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HCAIs, particularly those acquired in a critical care setting contribute significantly to morbidity and mortality, and health care costs. Critically ill patients have more comorbid diagnoses and higher severity of acute illness making them particularly susceptible to new infections while hospitalized. Indwelling catheters and increasing prevalence of multidrug-resistant (MDR) pathogens add to the risk and negative consequences of HCAIs. One in 20 patients acquires a HCAI while receiving medical care.1 The most frequent HCAIs include bloodstream infections (BSIs), VAPs, infections with C difficile, SSIs, and CAUTIs.
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Bloodstream Infections
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BSIs or bacteremias remain common in hospitalized patients both within the intensive care units (ICUs) and in hospital wards. About 90% of these BSIs are associated with a catheter in the bloodstream, usually a central line.2 CRBSIs are considered a preventable cause of morbidity and mortality and are a target of interventions aimed at improving quality of health care and cost-effectiveness.
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Risk Factors and microbiology
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Central lines are at risk for infection both during the process of insertion and subsequent access and maintenance. Factors associated with a lower incidence of CRBSIs include the following:
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Optimal catheter site selection (subclavian vs internal jugular, or femoral veins)
Use of proper hand hygiene
Maximal barrier precautions at the time of insertion
Chlorhexidine skin antisepsis, use of chlorhexidine-impregnated dressings, or use of catheters coated with antiseptic or antimicrobials
Tunneled insertion
Catheter site care and limited manipulation of the catheter
Daily review of line necessity and prompt removal of unnecessary lines
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Gram-positive aerobes are the most frequently isolated pathogens from the bloodstream of hospitalized patients. Coagulase-negative staphylococci and S aureus account for just over half of all nosocomial bacteremias (51%). Candida species and enterococci were each responsible for 9% of BSIs. Gram-negative bacteria, including many MDR species, accounted for most of the remainder.3
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Certain patient populations are at increased risk of CRBSIs and may have greater susceptibility to microbial pathogens not commonly responsible for infections otherwise. Patients receiving intravenous hyperalimentation or high concentrations of glucose via a central line are particularly susceptible to fungal infections especially Candida species. Gram-positive aerobes are the most commonly isolated pathogens from the bloodstream of patients who receive hemodialysis. Immunocompromised hosts, especially those who are neutropenic or receiving chemotherapy may translocate microbes from their gut into the bloodstream and therefore have a disproportionately high rate of infection with gram-negative bacilli. Burn victims are particularly susceptible to infections due to Pseudomonas species.
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The diagnosis of CRBSI is based on clinical criteria and microbiological confirmation. The clinical symptoms and signs of CRBSI can be protean and need not include typical indicators of infection such as fever, especially in critically ill patients. A high degree of suspicion should be maintained in a patient with a central line and clinical changes. Positive blood cultures in the absence of other identifiable source of infection suggest a CRBSI. Proper specimen collection prior to initiation of antimicrobial therapy and repeat sampling can help increase the yield of microbial cultures. Positive cultures taken from a peripheral site have the highest specificity; cultures drawn from the catheter have a high false-positive rate but excellent negative predictive value.
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Once CRBSI is confirmed, the treatment is focused on catheter management and antimicrobial treatment. In critically ill patients with a CRBSI and signs of sepsis or hemodynamic instability, the catheter should be removed promptly. Additionally, clinical practice guidelines recommend catheter removal if there is endocarditis or persistent bacteremia after 72 hours of appropriate antibiotic treatment, or fungemia.4 Catheter removal is also recommended in cases of infection with most organisms encountered in critical care settings: S aureus, gram-negative bacilli (including Pseudomonas), mycobacteria, and low-virulence organisms such as Bacillus species or Propionibacterium.
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Infrequently, salvage of long-term catheters with systemic antimicrobial therapy with or without an antibiotic lock may be attempted if none of the criteria for removal are met. Similarly, in a patient without sepsis or hemodynamic instability, a catheter may be exchanged over a guidewire if the risks of catheter reinsertion are considered to be unacceptably high. However, it is important to note that the success rate of these strategies is low and unpredictable and the data supporting catheter exchange are sparse and present only in small, uncontrolled studies.
