Secondary Logo

Journal Logo

CE

Infection in Acute Care

Evidence for Practice

Houghton, Douglas DNP, APRN, ACNPC, CCRN, FAANP

AJN The American Journal of Nursing: October 2019 - Volume 119 - Issue 10 - p 24–32
doi: 10.1097/01.NAJ.0000586160.03391.82
Feature Articles
Free
CE

ABSTRACT: Infection may be either a cause for admission to an acute care hospital or health care associated, a complication of receiving care for another illness in the acute care environment. In recent years, there has been significant research investigating risk factors for infection in the hospital setting, best practices for diagnosis and treatment, and ways to prevent many health care–associated infections. Multidrug-resistant organisms are a consequence of antibiotic overuse, poor environmental hygiene, and our increasing ability to keep chronically ill patients alive longer through invasive intensive care support. This article reviews the evidence on infection in acute care settings, with a focus on community- and hospital-acquired pneumonia, surgical site infections, and Clostridioides difficile infection. Recommendations for integrating this evidence into nursing practice are offered.

The author reviews the evidence on preventing and treating common infections in acute care settings, focusing on community- and hospital-acquired pneumonia, surgical site infections, and Clostridioides difficile infection.

Douglas Houghton is the director of Advanced Practice Providers at Jackson Memorial Hospital, Miami, FL. Contact author: dhoughton@jhsmiami.org. The author and planners have disclosed no potential conflicts of interest, financial or otherwise.

Infections have afflicted humans since the beginning of recorded history, often with devastating outcomes. An infection may be a cause for admission to an acute care hospital, as in cases of community-acquired pneumonia (CAP). An infection may also be health care associated, a complication of receiving care for another illness in a health care environment, as in cases of hospital-acquired pneumonia (HAP). While medical advances have brought lifesaving treatment for many diseases, such advances have also increased the risk of health care–associated infections (HAIs). The Centers for Disease Control and Prevention (CDC) defines an HAI as an infection diagnosed after admission that wasn't suspected or present at the time of admission.1 The CDC also publishes specific diagnostic surveillance definitions used to collect data on HAIs via the National Healthcare Safety Network.2

This article reviews the evidence for the three most commonly encountered infections in the acute care hospital environment: pneumonia (community acquired and hospital acquired, with the latter including ventilator-associated pneumonia [VAP]), surgical site infection, and gastrointestinal (GI) tract infection with Clostridioides difficile (previously known as Clostridium difficile3). It also offers recommendations for prevention and control. Readers should keep in mind that evidence and recommendations may not apply to special populations such as severely immunocompromised patients, pregnant women, or children.

Back to Top | Article Outline

THE SCOPE OF THE PROBLEM

A CDC survey of HAI prevalence in 2015 among more than 12,000 inpatients found that 3.2% had some type of HAI.4 Compared with results from a prior CDC survey in 2011, this represented a 16% reduction in overall risk of HAI and reflected decreases in the rates of surgical site and urinary tract infections; but the rates of HAP and C. difficile remained unchanged.4 The most common infections identified in the 2015 survey were pneumonia (25.8%); GI tract infection (21.3%), predominantly with C. difficile; and surgical site infections (16.2%). Nearly 24% of all infections were device related, including central line–associated bloodstream infections, catheter-associated urinary tract infections, and VAP. Fortunately, national efforts to strengthen infection prevention programs in hospitals are having positive effects, and the incidence of many types of HAIs has been decreasing steadily in recent years.5 That said, hospitalized patients are often at increased risk for developing infection; this includes patients with immune system deficiencies or who are on immunosuppressive agents, patients with invasive devices, and patients with diabetes, among others.

Figure

Figure

Multidrug-resistant organisms (MDROs). The development of numerous antibiotic agents during the last century resulted in drastic reductions in mortality rates from infection.6 But with the widespread use of these drugs, pathogens of every type have become increasingly resistant to their effects, and MDROs have become prevalent. MDROs can be found in almost every care setting, but they proliferate in acute care settings. Factors that predispose acutely ill patients to acquire MDROs include contact with multiple providers, environmental colonization with MDROs, greater antibiotic exposure, immunosuppression, the use of indwelling devices, the use of mechanical ventilation, hyperlipidemia, history of surgery, older age, and greater susceptibility associated with whatever malady led to acute care admission.7-10 (For more on the role of antibiotics, see Antibiotic Overuse: A Dangerous Trend.11-17)

It is within this complex context that nurses must provide care to patients with infections, whether community acquired or health care associated.

