have prompt resolution of symptoms, and 10–14 days of treatment is recommended for those with a delayed response. Oral therapy can be used for some or all of the treatment course if the organism is susceptible and the patient is well enough to take oral medication with adequate absorption.
Patients with CA_UTI who no longer require catheterization should have the catheter removed and receive appropriate antibiotic therapy. Patients who require extended catheterization should be managed by intermittent catheterization, if it is possible. If long term catheterization is needed and intermittent catheterization is not feasible, the catheter should be replaced at the initiation of antibiotic therapy.
The two most important strategies to prevent CA-UTI are not to use a urinary catheter and, if a catheter is necessary, to minimize the duration of use. Catheters should be inserted only when there are valid indications and removed as soon as they are no longer indicated.
Systemic antimicrobial prophylaxis should not be routinely used in patients with short-term or long-term catheterization, including patients who undergo surgical procedures, to reduce CA-bacteriuria or CA-UTI because of concern about selection of antimicrobial resistance.
Best practices for catheter insertion and care may delay infection acquisition and decrease risks of symptomatic infection. These include insertion techniques to minimize contamination and maintaining a closed drainage system to delay catheter colonization.
Catheter-acquired urinary tract infections must be acknowledged as an important patient safety issue, and the indwelling urethral catheter must be treated as an invasive intervention that carries a risk for patients. Attention to limiting catheter use, minimizing duration of use, and supporting optimal practices for catheter care should be implemented worldwide.
Hospital-acquired pneumonia and ventilator-associated pneumonia
Nosocomial pneumonia including hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP) are the second most frequent nosocomial infections and the first in terms of morbidity, mortality, and costs.
In recent years two different sets of guidelines for the management of hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP) were published: 2016 Clinical Practice Guidelines by the Infectious Diseases Society of America (IDSA) and the American Thoracic Society (ATS) and (2017) Guidelines of the European Respiratory Society (ERS), European Society of Intensive Care Medicine (ESICM), European Society of Clinical Microbiology and Infectious Diseases (ESCMID) and Asociación Latinoamericana del Tórax (ALAT).
Nosocomial pneumonia are generally classified into hospital-acquired pneumonia (HAP) and ventilator-associated pneumonia (VAP).
Hospital-acquired pneumonia (HAP) is defined as pneumonia occurring at least 48 hours after hospital admission, excluding any infection incubating at the time of admission.
Ventilator-associated pneumonia (VAP) is defined as a pneumonia occurring in patients under mechanical ventilation for at least 48 hours. It is a frequent issue in intensive care units, with a great impact on morbidity, mortality and cost of care. Treating VAP is a difficult task, as initial antibiotics have to be appropriate and prompt.
The term healthcare-associated pneumonia (HCAP) was included in the previous guidelines to identify patients coming from community settings at risk for multidrug-resistant (MDR) bacteria. HCAP referred to pneumonia acquired in healthcare facilities including nursing homes, hemodialysis centers and outpatient clinics or acquired in patients with previous hospitalization within the past 90 days. However HCAP was not included in recent guidelines because there is increasing evidence that aetiology in HCAP patients is similar to that of community-acquired pneumonia and that many patients with HCAP are not at high risk for MDR bacteria.
The pathogenesis of nosocomial pneumonia is multifactorial. The concomitant illnesses of hospitalized patients is a risk for nosocomial infections. in hospitalized patients alterations in immune function make patients more susceptible to invasive infections that would not occur in healthy individuals. Many hospitalized patients are in poor nutritional status, increasing their risk of infection. Severe illness and hemodynamic compromise are associated with increased rates of nosocomial pneumonia. Aspiration of oropharyngeal secretions may play a significant role in the development of nosocomial pneumonia. In hospitalized patients the combination of alterated immune function, impaired mucocilliary clearance of the respiratory tract and oropharynx colonization by enteric Gram-negative pathogens make aspiration an important contributor to pneumonia. Moreover supine positioning contributes greatly to the aspiration risk.