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Empiric antimicrobial therapy for CRBSIs usually includes antibiotics to cover resistant gram-positive organisms including S aureus, such as vancomycin. Additionally, empiric therapy should be tailored to the patient, based on host risk factors and susceptibility to certain infections as discussed earlier. Antimicrobial therapy should be reassessed and narrowed based on microbiological profile as soon as culture results are available.
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Typical duration of antimicrobial therapy in uncomplicated CRBSI is 10 to 14 days from the first day blood cultures turned negative. In suspected or confirmed endocarditis, treatment is usually continued for 4 to 6 weeks.
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Follow-Up and Outcomes
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After initiation of antimicrobial therapy, patients with BSIs should be followed closely and monitored with surveillance cultures until the bacteremia or fungemia resolves. Persistently positive cultures or lack of clinical improvement should prompt investigation of the causes of treatment failure: inappropriate antimicrobial therapy, failure to remove the catheter, or development of an associated complication such as a persistent secondary source of infection or a septic focus, endocarditis, or suppurative thrombophlebitis.
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CRBSIs are associated with increased hospital length of stay and costs and have an associated mortality of 25%.5 Every effort should be made to prevent CRBSIs.
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Hospital-acquired pneumonia (HAP) is defined as a pneumonia that occurs 48 hours or more after hospital admission that did not exist at the time of admission. VAP is defined as a pneumonia that occurs 48 hours after intubation and institution of mechanical ventilation. Health care–associated pneumonia (HCAP) includes pneumonia that occurs within 48 hours of hospital admission in patients who were hospitalized for 2 or more days within 90 days of the infection, or resided in a nursing home or long-term care facility, or received recent intravenous antibiotic therapy, chemotherapy or wound care within the past 30 days, or attended a hospital or hemodialysis clinic. Ventilator-associated event (VAE) is a recent surveillance definition developed by the Centers for Disease Control and Prevention (CDC) to create a more objective and systematic way of measuring VAPs. VAEs may not represent true clinical VAPs. In the VAE algorithm there are sequential tiers. The first tier is ventilator-associated condition (VAC) defined as an increase in the fraction of inspired oxygen (FIO2) of 0.20 for 2 or more days or an increase in positive end-expiratory pressure (PEEP) of greater than or equal to 3 cm H2O for 2 days after 2 or more days of stable or decreasing daily minimal values. Tier two is infection-related ventilator-associated condition (IVAC) which includes VAC plus a temperature greater than 38°C or less than 36°C or white blood cell count greater than or equal to 12,000 or less than or equal to 4000 cells/mm3, and initiation of a new antimicrobial agent that is continued for 4 or more days. The third tier is for patients that meet the IVAC definition and have purulent secretions (defined as ≥ 25 neutrophils and ≤ 10 squamous epithelial cells per low power field) or have a positive sputum or other specimen culture, for a designation of possible VAP. Qualification as a probable VAP does not allow use of sputum, instead the patient must have purulent secretions and a positive quantitative or semiquantitative aspirate or lavage or biopsy, or in the absence of purulent secretions, a positive pleural culture, lung pathology, or diagnostic serology for virus or Legionella.6 Note that the CDC VAE definitions exclude chest radiographs due to their subjectivity and variability in their technique, interpretation, and reporting.
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HAP is the second most common nosocomial infection in the United States and accounts for up to 16% of all hospital-acquired infections (HAIs) and up to 27% of HAIs in the ICU.7 HAPs can increase hospital stays up to 9 days and cost as much as $40,000 per patient. VAP can occur in 9% to 26% of all intubated patients. Attributable mortality ranges from 0% to 50%. In 2002, an estimated 250,000 HAPs developed in US hospitals and 36,000 of these were associated with deaths.6 Major risk factors for HAP include age more than 70, underlying chronic lung disease, immunosuppression, prolonged intubation, enteral feeding, and prior thoracoabdominal surgery.