Back to Top | Article Outline

PNEUMONIA

Together with influenza, pneumonia remains the eighth leading cause of death in the United States.18 Despite advances in antibiotic and antiviral therapies, mortality is higher in older populations.19

CAP was recently identified as the sixth leading diagnosis at hospital admission.20 Risk factors include older age; smoking; environmental exposure to toxins (such as certain gases, dust, metals); malnutrition; poor oral health; chronic lung disease; functional impairment; history of CAP within the past two years; and treatment with certain drugs, including immunosuppressive agents, oral steroids, and gastric acid–suppressing agents.21 Presentation can vary greatly. Some people have moderate symptoms of fever, cough, phlegm, and malaise that gradually worsen over time. Others may present with severe dyspnea and hypoxemia, requiring endotracheal intubation and mechanical ventilation. Diagnosis is usually based on clinical symptoms and chest radiography findings, although chest radiography has been found to have low diagnostic sensitivity compared with chest computed tomography (CT).22 Some experts have called for greater use of CT scans in diagnosing CAP.22 For more, see CDC Clinical Definitions for Pneumonia in Adults23 and Community-Acquired Pneumonia: Clinical Severity Scoring Systems.19, 24-30 (It's important to remember that surveillance definitions such as the CDC's differ somewhat from clinical diagnostic criteria.)

Box 1

Box 1

Box 2

Box 2

Identification of specific pathogens often isn't possible because of the difficulty of obtaining adequate specimens, although newer microbiological testing methods show promise. Thus treatment is often based on the likely pathogens and on the presenting level of severity. Most “textbook” lists of pathogens causing CAP begin with Streptococcus pneumoniae and include Chlamydophila, Haemophilus influenzae, Legionella species, Moraxella catarrhalis, Mycoplasma pneumoniae, Staphylococcus aureus, and group A streptococci.19 One recent study analyzed data for more than 2,200 patients for whom there was radiographic evidence of pneumonia and at least one specimen available for both bacterial and viral testing.31 It's worth noting that both human rhinovirus and influenza were detected more often than S. pneumoniae; the researchers suggested that improved “influenza-vaccine uptake and effectiveness” might decrease the incidence of CAP.31

Treatment. Prompt antibiotic therapy in any infectious process improves outcomes. Regimens for CAP vary, depending on the likely pathogen and the level of illness severity. Current guidelines for patients with CAP hospitalized in a non-ICU setting call for either a β-lactam and macrolide combination or a respiratory fluoroquinolone.30 In a randomized crossover trial, Postma and colleagues found β-lactam monotherapy to be “noninferior” to the two aforementioned strategies,32 but this is insufficient evidence to recommend a practice change. And in a study of patients sick enough to be admitted to an ICU, Pereira and colleagues confirmed that combination β-lactam with macrolide therapy resulted in lower in-hospital and six-month mortality rates.33

In patients hospitalized with CAP in an ICU setting, the most recent guidelines jointly issued by the Infectious Diseases Society of America (IDSA) and the American Thoracic Society (ATS) recommend more aggressive therapy.30 In general, treatment with a β-lactam antibiotic plus either azithromycin (Zithromax and others) or a respiratory fluoroquinolone is advised. In cases of community-acquired methicillin-resistant S. aureus (MRSA), vancomycin (Vancocin) or linezolid (Zyvox) should also be added. If Pseudomonas aeruginosa is suspected, treatment with an antipneumococcal, antipseudomonal β-lactam plus other drugs in various combinations is advised.

Patients with CAP should receive antibiotic therapy for at least five days, continuing until the patient has been afebrile for at least 48 hours and has no more than one CAP-associated sign of instability (such as continued need for oxygen therapy or an elevated white blood cell count).30 These discontinuation criteria were recently validated in a study by Uranga and colleagues.34

Box 3

Box 3

In cases of severe CAP and treatment failure, there is some evidence to support the use of adjunctive therapy with corticosteroids.35, 36 But this therapy remains controversial and further research is needed.19

HAP refers to pneumonia that develops during hospitalization. (An older term, health care–associated pneumonia, referred to pneumonia that developed in people who, though not hospitalized, had significant health care contact, such as by receiving dialysis or residing in nursing homes. This term has been removed from the most recent IDSA–ATS guidelines.) Additional risk factors for HAP include being hospitalized for more than 48 hours and being a surgical patient.37 Although VAP also usually develops during hospitalization, it is discussed separately in the literature and in this article.