Risk factors are also prolonged hospital length of stay, cigarette smoking, increasing age, uremia, prior antibiotic exposure, alcohol consumption, endotracheal intubation, coma, major surgery, malnutrition, multiple organ-system failure, and neutropenia. Importantly, the use of stress ulcer prophylaxis, such as proton pump inhibitors commonly used in critically ill patients, is associated with risk of nosocomial pneumonia. Finally, foreign bodies, such as endotracheal and nasogastric tubes, may provide a source for further colonization allowing migration of pathogens to the lower respiratory.
The guidelines recommend obtaining cultures of respiratory secretions and blood cultures from all patients with suspected HAP or VAP in order to guide antibiotic treatment. Noninvasive techniques such as endotracheal aspiration can be done more rapidly than invasive sampling, with fewer complications and resources, however may led to an over-identification of bacteria by initial direct examination of samples. Invasive bronchoscopic techniques such as bronchoalveolar lavage (BAL) or protected specimen brush (PSB) require the participation of qualified clinicians, may compromise gas exchange during the procedure and may be associated with higher direct costs.
Microbiology can be confirmed by both semiquantitative culture results (with growth of microorganism(s) reported as light/few, moderate, or abundant/many) and quantitative culture results (growth thresholds considered significant at 103 colony-forming units [CFU]/mL for PSB or 104 CFU/mL for BAL). However, there is no still consensus in the clinical microbiology community as to whether these specimens should be cultured quantitatively, using the aforementioned designated bacterial cell count to designate infection, or by a semiquantitative approach.
Once HAP or VAP is suspected clinically, antibiotic therapy should be started. In patients with sepsis or septic shock, antibiotics should be started as soon as possible (within 1 hour).
Delaying empiric antibiotic treatment and failing to give an appropriate regimen are both associated with higher mortality rates.
Choice of a specific regimen for empiric therapy should be based on:
· patient’s clinical conditions,
· knowledge of the prevailing pathogens within the healthcare setting
· the individual patient’s risk factors for multidrug resistance.
Knowledge of the predominant bacteria, and particularly their susceptibility patterns, should greatly impact the choice of empiric therapy. Awareness and knowledge of local resistance patterns is critical to decide empiric antibiotic therapy for HAP and VAP.
According to the European guidelines, a narrow-spectrum empiric antibiotic therapy with activity against non-resistant Gram-negative and methicillin-sensitive S. aureus (MSSA) is suggested in low risk patients and early-onset HAP/VAP. Low risk patients are those who present HAP/VAP without septic shock, with no other risk factors for MDR bacteria and those who are not in hospitals with a high background rate of resistant pathogens.
Conversely, broader-spectrum initial empiric therapy covering Gram-negative bacteria and include antibiotic coverage for MRSA is suggested in high-risk patients. High-risk patients are those with septic shock and/or who have the following risk factors for potentially resistant bacteria including hospital settings with high rates of MDR bacteria, previous antibiotic use, recent prolonged hospital stay and previous colonization with MDR bacteria.
The traditional intermittent dosing of each agent for VAP may be replaced with prolonged infusions of certain beta-lactam antibiotics to optimize pharmacokinetic/pharmacodynamic principles, especially in critically ill patients with infections caused by Gram-negative bacilli and overall for those patients with infections caused by Gram-negative bacilli that have elevated but susceptible MICs to the chosen agent.
Longer treatment corse increases the risks of both Clostridium difficile infections and antimicrobial resistance. A 7–8 day course of antibiotic therapy in patients with HAP/VAP without immunodeficiency, cystic fibrosis, empyema, lung abscess, cavitation or necrotising pneumonia and with a good clinical response to therapy is generally suggested. In these patients prolonged regimens do not improve patients outcome.