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The common causes of VAPs are microaspiration of oropharyngeal organisms, inhalation of aerosols containing bacteria, infected biofilm in the endotracheal tube with subsequent embolization to the distal airways, and less commonly hematogenous spread via infected intravenous catheters and gut translocation. Aspiration is the most common cause of HAP and VAP in hospitalized patients with risks that are often increased due to intubation, sedation, and bacterial colonization of the oropharynx with gram-negative organisms. Intubated patients are at the highest risk for VAP due to the common use of sedation, reduced cough, and the leakage of oropharyngeal contents and organisms around the high volume, low-pressure cuffs of the endotracheal tube, as well as the formation of a biofilm and subsequent colonization with bacteria. The risk of pneumonia increases each day the patient is intubated and can be as high as 3% for the first 5 days, 2% from days 5 to 10, and 1% per day afterward. The most common causes for HAP/HCAP/VAP are aerobic gram-negative bacilli such as P aeruginosa, K pneumoniae, and Acinetobacter species and less commonly gram-positive organisms such as S aureus. Anaerobes are an uncommon cause of VAP. Early-onset VAP occurs within 96 hours of admission, is usually caused by antibiotic-sensitive bacteria, and has a more favorable prognosis. Late-onset VAP occurs after 96 of ICU admission and is commonly caused by MDR pathogens. Risk factors for MDR pathogens include immunosuppression, prior antibiotic use, HCAP risk factors, and high frequency of resistance in the community or hospital unit.
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The diagnosis of HAP or VAP can be challenging. The clinical approach includes a chest radiograph that shows a new infiltrate plus at least 2 of the following features: temperature greater than 38°C or less than 36°C, leukocytosis greater than 12,000 or leukopenia less than 4000 cells/mm3, and purulent secretions. As opposed to the VAE surveillance criteria, chest radiographs are clinically recommended to assess for the severity of pneumonia (such as multilobar involvement), and to detect complications like pleural effusion, cavitation, and pneumothorax. Given the high sensitivity but very low specificity of this approach as well as the emergence of more MDR pathogens and the polymicrobial nature of HAPs and VAPs, the search for the causative organism(s) should be attempted with blood cultures and semiquantitative sputum cultures prior to the start of empiric antibiotics. Furthermore, if available and logistically possible the ideal approach is a quantitative sampling of the lower respiratory tract with an endotracheal aspirate, bronchoalveolar lavage (BAL), or protected brush sampling. The diagnostic thresholds for BAL are 104 to 105 CFU/mL, and for protected brush sample 103 CFU/mL. A diagnostic thoracentesis should be performed if the pleural effusion is large or if the patient appears toxic. The Clinical Pulmonary Infection Score (CPIS) includes temperature, white blood cell count, tracheal secretions, oxygenation (PaO2/FIO2), chest radiography, and microbiological data. A score of greater than or equal to 6 suggests pneumonia and a score less than 6 suggests that antibiotics can be safely discontinued. However, due to the overall low sensitivity and specificity of the CPIS it has not been widely used clinically to diagnose VAP. Procalcitonin (PCT) is a biomarker that has been studied in hospitalized as well as outpatients to help diagnose sepsis and pneumonia. It has shown to have a high specificity for bacterial infections rather than for viral infections. Unfortunately, PCT is elevated in many noninfectious inflammatory disorders such as burns, major surgery, trauma, and pancreatitis, as well as sepsis from any etiology. The use of PCT in the critically ill has yet to be fully realized. There is data suggesting that a very low or a significant decrease in PCT levels can allow for safe and earlier discontinuation of antibiotics.
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The key decision in the initial empiric antimicrobial treatment of patients with VAP or HAP rests on whether the patient has risk factors for MDR pathogens. If patients have the previously mentioned risk factors or if they have been intubated or in the hospital for more than 96 hours, coverage for MDR pathogens is required. Several studies have showed an increase in mortality by 2- to 3-fold if inappropriate or delayed (> 24 hours) antibiotics are given. The American Thoracic Society/Infectious Diseases Society of America guidelines published in 2005 can help with the initial choice of antimicrobial agents and are shown in Table 40–1.