Treatment. The most significant difference between CAP and HAP is the greater risk hospitalized patients have for the development of MDRO pneumonia.38, 39 Thus, treatment recommendations vary somewhat from those for CAP, and are based on a patient's risk of mortality and MDROs; they are similar to those for VAP, described below. The IDSA–ATS guidelines for HAP strongly recommend antibiotic therapy for seven days in duration, despite a “very low quality” of evidence.39 Shorter courses of therapy for HAP have been studied, but there is insufficient evidence with regard to nonventilated patients in particular to support a change in practice.40

VAP. The CDC defines VAP as a pneumonia that develops when the patient has been on mechanical ventilation for more than two days.23 Additional risk factors for VAP include having suffered major trauma or brain injury.37 Overall, VAP rates have been decreasing.41 This may be owing to a heightened focus on preventive practices such as daily “sedation vacations,” endotracheal tubes with subglottic secretion drainage ports, elevating the head of the bed, early mobility, oral care with chlorhexidine, and more aggressive extubation.42 Nonetheless, clinical surveys indicate that as many as 5% to 15% of patients on ventilators develop pneumonia.42, 43

For diagnostic purposes, noninvasive sampling with semiquantitative cultures is recommended (such as endotracheal suction tube specimens), rather than more invasive methods (such as mini-bronchoalveolar lavage or bronchoscopic specimens).39 The use of clinical scoring systems such as the Clinical Pulmonary Infection Score is not recommended.

Treatment. Many institutions use procalcitonin and C-reactive protein levels to discern the need for antibiotic therapy in cases of suspected infection. But because of insufficient evidence, the current IDSA–ATS guidelines for treating HAP and VAP do not recommend their routine use when considering whether to begin antibiotic therapy.39 This may change (at least for the sickest patients), as a recent meta-analysis of procalcitonin use in guiding antibiotic treatment decisions showed a lower 30-day mortality rate (21.1% versus 23.7%) and a one-day decrease in antibiotic use in the group whose treatment was guided by procalcitonin levels compared with controls.44 Because high procalcitonin levels may also be found in inflammatory processes such as severe trauma, surgery, cardiogenic shock, and autoimmune disease caution must be used in their interpretation.

Treatment for VAP should begin with aggressive empiric antibiotic therapy as soon as VAP is suspected. It should be based on local antibiogram data regarding the prevalence of MDROs in the clinical area and on guideline recommendations. Precise regimens for VAP vary, depending on the likely pathogen and the level of illness severity. At minimum, treatment should include broad-spectrum antibiotics that target S. aureus, P. aeruginosa, and other gram-negative bacteria.39 In areas with greater than 10% prevalence of multidrug-resistant P. aeruginosa, an anti-MRSA agent is also recommended, at least until definitive culture results are obtained. Once such results are in, this broad-spectrum regimen should be scaled back to a more targeted regimen, in order to lower the risk of development of MDROs in both the patient and the clinical environment. The IDSA–ATS guidelines for VAP strongly recommend antibiotic therapy of seven days in duration, based on moderate-quality evidence.39

Prevention and treatment. In summary, evidence-based recommendations for managing hospitalized patients at risk for or who have CAP, HAP, or VAP include the following.19, 30, 39, 42, 45

Treatment.

  • Begin empiric antibiotic therapy quickly, ideally within three hours of initial symptoms.
  • In patients with CAP, use a validated severity scoring method to gauge level of illness and risk of worsening.
  • Use short durations of antibiotic therapy if symptoms resolve (CAP, five days; VAP or HAP, seven days).
  • Choose antibiotics for HAP or VAP based on local data per hospital antibiogram.

Prevention.