Central-venous-catheter-related bloodstream infections
About half of nosocomial bloodstream infections occur in intensive care units, and the majority of them are associated with intravascular device. Central-venous-catheter-related bloodstream infections (CRBSIs) are an important cause of healthcare-associated infections.
Central venous catheters (CVCs) are integral to the modern clinical practices and are inserted in critically-ill patients for the administration of fluids, blood products, medication, nutritional solutions, and for hemodynamic monitoring. They are the main source of bacteremia in hospitalized patients and therefore should be used only if they are really necessary.
Risk factors for CRBSI include patient-, catheter-, and operator-related factors. Several factors have been proposed to participate in the pathogenesis of CRBSI.
Hospitalized patients with neutropenia are at high risk. However other host risk factors also include immune deficiencies in general, chronic illness, and malnutrition.
The catheter itself can be involved in 4 different pathogenic pathways:
- colonization of the catheter by microorganisms from the patient’s skin and occasionally the hands of healthcare workers,
- intraluminal or hub contamination,
- secondary seeding from a bloodstream infection, and, rarely,
- administration of contaminated infusate or additives
The diagnosis of CRBSI is often suspected clinically in a patient using a CVC who presents with fever or chills, unexplained hypotension, and no other localizing sign.
Diagnosis of CRBSI requires establishing the presence of bloodstream infection and demonstrating that the infection is related to the catheter.
Blood cultures should not be drawn solely from the catheter port as these are frequently colonized with skin contaminants, thereby increasing the likelihood of a false-positive blood culture
According to IDSA guidelines a definitive diagnosis of CRBSI requires culture of the same organism from both the catheter tip and at least one percutaneous blood culture. Alternatively culture of the same organism from at least two blood samples (one from a catheter hub and the other from a peripheral vein or second lumen) meeting criteria for quantitative blood cultures or differential time to positivity. Most laboratories do not perform quantitative blood cultures, but many laboratories are able to determine differential time to positivity. Quantitative blood cultures demonstrating a colony count from the catheter hub sample ≥3-fold higher than the colony count from the peripheral vein sample (or a second lumen) supports a diagnosis of CRBSI. Differential time to positivity (DTP) refers to growth detected from the catheter hub sample at least two hours before growth detected from the peripheral vein sample.
The CVC and arterial catheter, if present, should be removed and cultured if the patient has unexplained sepsis or erythema overlying the catheter insertion site or purulence at the catheter insertion site.
Antibiotic therapy for catheter-related infection is often initiated empirically. The initial choice of antibiotics will depend on the severity of the patient’s clinical disease, the risk factors for infection, and the likely pathogens associated with the specific intravascular device. Resistance to antibiotic therapy due to biofilm formation also has an important role in the management of bacteremia. In fact the nature of biofilm structure makes micro-organisms difficult to eradicate and confer an inherent resistance to antibiotics.
CRBSIs can be reduced by a range of interventions including closed infusion systems, aseptic technique during insertion and management of the central venous line, early removal of central venous lines and appropriate site selection.
Different measures have been implemented to reduce the risk for CRBSI, including use of maximal barrier, precautions during catheter insertion, effective cutaneous anti-sepsis, and preventive strategies based on inhibiting micro-organisms originating from the skin or catheter hub from adhering to the catheter.
Simultaneous application of multiple recommended best practices to manage CVCs has been associated with significant declines in the rates of CRBSI.
Education, and training of health care workers, and adherence to standardized protocols for insertion and maintenance of intravascular catheters significantly reduced the incidence of catheter-related infections and represent the most important preventive measures.
Clostridium difficile infection
In the last two decades, the dramatic increase in incidence and severity of Clostridium difficile infection (CDI) in many countries worldwide, has made CDI a global public health challenge. CDI may be a particular concern in surgical patients, as surgery may predispose patients to CDI and surgery itself needs to treat severe cases of CDI. Optimization of CDI management in the peri-operative setting, has become increasingly necessary to decrease the cost, morbidity and mortality that may result from CDI.