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General strategies that have been found to influence the risk of VAP include active surveillance for VAP. The Institute for Healthcare Improvement (IHI) endorses the ventilator bundle checklist. Although not all the elements are aimed at VAP prevention, it represents the best practices for patients on mechanical ventilation. The elements include keeping the head of the bed elevated 30° to 45°, daily sedation interruption and assessment of readiness to extubate, daily oral care with chlorhexidine, peptic ulcer disease prophylaxis, and deep venous thrombosis prophylaxis. Another essential element is the emphasis on adherence to the hand hygiene guidelines. Other strategies that appear helpful include using standardized weaning protocols, using noninvasive positive pressure ventilation (NIPPV) whenever possible, educating the staff about VAP prevention, using subglottic drainage (shown to decrease early-onset VAP),8 changing the ventilator circuit only when visibly soiled or malfunctioning, using a closed in-line suctioning system, and avoiding nasotracheal intubation (which may result is sinusitis that will increase the risk of VAP). However, the most important element of all is the implementation strategy. For such a strategy to be effective it is important to have complete buy-in and accountability of the senior clinical and administrative leadership on the importance of VAP prevention, education of the staff, monitoring of practice, and feedback to all staff on the outcomes, risk factors, and local epidemiology. It is essential to measure the occurrence of VAP as well as compliance with performance measures such as adherence to the ventilator bundle elements and hand hygiene.9 A checklist is not enough; there must be cultural (adaptive) change to effect true change in practice.
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Infection With C Difficile
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C difficile is the most commonly reported nosocomial pathogen and causes about 12% of HCAIs.10 The spectrum of disease caused by C difficile can range from an asymptomatic carrier state to varying severity of colitis with diarrhea. Both the incidence and severity of C difficile infections (CDIs) have increased dramatically since the late 1990s. In North America, the overall incidence of CDI went up 5-fold and the attributable mortality rate has increased 4-fold. Those above the age of 65 are particularly susceptible and the incidence of CDI in the elderly increased 8-fold.11 In the United States alone, an estimated 500,000 cases of CDI occur annually and about 15,000 to 20,000 patients die from CDI each year.5
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The single greatest risk factor for CDI is antibiotic use. Antibiotics disrupt the natural flora in the gut, and this along with high resistance of C difficile to the most commonly used antibiotic agents allows C difficile to proliferate and CDI to occur. The risk of CDI is higher with the use of multiple antibiotics, broader-spectrum agents, and longer duration of therapy. Almost all antibiotics have been associated with CDI but the risk is highest with clindamycin, broad-spectrum cephalosporins, and fluoroquinolones. Notably, fluoroquinolone resistance of the NAP1/BI/027 strain is believed to be an important factor in the increased virulence of C difficile.
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Patients above the age of 65 are at increased risk of severe CDI. Use of gastric acid suppressants (proton pump inhibitors and H2 receptor blockers) is also a possible risk factor for CDI. Immunosuppressive agents such as methotrexate and the presence of chronic inflammatory bowel disease have also been associated with CDI. Hospitalization or residence in a long-term care facility bring together multiple risk factors for CDI and are therefore responsible for almost all the cases.
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C difficile can cause a wide range of disease in patients: at one end is asymptomatic infection in a silent carrier state, and at the other end, fulminant disease associated with severe sepsis and death.
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Asymptomatic carriage: About 20% to 30% of hospitalized patients and 50% of residents of long-term care facilities are silent carriers of C difficile. They have no symptoms but serve as a reservoir of infection and can play an important role in transmission of C difficile.12
C difficile diarrhea (CDAD): This presents as antibiotic-associated diarrhea and is one of the most frequent manifestations of CDI. Systemic symptoms such as fever and leukocytosis are less frequent.
C difficile colitis: This is a more severe form of CDAD and presents with high-volume watery, foul-smelling diarrhea with fever and leukocytosis. Pseudomembranes are not seen.
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Pseudomembranous colitis: Diarrhea is more severe and may progress to a protein-losing enteropathy. Fever and leukocytosis are common. Pseudomembranes are seen on sigmoidoscopy.
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Fulminant colitis: This is the most serious, life-threatening form of CDI occurring in about 3% of patients. Prolonged ileus, toxic megacolon, colonic perforation, severe sepsis, and death may occur. Diarrhea may be much less prominent due to ileus.
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CDI should be suspected in any patient with diarrhea and antibiotic exposure or another risk factor. Different methods for laboratory confirmation of CDI are available. A cytotoxin assay that detects the cell toxicity of toxin B is considered the gold standard with a sensitivity of 67% to 100% and a specificity of 85% to 100%.13 It is a tissue culture test and results can take up to 3 days.