  • Keep the head of the patient's bed elevated at 30° or more to prevent aspiration.
  • Use endotracheal tubes with subglottic suction.
  • Encourage early ambulation.
  • Aggressively manage electrolytes and fluid balance and hypoxemia.
  • General infection prevention strategies, such as proper handwashing and encouraging at-risk populations to get the influenza vaccine, are also important.
Back to Top | Article Outline

SURGICAL SITE INFECTIONS

Surgical site infections (SSIs) account for nearly 20% of all HAIs and are associated with significantly longer hospital stays and an increased risk of death.46 Overall, approximately 2% to 5% of patients undergoing surgery are affected.46 But the rate for patients undergoing specific surgeries and facing associated risk factors can vary widely. For example, in a recent study by Sanger and colleagues of 851 patients undergoing abdominal surgeries, 19.6% developed SSIs while recovering in the hospital.47 It's estimated that up to 60% of SSIs are preventable.48

Risk factors may be patient or procedure related, with patient-related factors classified as modifiable or nonmodifiable.46, 48 Modifiable risk factors include alcohol use, smoking, glycemic control (in people with diabetes), obesity, preoperative hypoalbuminemia, and use of immunosuppressive medications. Nonmodifiable factors include age, history of radiotherapy, and recent skin or soft tissue infection. Clinical evidence of SSI may include fever; an elevated white blood cell count; edema, erythema, or excessive pain at the surgical site; wound dehiscence; foul odor; and purulent drainage at the surgical site. It can be initially difficult to distinguish normal postoperative surgical wound appearance from an infected surgical site. Frequent, serial examinations of the site, preferably by the same person, can be helpful. There is evidence supporting daily clinical wound assessment as a significant early predictor of SSI.47

Prevention and treatment. Strategies to prevent SSIs are well documented and supported by several evidence-based professional guidelines.46, 48, 49 These strategies include smoking cessation, glucose control, not shaving the surgical site (clipping only if necessary), and maintaining perioperative normothermia. Antibiotic prophylaxis is recommended only when indicated; when so indicated, it should be administered within one hour of incision with an appropriate agent (within two hours for vancomycin or fluoroquinolones), and should be discontinued within 24 hours of surgery.46, 48, 50

Further recommendations include preoperative bathing with chlorhexidine, perioperative administration of supplemental oxygen for patients undergoing general anesthesia, and consideration of the use of antibiotic sutures for wound closure.46, 49 Although preoperative chlorhexidine bathing is recommended, optimal timing and number of applications remain unclear. Postoperatively, early showering (12 hours after surgery) has not been shown to increase SSI rates.46 The use of wound vacuum therapy is increasingly common in treating SSIs and is recommended for certain wounds.46, 49 But both topical wound antibiotic treatment and the use of silver-containing dressings have shown mixed results in the literature, and neither is routinely recommended by current guidelines.46, 49

Once an SSI is diagnosed, treatment recommendations include opening the wound to allow drainage.51 This involves removing staples or sutures and possible incision and drainage at the site if indicated. Depending on the site and severity of infection, IV or oral antimicrobial treatment may be ordered for some patients, particularly if the patient is immunocompromised or physically weak owing to age or comorbidities.51

In all surgical patients, postoperative monitoring for necrotizing fasciitis is crucial. Patients most at risk are those who have diabetes, are immunocompromised, or have suffered traumatic wounds.52 Clinical findings suggestive of necrotizing fasciitis include excessive pain or tenderness (disproportionate to what is usual for a given surgery), fever, soft-tissue edema, and skin bullae or necrosis. Imaging may show gas in the tissues (suggestive of group A streptococcal infection), although the absence of gas doesn't rule out necrotizing fasciitis. If necrotizing fasciitis is suspected, immediate consultation with a surgeon experienced with this infection is warranted, as open surgical inspection and biopsy are the most definitive means of diagnosing and treating the infection.