C. difficile is an anaerobic, spore forming Gram-positive bacillus, which may form part of the normal intestinal microbiota in healthy newborns but which is rarely present in the gut of healthy adults. The organism is spread via the oral-fecal route and in hospitalized patients may be acquired through the ingestion of spores or vegetative bacteria spread to patients by healthcare personnel or from the environment. Since CDI is a toxin mediated infection, toxins negative C. difficile strains are non-pathogenic.
Risk factors for CDI may be divided into three general categories: host factors (immune status, co-morbidities), exposure to C. difficile spores (hospitalizations, community sources, long-term care facilities) and factors that disrupt normal colonic microbiome (antibiotics, other medications, surgery). Risk factors have included, age more than 65 years, comorbidity or underlying conditions, inflammatory bowel diseases, immunodeficiency (including human immunodeficiency virus infection), malnutrition, and low serum albumin level. Patients with inflammatory bowel disease (IBD) are at increased risk of developing CDI, they may have worse outcomes, including higher rates of colectomy, and they experience higher rates of recurrence.
It is well known that antibiotics play a central role in the pathogenesis of CDI, presumably by disruption of the normal gut flora, thereby providing a perfect setting for C. difficile to proliferate and produce toxin. Although nearly all antibiotics have been associated with CDI, clindamycin, third-generation cephalosporins, penicillins and fluoroquinolones have traditionally been considered at greatest risk. A controversial risk factor is related to the exposure to gastric acid-suppressive medications, such as histamine-2 blockers and proton pump inhibitors (PPIs). Recent studies have suggested the association between use of stomach acid–suppressive medications, primarily PPIs, and CDI.
The spectrum of symptomatic CDI ranges from mild diarrhoea to severe disease or fulminant colitis and as many as 30% of patients may develop recurrent CDI. Diarrhea is the hallmark symptom, however, patients may not present with initial symptoms of diarrhea due to colonic dysmotility either from previous underlying conditions or possibly from the disease process itself. Diarrhea may in fact be absent. This is especially important in surgical patients who may have a concomitant ileus. Therefore it is important to have a high index of suspicion. Diarrhea usually may be accompanied by abdominal pain and cramps and if prolonged may result in altered electrolyte balance and dehydration.
Severe forms of the disease are associated with increased abdominal cramping and pain and signs of systemic inflammation, such as fever, leukocytosis, and hypoalbuminemia. Diarrhoea may be absent in some patients with CDI. Sometimes, it may signal the progression of the infection to its fulminant form. The progression to fulminant C. difficile colitis is quite infrequent (1%–3% of all CDI); however, mortality in this group of patients remains high due to the development of toxic megacolon and colonic perforation, peritonitis and septic shock, and subsequent organ dysfunction.
Prompt and precise diagnosis is an important aspect of effective management of CDI. Early identification of CDI allows early treatment and can potentially improve outcomes. Rapid isolation of infected patients is important in controlling the transmission of C. difficile.
This is particularly important in reducing environmental contamination as spores can survive for months in the environment, despite regular use of environmental cleaning agents. Contact (enteric) precautions patients with CDI should be maintained until the resolution of diarrhea, which is demonstrated by passage of formed stool for at least 48 hours. Patients with known or suspected CDI should ideally be placed in a private room with en-suite hand washing and toilet facilities. If a private room is not available, as often occurs, known CDI patients may be cohort nursed in the same area though the theoretical risk of transfection with different strains exists.
Hand hygiene with soap and water and the use of contact precautions along with good cleaning and disinfection of the environment and patient equipment, should be used by all health-care workers contacting any patient with known or suspected CDI. Hand hygiene is a cornerstone of prevention of nosocomial infections, including C. difficile. Alcohol-based hand sanitizers are highly effective against non–spore-forming organisms, but they may not kill C. difficile spores or remove C. difficile from the hands.
The most effective way to remove them from hands is through hand washing with soap and water.
Be aware of your role!