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An enzyme-linked immunosorbent assay (ELISA) is also available. While the ELISA is rapid and can provide results within a few hours, it has a relatively low sensitivity (75%-85%) but a high specificity (95%-100%); thus false-negative results are not infrequent.13 C difficile can be isolated in anaerobic stool culture but cannot distinguish between toxigenic and nontoxigenic strains. Molecular methods such as polymerase chain reaction (PCR) are rapid and sensitive tests for detection of C difficile that are being increasingly used.
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First-line treatment is based on the severity of CDI. Oral metronidazole is the initial treatment recommended for mild and moderate CDI. Oral vancomycin is superior to metronidazole for treatment for severe CDI. For patients with the most severe form of disease, or complications such as ileus or toxic megacolon, current guidelines recommend treatment with a combination of oral vancomycin and intravenous metronidazole. Surgery with colectomy may be needed as a lifesaving measure in extreme cases. Many newer approaches and antimicrobial agents for the treatment of CDI are under development but none are recommended for routine use at this time. Studies of probiotics aimed at restoring normal gut flora are inconclusive for treatment of CDI. Supportive care and management of fluid status and electrolytes are important adjuncts to treatment of CDI. Antibiotics that may have contributed to the development of CDI should be stopped as soon as possible.
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Twenty percent of patients with one episode of CDI develop recurrent infection and 60% of those who have had 2 episodes will develop recurrence. About half of the recurrences are due to new infections and not relapses per se. Persistence of risk factors for CDI and depletion of normal gut flora contribute to recurrence. The first recurrence is treated in a manner similar to the initial episode with metronidazole and/or vancomycin based on the severity of illness. Further recurrences may benefit from a prolonged taper of oral vancomycin. Fecal transplant can help restore normal flora and may be effective in the management of recurrent CDI.
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Prevention of CDI involves measures targeted at the individual patient and other interventions designed to prevent the spread of C difficile spores within the hospital environment. Judicious use of antibiotics and avoidance of high-risk agents can help reduce the incidence of CDI. Acid suppressants should only be used when clearly indicated.
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On a broader scale, containment of C difficile infections within hospital and health care facilities is essential to prevent spread between patients. C difficile is transmitted when spores infect patients via the fecal-oral route. The spores can be transferred between patents via equipment or the hands of health care providers. Rapid and reliable detection of CDI is critical to early isolation of infected patients. Contact precautions with the use of gowns and gloves for all visitors and health care providers should be strictly enforced. Hand washing with soap and water is essential after caring for a patient with CDI since commonly used antimicrobial hand gels are ineffective against spores of C difficile. These spores are hardy and resistant to desiccation, chemicals, and extremes of temperatures. They can survive on surfaces for months. Environmental decontamination should be diligently performed to prevent transmission of CDI.
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Surgical Site Infections
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SSIs are a very common cause of HCAIs. From 2007 to 2010, SSIs accounted for approximately 23% of all HCAIs.14 More than 5% of all surgical patients acquire an SSI and many (40%-60%) are preventable.15 SSIs are classified as being either incisional or organ/space infections. Incisional SSIs are further divided into those involving only skin and subcutaneous tissue (superficial incisional SSI) and those involving deeper soft tissues of the incision (deep incisional SSI). Organ/space SSIs involve any part of the anatomy that was opened or manipulated during an operation, other than incised body wall layers.
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S aureus, coagulase-negative staphylococci, Enterococcus spp., and Escherichia coli remain the most frequently isolated pathogens. An increasing proportion of SSIs are caused by MDR pathogens, such as methicillin-resistant S aureus (MRSA), or by Candida albicans.
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Microbial contamination of the surgical site is a necessary precursor of SSI. The risk of SSI can be conceptualized according to the following relationship16:
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Quantitatively, if a surgical site is contaminated with greater than 105 microorganisms per gram of tissue, the risk of SSI is markedly increased. However, the dose of contaminating microorganisms required to produce infection may be much lower when foreign material is present at the site (ie, 100 staphylococci per gram of tissue introduced on silk sutures).