Back to Top | Article Outline

GI INFECTION: C. DIFFICILE

Incidence rates of C. difficile infection (CDI) have steadily and dramatically risen during the past 20 years in both community and inpatient populations. One surveillance study showed a near doubling of such rates in hospitalized adults between 2001 and 2010, from 4.5 to 8.2 cases per 1,000 patient discharges.53 Although estimates vary, CDIs reportedly account for 15.5% to 21.3% of HAIs3, 4 and cause from 14,000 to 29,000 deaths annually.54, 55 Multiple recurrences of CDI are common in both inpatient and community settings.54, 56

The top three risk factors for CDI are antibiotic use, exposure to the organism, and serious comorbidities; other factors include GI surgery or manipulation (such as colonoscopy), immunocompromise, longer lengths of stay, older age, and proton pump inhibitor use.54, 57, 58 Risk factors for recurrence include chronic kidney disease; female sex; nursing home residency; and the use of antibiotics, proton pump inhibitors, or corticosteroids within 90 days of CDI diagnosis.54

Diagnosis of CDI should involve use of a multistep testing algorithm. The current guidelines, jointly issued by the IDSA and the Society for Healthcare Epidemiology of America (SHEA), recommend testing patients who have three or more unformed stools in 24 hours with no laxative use.59 Screening proceeds by following a testing algorithm, often first testing for glutamate dehydrogenase, which is an enzyme produced by all strains of C. difficile. This test has a high negative predictive value60; thus, if the result is negative, no further testing is needed. If the result is positive, this should be confirmed with either a toxin test or a nucleic acid amplification test, such as the polymerase chain reaction test.59 For an evidence-based testing algorithm, see Figure 1.59

Figure 1

Figure 1

Prevention and treatment. As soon as CDI is suspected, it is appropriate to institute contact precautions and conduct room disinfection with a sporicidal cleaning product, according to the IDSA–SHEA guidelines.59 For routine use, either soap and water or alcohol-based hand rubs or sanitizers are acceptable for hand hygiene. During outbreaks or in hyperendemic settings, staff should use soap and running water with vigorous rubbing to remove any spores present, although the quality of supporting evidence is low. Once a patient is discharged or if contact precautions are discontinued, terminal cleaning of the room and equipment are recommended. Adjunctive disinfection methods such as with ultraviolet light may be helpful. Contact precautions may be discontinued once the patient has at least 48 hours without diarrhea, but institutions with higher rates of CDI should continue using contact precautions until the patient is discharged.

Treatment of CDI previously consisted of oral or IV metronidazole (Flagyl); newer data support the use of oral vancomycin or fidaxomicin (Dificid) instead.59 Severe infection should be treated with oral vancomycin. If ileus is present or if absorption is questionable owing to poor gut function, the recommended treatment is vancomycin per rectum along with IV metronidazole.

A recent large study of patients with CDI who were treated with either vancomycin or metronidazole found no difference in risk of recurrence between the groups; but in cases of severe CDI, the risk of 30-day mortality was significantly lower among those who received vancomycin.56 The IDSA–SHEA guidelines recommend treating recurrences aggressively with one of three options: a prolonged “taper and pulse” course of vancomycin; a 10-day course of fidaxomicin; or, if metronidazole was used initially, a 10-day course of vancomycin.59

Back to Top | Article Outline

NURSING IMPLICATIONS

Given the profound effects that HAIs can have on patient outcomes and health care costs, it's clear that infection prevention and control measures are paramount. Good antibiotic stewardship has been associated with decreased incidences of and colonization by many MDROs, including gram-negative bacteria and MRSA, as well as a lower incidence of CDI,61 and should be routine practice in every setting. Nurses in clinical practice can contribute to HAI prevention and control in the following ways.

  • Promote good antibiotic stewardship. Encourage daily medical team review of the need for any antibiotics the patient is receiving and discuss the potential for deescalation to the most narrow-spectrum agent that would be effective.
  • Practice and preach good hygiene and contact precautions. Wash hands before and after each patient or environmental contact. Maintain strict contact precautions for those patients who are infected or colonized with MDROs or C. difficile. Keep long hair contained. Adhere to the evidence-based practice recommendations described above, and continue learning about infection prevention.
  • Promote a clean patient environment. Encourage leadership to consider the use of adjunctive environmental cleaning methods such as ultraviolet light.
  • Recognize and report early symptoms of infection to the medical team.
  • Support the patient's nutritional status with enteral nutrition as soon as feasible.

Improving patient outcomes and decreasing infection rates require a multidisciplinary approach with strong leadership support, impeccable nursing assessment and care, and adherence to evidence-based guidelines for medical treatment.

Back to Top | Article Outline

REFERENCES

1. Horan TC, et al CDC/NHSN surveillance definition of health care-associated infection and criteria for specific types of infections in the acute care setting. Am J Infect Control 2008;36(5):309–32.
2. National Healthcare Safety Network. Chapter 17. CDC/NHSN surveillance definitions for specific types of infections. Atlanta: Centers for Disease Control and Prevention; 2019 Jan. NHSN patient safety component manual; https://www.cdc.gov/nhsn/pdfs/pscmanual/pcsmanual_current.pdf.
3. Lawson PA, et al Reclassification of Clostridium difficile as Clostridioides difficile (Hall and O'Toole 1935) Prevot 1938. Anaerobe 2016;40:95–9.
4. Magill SS, et al Changes in prevalence of health care-associated infections in U.S. hospitals. N Engl J Med 2018;379(18):1732–44.
5. Centers for Disease Control and Prevention. 2016 National and state healthcare-associated infections progress report. Atlanta; 2016. Current HAI progress report; https://www.cdc.gov/hai/data/portal/progress-report.html.
6. Friedman ND, et al The negative impact of antibiotic resistance. Clin Microbiol Infect 2016;22(5):416–22.
7. Labricciosa FM, et al Epidemiology and risk factors for isolation of multi-drug-resistant organisms in patients with complicated intra-abdominal infections. Surg Infect (Larchmt) 2018;19(3):264–72.
8. Lat I, et al A multicenter, prospective, observational study to determine predictive factors for multidrug-resistant pneumonia in critically Iill adults: the DEFINE study. Pharmacotherapy 2018.
    9. Magira EE, et al Multi-drug resistant organism infections in a medical ICU: association to clinical features and impact upon outcome. Med Intensiva 2018;42(4):225–34.
      10. Mody L, et al Prevalence of and risk factors for multidrug-resistant Acinetobacter baumannii colonization among high-risk nursing home residents. Infect Control Hosp Epidemiol 2015;36(10):1155–62.
      11. Linder JA, et al Non-visit-based and non-infection-related ambulatory antibiotic prescribing [conference abstract]. Open Forum Infect Dis 2018;5(suppl 1):S43.
      12. Baggs J, et al Estimating national trends in inpatient antibiotic use among US hospitals from 2006 to 2012. JAMA Intern Med 2016;176(11):1639–48.
        13. Centers for Disease Control and Prevention. Antibiotic prescribing and use in hospitals and long-term care. 2017. https://www.cdc.gov/antibiotic-use/healthcare/index.html.
          14. Klein EY, et al Global increase and geographic convergence in antibiotic consumption between 2000 and 2015. Proc Natl Acad Sci U S A 2018;115(15):E3463–E3470.
            15. Centers for Disease Control and Prevention. Antibiotic resistance threats in the United States, 2013. Atlanta; 2013 Apr. https://www.cdc.gov/drugresistance/pdf/ar-threats-2013-508.pdf.
              16. Thorpe KE, et al Antibiotic-resistant infection treatment costs have doubled since 2002, now exceeding $2 billion annually. Health Aff (Millwood) 2018;37(4):662–9.
                17. Tamma PD, et al Association of adverse events with antibiotic use in hospitalized patients. JAMA Intern Med 2017;177(9):1308–15.
                18. Heron M. Deaths: leading causes for 2016. Natl Vital Stat Rep 2018;67(6):1–77.
                19. Wunderink RG, Waterer G. Advances in the causes and management of community acquired pneumonia in adults. BMJ 2017;358:j2471.
                20. McDermott KW, et al. Trends in hospital inpatient stays in the United States, 2005-2014. Rockville, MD: Healthcare Cost and Utilization Project (HCUP), Agency for Healthcare Research and Quality; 2017 Jun. HCUP statistical brief # 225; https://www.hcup-us.ahrq.gov/reports/statbriefs/sb225-Inpatient-US-Stays-Trends.jsp.
                21. Almirall J, et al Risk factors for community-acquired pneumonia in adults: a systematic review of observational studies. Respiration 2017;94(3):299–311.
                22. Claessens YE, et al Early chest computed tomography scan to assist diagnosis and guide treatment decision for suspected community-acquired pneumonia. Am J Respir Crit Care Med 2015;192(8):974–82.
                23. National Healthcare Safety Network. Chapter 6. Pneumonia (ventilator-associated [VAP] and non-ventilator-associated pneumonia [PNEU]) event. Atlanta: Centers for Disease Control and Prevention; 2019 Jan. NHSN patient safety component manual; https://www.cdc.gov/nhsn/pdfs/pscmanual/pcsmanual_current.pdf.