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SSIs are associated with considerable morbidity with over one-third of postoperative deaths related, at least in part, to SSIs. SSIs can double the length of time a patient stays in the hospital and thereby can increase the cost of health care.
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Essential processes for prevention of SSIs are core measures in the Surgical Care Improvement Project: Hospital Compare Hospital Quality Initiatives.17 The essential elements of the SSI bundle18 are appropriate use of prophylactic antibiotics; appropriate hair removal, controlled postoperative serum glucose in patients after cardiac surgery, and immediate postoperative normothermia in patients with colorectal surgery.
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It is important to standardize the administration process of delivering prophylaxis so that antibiotics can consistently be given within 1 hour prior to incision. Overuse, underuse, improper timing, and misuse of antibiotics occurs in 25% to 50% of operations. A large number of hospitalized patients develop infections caused by C difficile and inappropriate use of broad-spectrum antibiotics or prolonged courses of prophylactic antibiotics puts all patients at risk of developing antibiotic-resistant pathogens.
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Avoid hair removal unless necessary for the procedure. Razors should never be used and generally shaving should be avoided before surgery. When necessary, hair should be removed with clippers right before surgery—but not in the operating room itself.
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Tight glucose control is important in patients who undergo cardiac surgery. Note that “glucose control” here is defined as serum glucose levels below 200 mg/dL, collected at or closest to 6:00 AM on each of the first 2 postoperative days.
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The literature indicates that patients undergoing colorectal surgery have a decreased risk of SSI and other complications if they are not allowed to become hypothermic during the perioperative period.19
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The CDC recommends the following practices as those with the best evidence to minimize the risk of SSIs:
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Whenever possible, identify and treat all infections remote to the surgical site before elective operation and postpone elective operations on patients with remote site infections until the infection has resolved.
Encourage tobacco cessation. At a minimum, instruct patients to abstain for at least 30 days before elective operation from smoking cigarettes, cigars, pipes, or any other form of tobacco consumption.
Require patients to shower or bathe with an antiseptic agent on at least the night before the operative day.
Thoroughly wash and clean at and around the incision site to remove gross contamination before performing antiseptic skin preparation.
Keep nails short and do not wear artificial nails.
Perform a preoperative surgical scrub for at least 2 to 5 minutes using an appropriate antiseptic and scrub the hands and forearms up to the elbows.
Protect an incision that has been closed primarily with a sterile dressing for 24 to 48 hours postoperatively.
Provide positive pressure ventilation in the operating room with at least 15 air changes per hour, of which 3 should be of fresh air.
Keep the operating rooms' doors closed and minimize traffic.
Sterilize all surgical instruments according to published guidelines. Perform flash sterilization only for patient care items that will be used immediately (eg, to reprocess an inadvertently dropped instrument). Do not use flash sterilization for reasons of convenience, as an alternative to purchasing additional instrument sets, or to save time.
Wear a surgical mask that fully covers the mouth and nose when entering the operating room if an operation is about to begin or already under way, or if sterile instruments are exposed. Wear the mask throughout the operation.
Wear a cap or hood to fully cover hair on the head and face when entering the operating room.
Handle tissue gently, maintain effective hemostasis, minimize devitalized tissue and foreign bodies (ie, sutures, charred tissues, necrotic debris), and eradicate dead space at the surgical site.
Use delayed primary skin closure or leave an incision open to heal by second intention if the surgeon considers the surgical site to be heavily contaminated.
Obtain cultures and exclude from duty, surgical personnel who have draining skin lesions until infection has been ruled, out or personnel have received adequate therapy and infection has resolved.
If drainage is necessary, use a closed suction drain. Place a drain through a separate incision distant from the operative incision. Remove the drain as soon as possible.
Report appropriately stratified operation-specific, SSI rates to surgical team members. The optimum frequency and format for such rate computations will be determined by stratified caseload sizes (denominators) and the objectives of local, continuous quality improvement initiatives.