                24. Lim WS, et al Defining community acquired pneumonia severity on presentation to hospital: an international derivation and validation study. Thorax 2003;58(5):377–82.
                25. Liu JL, et al Expanded CURB-65: a new score system predicts severity of community-acquired pneumonia with superior efficiency. Sci Rep 2016;6:22911.
                  26. Fine MJ, et al A prediction rule to identify low-risk patients with community-acquired pneumonia. N Engl J Med 1997;336(4):243–50.
                    27. Charles PG, et al SMART-COP: a tool for predicting the need for intensive respiratory or vasopressor support in community-acquired pneumonia. Clin Infect Dis 2008;47(3):375–84.
                      28. Ehsanpoor B, et al Validity of SMART-COP score in prognosis and severity of community acquired pneumonia in the emergency department. Am J Emerg Med 2018 Oct 21 [Epub ahead of print].
                        29. Lim HF, et al IDSA/ATS minor criteria aid pre-intensive care unit resuscitation in severe community-acquired pneumonia. Eur Respir J 2014;43(3):852–62.
                          30. Mandell LA, et al Infectious Diseases Society of America/American Thoracic Society consensus guidelines on the management of community-acquired pneumonia in adults. Clin Infect Dis 2007;44 Suppl 2:S27–S72.
                          31. Jain S, et al Community-acquired pneumonia requiring hospitalization among U.S. adults. N Engl J Med 2015;373(5):415–27.
                          32. Postma DF, et al Antibiotic treatment strategies for community-acquired pneumonia in adults. N Engl J Med 2015;372(14):1312–23.
                          33. Pereira JM, et al Impact of antibiotic therapy in severe community-acquired pneumonia: data from the Infauci study. J Crit Care 2018;43:183–9.
                          34. Uranga A, et al Duration of antibiotic treatment in community-acquired pneumonia: a multicenter randomized clinical trial. JAMA Intern Med 2016;176(9):1257–65.
                          35. Chen LP, et al Efficacy and safety of glucocorticoids in the treatment of community-acquired pneumonia: a meta-analysis of randomized controlled trials. World J Emerg Med 2015;6(3):172–8.
                          36. Torres A, et al Effect of corticosteroids on treatment failure among hospitalized patients with severe community-acquired pneumonia and high inflammatory response: a randomized clinical trial. JAMA 2015;313(7):677–86.
                          37. Torres A, et al International ERS/ESICM/ESCMID/ALAT guidelines for the management of hospital-acquired pneumonia and ventilator-associated pneumonia: guidelines for the management of hospital-acquired pneumonia (HAP)/ventilator-associated pneumonia (VAP) of the European Respiratory Society (ERS), European Society of Intensive Care Medicine (ESICM), European Society of Clinical Microbiology and Infectious Diseases (ESCMID) and Asociacion Latinoamericana del Torax (ALAT). Eur Respir J 2017;50(3).
                          38. Ekren PK, et al Evaluation of the 2016 Infectious Diseases Society of America/American Thoracic Society guideline criteria for risk of multidrug-resistant pathogens in patients with hospital-acquired and ventilator-associated pneumonia in the ICU. Am J Respir Crit Care Med 2018;197(6):826–30.
                          39. Kalil AC, et al Management of adults with hospital-acquired and ventilator-associated pneumonia: 2016 clinical practice guidelines by the Infectious Diseases Society of America and the American Thoracic Society. Clin Infect Dis 2016;63(5):e61–e111.
                          40. Sandoval CP. Short-course versus prolonged-course antibiotic therapy for hospital-acquired pneumonia in critically ill adults. Crit Care Nurse 2016;36(4):82–3.
                          41. Skrupky LP, et al A comparison of ventilator-associated pneumonia rates as identified according to the National Healthcare Safety Network and American College of Chest Physicians criteria. Crit Care Med 2012;40(1):281–4.
                          42. Klompas M, et al Strategies to prevent ventilator-associated pneumonia in acute care hospitals: 2014 update. Infect Control Hosp Epidemiol 2014;35(8):915–36.