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Many of these elements have been incorporated in a systemic fashion using the surgical checklist. There have been studies that use a before-and-after methodology demonstrating the effectiveness of a surgical checklist. In 2009, Haynes and Gawande reported the effective use of a 19-item checklist in 8 countries in reducing mortality by 46%, complications by 36%, and SSIs by 45%.20 To date there have been few randomized trials that have shown benefits of surgical checklists. The most recent clustered randomized trial was a study of 2 Norwegian hospitals and more than 4000 operations, where complications dropped 42% and length of stay was reduced by 0.8 days with the use of a surgical checklist. Mortality did not change significantly.21 The value of the checklists and their elements are based on the best evidence we have to date, but their implementation may be the key to minimizing surgical complications including SSIs.
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Catheter-Associated Urinary Tract Infections
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CAUTIs are extremely common and costly complications in hospitalized patients. CAUTIs are the most common type of HCAI accounting for more than 30% of all hospital infections. An estimated 13,000 deaths are associated with UTIs each year.5 According to the CDC, 75% of UTIs are catheter associated, and 15% to 25% of patients receive a urinary catheter during their hospital stay.22 In the ICU, the incidence of CAUTIs can range from 3.1 to 7.4 per 1000 urinary catheter days.23 Over $340 million is estimated to be spent in health care costs attributable to CAUTIs in the United States each year.24 As of October 1, 2008, the Centers for Medicare and Medicaid Services (CMS) no longer reimburse hospitals for the additional costs for caring for patients with CAUTI and consider CAUTI a “reasonably preventable” infection. Since the single most significant risk factor for a CAUTI is the prolonged use of the urinary catheter, the overriding principle for the prevention of CAUTIs is to minimize any unnecessary catheters by employing systems that ensure that patients have an acceptable indication for a urinary catheter and that catheters are removed as soon as possible.
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Appropriate indications for the use of indwelling urinary catheters include urinary tract obstruction, neurogenic bladder dysfunction and urinary retention, and urologic studies or surgery on contiguous structures. Additionally, urinary catheter use is considered appropriate in patients with urinary incontinence and stage III or IV sacral pressure ulcers, as well as for end-of-life care.23 Other indications for the placement of a urinary catheter in critically ill patient on mechanical ventilation include sepsis (for the first 24 hours), acute respiratory distress syndrome on continuous sedation or who require paralytic agents, continuous renal replacement therapy, acute renal failure, use of vasopressors with titration, temperature management systems, intra-aortic balloon pump, and subarachnoid hemorrhage with triple-H therapy (hypertension, hypervolemia, and hemodilution). Other strategies that are thought to be effective in reducing catheter use and thereby preventing infection include the routine use of a bladder scan to help caregivers identify patients who have urinary obstruction, daily review of the necessity of the urinary catheter, proper insertion technique and maintenance, and decision support tools (both electronic or with paper stop order sets) that are either nurse initiated or nurse prompted to ensure early removal of unnecessary urinary catheters.
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In 2007, The Michigan Health and Hospital Association Keystone Center implemented a statewide initiative to reduce unnecessary urinary catheters. The initiative was based on nurse-led multidisciplinary rounds with the use of the “bladder bundle” to aid in the prompt removal of catheters. The efforts lead to a 45% reduction in inappropriate catheter use. The key elements of the “bladder bundle” include the following25:
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Nurse-initiated urinary catheter discontinuation protocol
Urinary catheter reminders and removal prompts
Alternatives to indwelling urinary catheterization (such a condom catheters)
Portable bladder ultrasound monitoring
Insertion care and maintenance
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Unfortunately, data from the CDC's National Healthcare Safety Network (NHSN) reveal that CAUTI rates remain high. There are many possible reasons for this; priority is given to other infections such as VAP, CRBSI, and SSI, and the morbidity and mortality of CAUTI is underappreciated. Most hospitals in the United States do not have a program for CAUTI surveillance, education, or adopt any of the previously mentioned prevention strategies.26
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In 2013, the federal government released The National and State Healthcare-Associated Infections Progress Report revealing a 3% increase in CAUTIs between 2009 and 2012.27 At the 2013 Action Planning Conference, a document proposing new targets for the prevention of HAIs was identified in the National Action Plan to Prevent Healthcare-Associated Infections (HAI): Road Map to Elimination. One of the proposal's goals was to reduce CAUTIs in ICU and ward patients. Based on the CDC's NHSN data, the proposed 2020 target is a 25% reduction from the 2015 baseline.28