                          43. Metersky ML, et al Trend in ventilator-associated pneumonia rates between 2005 and 2013. JAMA 2016;316(22):2427–9.
                          44. Wirz Y, et al Effect of procalcitonin-guided antibiotic treatment on clinical outcomes in intensive care unit patients with infection and sepsis patients: a patient-level meta-analysis of randomized trials. Crit Care 2018;22(1):191.
                          45. Damas P, et al Prevention of ventilator-associated pneumonia and ventilator-associated conditions: a randomized controlled trial with subglottic secretion suctioning. Crit Care Med 2015;43(1):22–30.
                          46. Ban KA, et al American College of Surgeons and Surgical Infection Society: surgical site infection guidelines, 2016 update. J Am Coll Surg 2017;224(1):59–74.
                          47. Sanger PC, et al A prognostic model of surgical site infection using daily clinical wound assessment. J Am Coll Surg 2016;223(2):259–70.e2.
                          48. Anderson DJ, et al Strategies to prevent surgical site infections in acute care hospitals: 2014 update. Infect Control Hosp Epidemiol 2014;35(6):605–27.
                          49. Berríos-Torres SI, et al Centers for Disease Control and Prevention guideline for the prevention of surgical site infection, 2017. JAMA Surg 2017;152(8):784–91.
                          50. Bratzler DW, et al Antimicrobial prophylaxis for surgery: an advisory statement from the National Surgical Infection Prevention Project. Clin Infect Dis 2004;38(12):1706–15.
                          51. Stevens DL, et al Practice guidelines for the diagnosis and management of skin and soft tissue infections: 2014 update by the Infectious Diseases Society of America. Clin Infect Dis 2014;59(2):e10–e52.
                          52. Stevens DL, Bryant AE. Necrotizing soft-tissue infections. N Engl J Med 2017;377(23):2253–65.
                          53. Reveles KR, et al The rise in Clostridium difficile infection incidence among hospitalized adults in the United States: 2001-2010. Am J Infect Control 2014;42(10):1028–32.
                          54. Ma GK, et al Increasing incidence of multiply recurrent Clostridium difficile infection in the United States: a cohort study. Ann Intern Med 2017;167(3):152–8.
                          55. Palli SR, et al Cost drivers associated with Clostridium difficile-associated diarrhea in a hospital setting. J Clin Outcomes Manag 2015;22(3):111–20.
                          56. Stevens VW, et al Comparative effectiveness of vancomycin and metronidazole for the prevention of recurrence and death in patients with Clostridium difficile infection. JAMA Intern Med 2017;177(4):546–53.
                          57. Centers for Disease Control and Prevention. FAQs for clinicians about C. diff. 2018 https://www.cdc.gov/cdiff/clinicians/faq.html.
                          58. Surawicz CM, et al Guidelines for diagnosis, treatment, and prevention of Clostridium difficile infections. Am J Gastroenterol 2013;108(4):478–98.
                          59. McDonald LC, et al Clinical practice guidelines for Clostridium difficile infection in adults and children: 2017 update by the Infectious Diseases Society of America (IDSA) and Society for Healthcare Epidemiology of America (SHEA). Clin Infect Dis 2018;66(7):e1–e48.
                          60. Crobach MJ, et al European Society of Clinical Microbiology and Infectious Diseases: update of the diagnostic guidance document for Clostridium difficile infection. Clin Microbiol Infect 2016;22 Suppl 4:S63–S81.
                          61. Baur D, et al Effect of antibiotic stewardship on the incidence of infection and colonisation with antibiotic-resistant bacteria and Clostridium difficile infection: a systematic review and meta-analysis. Lancet Infect Dis 2017;17(9):990–1001.

                          For 56 additional continuing nursing education activities on the topic of preventing hospital-acquired infections, go to www.nursingcenter.com/ce.

                          Keywords:

                          Clostridioides difficile; community-acquired pneumonia; health care–associated infection; hospital-acquired pneumonia; multidrug-resistant organisms; surgical site infection; ventilator-associated pneumonia

                          Copyright © 2019 Wolters Kluwer Health, Inc. All rights reserved.